The Fellow on Call

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This week, we kick off a new series, this time focusing on follicular lymphoma! This series will build on a lot of fundamentals that we discussed in our prior series. In this first episode, we start with an introduction to how to approach management of this disease.

Episode contents:

What is the best approach to biopsy?
What is the differential for CD10+ cells on flow?
How is follicular lymphoma classified?
What is the workup for a new suspected FL?

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This week, we round out our discussion we started in our prior episode on APLS, this time focusing on management. Stick around until the end to hear Dan and Vivek battle it out about the optimal time to recommend APLS testing for your patients!

If you have not done so already, we highly recommend you check out episode 134 (diagnosis of APLS) prior to jumping into this one!

Episode contents:

What is the best choice of anticoagulant?
Is a higher INR better for warfarin?
Are DOACs acceptable options?
What is the optimal time to send APLS testing?

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This week, we continue our series focusing on venous thromboembolism. In this episode, we begin our discussion of antiphospholipid syndrome.

Episode contents:

What is "antiphospholipid antibody syndrome"?
How do we make this diagnosis?
What is the optimal time to test for these antibodies?

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This week, we discuss another set of high yield topic for anyone who cares for patients on anticoagulation - how to safely hold anticoagulation prior to a procedure and how to reverse the effects of the drug in the even of an emergent situation. We discuss our approach to how we discuss this with our patients and our medical colleagues! Dan also shares his dotphrases for your reference!

Episode contents:

How do we approach peri-operative anticoagulation management? When do we hold? How long do we hold? Do they need bridging? No bridging?
In the case of a severe bleed, how do we reverse the effects of anticoagulation?

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This week, we talk all about hypercoagulable testing - a very common referral in outpatient hematology. Who do we consider testing on? Who should we encourage not to test? We discuss this and more here.

Episode contents:

What are situations in which to consider hypercoaguable testing?
What are situations to avoid doing so?

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This week, we kick off a new, highly-anticipated and highly-requested series, covering venous thromboembolism (VTE). In this first episode, we discuss how we make the initial diagnosis and how we approach initial management. As a clinician, you will undoubtedly come across the need to make this decision. This episode and this series will set you up for success!

Episode contents:

-What is venous thromboembolism?

How do we diagnose patients with VTE?
How do we initially management patients with VTE?
How do we select anticoagulants for VTE?

****This episode is sponsored by our Global Research Partners! Get paid to participate in market research surveys: https://affiliatepanel.members-only.online/FOC_24?utm_campaign=FOC&utm_source=email&utm_medium=email

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This week, we welcome Dr. Amar Kishan to our show to discuss the role of radiation oncology in the management of patients with testicular cancer. As our listeners know by now, the management of patients with testicular cancer spans multiple specialities. We always appreciate hearing from our colleagues about their perspective.

Episode contents:

What are important studies to send to radiation oncology prior to their appointment?
How radiation is planned for seminoma patients and a discussion of the treatment course
Implications on spermatogenesis, organ function, and infertility
Role of proton therapy?
Emerging therapies

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This week, we talk all about disseminated testicular cancer, highlighting our current treatment modalities and why we do what we do. We also cover refractory disease. This episode builds on our prior discussions in Parts 1 and 2, so be sure to check these out if you haven’t already!

Episode contents:

A history lesson about how we developed our current risk stratification model
Our current treatment paradigms and regimens for disseminated seminoma and non-seminoma
To resect or not to resect?
How we approach relapsed/refractory disease

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This week, we continue on our testicular cancer journey, focusing on Stage 1 and 2 disease. If you haven’t done so, we highly recommend checking out Episode 127 for our overview of this disease!

Episode contents:

What it the approach to stage 1 seminoma and non-seminoa? Radiation? Chemotherapy? Surgery?
What about stage 2 disease?
What are the pivotal trials that shape today's treatment landscape?

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It’s time for another new series, this time focusing on Testicular Cancer. In this first episode, we lay the foundation for our future discussions and discuss the basics of Testicular Cancer.

Episode contents:

What are germ cell tumors?
What are important tumor markers to monitor for germ cell tumors?
Seminoma vs. Non-seminoma
Staging of germ cell tumors
Overview of management

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This week, we round out our AML series with a detailed discussion about the approach to management of relapsed and refractory disease. This has been a VERY long road going through all management of AML. We hope that you have continued to build on our discussions week-to-week. An exciting treatment paradigm that is ever-evolving!

Episode contents:

How do we define primary induction failure in AML?
What are options for treatment of refractory disease? What is the mechanism of action of these treatment options?
What are options for relapsed disease?
What targeted therapies are available for relapsed AML?

****This episode is sponsored by our global research partners! Get paid to participate in market research surveys: https://affiliatepanel.members-only.online/FOC_24?utm_campaign=FOC&utm_source=email&utm_medium=email

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In today’s episode, we discuss how to approach AML treatment for patients who are unfit for intensive therapy.

Episode contents:

How do we assess fitness for intensive AML?
What are options for patients who are unfit for intensive chemotherapy for AML?
What are important genetic mutations are important to check for?
What are the key trials that inform our management in this space?
How do we dose venetoclax?
How do we sequence the available agents?

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In today’s episode, we welcome back Dr. Amar Kelkar for part 2 of our two-part discussion on allogeneic transplant. In this episode, we build on our prior discussion regarding transplant, this time focusing on transplant for the treatment of AML.

Episode contents:

What are the different conditioning regimens available?
How do we decide which regimen is optimal for our patients?
What is the role of MRD testing?
What is the role of maintenance therapy post-transplant?
What are treatment options for GVHD?
A discussion on racial disparities in transplant

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** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In today’s episode, we welcome back Dr. Amar Kelkar for part 1 of our two-part discussion on allogeneic transplant. In this episode, we discuss the fundamental approach to patient selection and stem cell source selection. As you all know from this series, allogeneic transplants play a pivotal role in the management of AML. Dr. Kelkar’s pearls of wisdom help make this confusing topic so much more approachable!

Episode contents:

What factors do we incorporate when considering a patient for allogeneic transplant?
How do we use HLA-matching?
What are the pros and cons of the different sources of stem cells?

****Get paid to participate in market research surveys: https://affiliatepanel.members-only.online/FOC_24?utm_campaign=FOC&utm_source=email&utm_medium=email

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This week, we continue our series focusing on acute myeloid leukemia. In this episode, we talk about maintenance therapies in AML.

Episode contents:

A recap of cytarabine consolidation
Why do we do maintenance therapy?
What are hypomethylating agents and how do they work?
Important targeted agents that play a role in maintenance therapy

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we continue our discussion on consolidation and maintenance therapies for AML, this time highlighting the role of allogeneic stem cell transplants. This episode builds on our prior episode, so if you have not listened to this just yet, we highly recommend doing so!

Episode contents:

A recap on approach to AML consolidation
The role of allogeneic transplants
The role of MRD testing in AML management

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This week, we move to our next phases of therapy for AML, which are consolidation and maintenance. Be sure to check out our prior episodes for a discussion on initial workup and how we incorporate recurrent genetic abnormalities into how we think about AML. Check out figure 1 from this paper for a helpful diagram!

Episode contents:

A recap on approach to AML treatment
Who do we consider for allogeneic transplant?
What are common therapy-related AML cytogenetic abnormalities to be aware of?
How do we approach consolidation? Role of G-CSF?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we round out our discussion regarding AML induction, this time focusing on the treatment options in the first line setting. We go through the various options, the dosing strategies, and the data behind them.

Be sure to check out parts one and two of this three-part induction discussion, as we continue to build on these concepts! Also, if you have not done so, please do check out our hemepath series to ensure you can more easily follow along with this conversation!

Episode contents:

What are our options for upfront induction therapy?
How do we select patients for the "add-ons" to induction therapy?
What is the data behind these options?

****This episode is sponsored by our Global Research Partners! Have some time and want to make some extra money? Get paid to participate in market research surveys: https://affiliatepanel.members-only.online/FOC_24?utm_campaign=FOC&utm_source=email&utm_medium=email

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In this week’s episode, we continue onto part two of our three-part discussion on AML induction, this week focusing on selecting our up-front regimen.

Be sure to check out last week’s episode, as this one builds on that one. Also, if you have not done so, please do check out our hemepath series to ensure you can more easily follow along with this conversation!

Episode contents:

What is "7+3"?
How do we pick our approach to management?
Do we ever add anything else to our induction back bone?

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In this week’s episode, we start our three-part discussion on AML induction, this week focusing on key definitions and an overview of treatment. Also, if you have not done so, please do check out our hemepath series to ensure you can more easily follow along with this conversation!

Episode contents:

What are "blasts"?
If there is concern for AML, then what?
Role of leukapheresis or cytoreduction
Diagnostic workup
Risk stratification
Approach to treatment

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this week’s episode, we discuss the diagnostic criteria and risk stratification for myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), building on our discussion from last week. Also, if you have not done so, please do check out our hemepath series to ensure you can more easily follow along with this conversation!

Episode contents:

A review of what to look at on the bone marrow biopsy report
WHO and ICC classification for AML and MDS
Disease-defining cytogenetic markers to be aware of and their prognostic implications

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we kick off a new series focusing on myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). In this first episode, we discuss the alphabet soup of premalignant hematologic conditions including CHIP, CCUS, and ICUS, before moving onto MDS and AML in future episodes.

Episode contents:

What is CHIP vs. CCUS vs. ICUS?
What is the mechanism of hematopoiesis?
What is clonality?
What is a variant allele frequency?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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By popular demand, our next series that we are excited to share with you is on MDS/AML! As we prepare for the release of the first episode next week, let’s throw it back to Episode 019 in our Heme/Onc Emergencies Series and talk about APL!

Episode contents:

How do we diagnose APL?
What are characteristic findings of APL?
What is the acute management of this disease?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we have an INCREDIBLE episode for you. We welcome Titilope Fasipe, MD, PhD, who not only is the Co-Director of the Sickle Cell and Thalassemia Program at Texas Children’s and an Assistant Professor in the Department of Pediatrics at the Baylor College of Medicine, she herself also has sickle cell disease! Dr. Fasipe takes us through her life story, from childhood to now. Conducting this interview was such an eye-opening experience for us, and we hope that her message resonates with you when you care for your patients with sickle cell disease.

Contents:

What it is like growing up with sickle cell disease?
Pearls to ensure that our practice provides excellent care for our patients with SCD
Important resources when caring for patients

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this week’s episode, we discuss the management of sickle cell disease in the chronic setting. This is a follow up to episode 111 where we discussed acute management of SCD. And furthermore, this is also in addition to our prior discussion about long-term chronic complications from SCD in episode 110. We highly recommend checking out these prior episodes if you haven’t done so already!

Contents:

Use of hydroxyurea in SCD management
Newer adjunctive therapies for SCD management
Perioperative management

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In this week’s episode, we discuss the management of acute complications of sickle cell disease including acute pain episodes and acute chest syndrome as well as a discussion of hyperhemolytic syndrome.

Contents:

How to manage patients with sickle cell disease presenting for acute pain crises
How to approach management of acute chest syndrome
What is hyperhemolytic crisis?
What is splenic and hepatic sequestration syndrome?

**This episode is sponsored by our global research partners! Have some time and want to make some extra money? Get paid to participate in market research surveys: https://affiliatepanel.members-only.online/FOC_24?utm_campaign=FOC&utm_source=email&utm_medium=email

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In this week’s episode, we discuss chronic complications that can arise in patients with sickle cell disease. The reality is, that unless we have an outpatient clinic or rotate through an outpatient clinic, there is a small chance that we will come across many of these issues. However, screening for and managing these chronic complications can have significant implications on our patients’ lives.

Contents:

What are the current screening guidelines for sickle cell disease complications?
What are key studies in pediatric SCD management?
Management of stroke, avascular necrosis, pain, pulmonary hypertension, kidney disease, iron overload, and other important complications to be aware of

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It’s time for another new series, this time focusing on Sickle Cell Disease! In this first episode, we lay the foundation for our future discussions. This episode can be dense, but rest assured we will revisit these concepts and expand on them throughout the series.

Contents:

What is hemoglobin?
What is the underlying problem in sickle cell disease genotypically?
Why is the presence of sickled cells problematic?
What is sickle cell trait?
What are other presentations similar to sickle cell disease/HbSS?
What are common electrophoresis patterns?
What is "hereditary persistence of hemoglobin"?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we round out our discussion on metastatic colorectal cancer, focusing on more targeted therapies for this disease. If you have not done so already, be sure to check out episode 107 for the first part of our metastatic colorectal cancer discussion.

Contents:

What is the role of immunotherapy?
What is the role of BRAF inhibition?
Can we use HER2 targeted therapies?
What is the role of more intensive chemotherapy regiments for patients?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we continue our discussion of colorectal cancer, turning our attention to metastatic disease, specifically for cancers without targetable mutations. If you have not done already, we highly recommend you check out episode 104 for our GI oncology pharmacology discussion!

Contents:

What information do we need when we approach a new patient with metastatic colorectal cancer?
How did we get to our current treatment paradigm?
Is there a role for maintenance 5-FU?
What is the role of EGFR-inhibitor bevacizumab?
Why does mutational analysis matter?
Why does sidedness of the tumor matter?
Is there a role for treatment holidays?
What do we do at the time of disease progression?

**This episode is sponsored by our Global Research Partners! Get paid to participate in market research surveys: https://affiliatepanel.members-only.online/FOC_24?utm_campaign=FOC&utm_source=email&utm_medium=email

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** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

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An exciting new academic year is about to begin. We know this can be daunting, especially for our newest hematology/oncology fellows. Over the next two weeks, we re-boot some of our high yield episodes you need to know to prepare for your first days as a new fellow and your nights on call.

Next up: When anticoagulation fails, Part 1! [Originally episode 079]

Content:

How to approach a "DOAC failure" situation
When to consider warfarin

** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Next up: Heparin-induced thrombocytopenia! [Originally episode 071]

Contents:

What is HIT? How is this different than HITT?
How do we make this diagnosis?
How do we treat HIT/HITT?

** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Next up: Cord compression! [Originally episode 014]

Contents:

Differential diagnosis
What is the acute management?
What other consultants need to be involved in decision-making?

** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Next up: Superior vena cava (SVC) syndrome ! [Originally episode 012]

What is the workup?
What is the differential diagnosis?
What do we do once we get the phone call about this emergency?
Who should we be consulting?

** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Next up: Metastatic Cancer of “Origin TBD,” a common question that comes up on solid oncology consults! [Originally episode 008]

Points covered:

Initial workup
What additional imaging is needed?
What to biopsy?
When to send molecular testing?

** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Next up: immune thrombocytopenic purpura [Originally episode 015]

Episode contents:

What is the workup for thrombocytopenia?
What is ITP? Not to be confused with TTP.
How do you diagnose ITP?
How do you treat ITP?

** Be sure to check out our rotation guide for more show notes and episodes organized by disease type: https://www.thefellowoncall.com/rotation-guides

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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First up: thrombotic thrombocytopenic purpura (TTP) [Originally episode 018]

Episode contents:

What is the workup for thrombocytopenia?
What is TTP?
How do we diagnose TTP?
How do we treat TTP?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In a recent American Cancer Society publication, there are increasing data that rates of colorectal cancer are rising rapidly among people in their 20s, 30s and 40s. This has certainly caught the attention of the lay press, most recently in a widely circulated New York Times article published in March 2024. Today, we welcome Dr. Chris Cann, who is an Assistant Professor of Hematology/Oncology at the Fox Chase Cancer Center in Philadelphia where he focuses on GI oncology and has a particular area of interest in early onset colorectal cancer. In his short career thus far, Dr. Cann is already making a name for himself in this space on a national level and so we are so glad he was able to join us for this special discussion. Dr. Cann sheds light on what we know and what we don’t know about this phenomenon. Definitely an episode to check out!

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we incorporate medical oncology back into our discussion with our Radiation Oncologist, Dr. Sanford, and our Surgical Oncologist, Dr. Bailey. We discuss how we approach the management of localized rectal cancer. Note that we will be heavily building off our discussions with our specialist. We recommend listening to these episodes if you have not done so already.

Content:

What information do we need upfront for patients with newly diagnosed rectal cancer?
How did we get to the current treatment paradigm?
What is the data for long course vs. short course radiation?
What is total neoadjuvant therapy?
What are high risk features in rectal cancer?
Is surgery always needed?
Is radiation therapy always needed?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We have another guest joining us this week! Dr. Allison Schepers, PharmD, BCOP is a Clinical Pharmacist Specialist at the Rogel Cancer Center at the University of Michigan where she focuses on GI, GU, and Thoracic malignancies! In this episode, Allison discusses the high yield points we need to know about important drugs we use in the colorectal cancer treatment space and how she approaches counseling her patients. Another great episode from our pharmacy colleagues you do NOT want to miss!

Content:

Important considerations about capecitabine, oxaliplain, and irinotecan, backbones of our colorectal cancer management
An overview of targeted agents?
If someone has a reaction, can we retrial any of these drugs in the future?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we are joined by Dr. Christina Bailey, Associate Professor of Surgery and Program Director of the General Surgery Residency at Vanderbilt University Medical Center in Nashville, Tennessee, for a discussion about the role of surgery in the management of patients with colorectal cancer. This is another amazing multidisciplinary colorectal surgery episode you do not want to miss!

Content:

Why are MRIs important as part of workup for patients with rectal cancer?
What is an "LAR" vs. "APR" and how do you decide which to use?
What are long term complications associated with rectal cancer surgery?
How much colon should be removed in a patient with colon cancer undergoing surgery?
How to counsel patients about colon resection?
How long after surgery should we wait for adjuvant chemotherapy in colon cancer?
Is there a role for neoadjuvant therapy in metastatic colon cancer?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we are joined by Dr. Nina Sanford, Assistant Professor and Chief of Gastrointestinal Radiation Oncology Service, UT Southwestern Medical Center in Dallas, Texas, for a discussion about the role of radiation in colorectal cancer, with an emphasis on the role of radiation in rectal cancer. Dr. Sanford is a wealth of knowledge so this is an episode you do NOT want to miss.

Of note, rectal cancer episodes will be released in a few weeks so if all of this does not make sense, don’t worry. It nicely sets the stage for what is to come!

Content:

What is the role of radiation in rectal cancer vs. colon cancer? Why do we use it more in rectal cancer?
How to evaluate your patients for radiation and how to decide long course vs. short course radiation
Side effects of radiation therapy for rectal cancer
Role of radiation for oligmetastatic colorectal cancer

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this week’s episode, we discuss the management of stage II colon adenocarcinoma, which is defined by a lack of nodal involvement and invasion through the muscularis layer of the colon. If you have not done so already, be sure to check out episode 099 (overview of colorectal cancer) and episode 100 for stage III colon cancer, as we will building on concepts discussed already.

Content:

Is there a role for adjuvant chemotherapy in stage II colon cancer patients?
What is the impact on MSI/MMR testing in stage II colon cancer patients?
Is there a role for evaluating circulating tumor DNA (ctDNA) in colon cancer patients?
Is there a role for immunotherapy in the adjuvant setting?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we kick off our discussion of adjuvant systemic treatment in colon cancer, beginning with Stage III colon cancer. We will review the evidence basis for adjuvant therapy as well as the two main chemotherapy regimens including duration and side effects.

Content:

Why do we need adjuvant therapy in stage III colon cancer?
What is FOLFOX? What is CAPOX? When do we use what?
What is the optimal duration of therapy?
What are the characteristics deemed high risk?
Can we discontinue oxaliplatin early?
What is the role of oxaliplatin in older patients?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Colorectal cancer is one of the most common cancers diagnosed each year worldwide. This highly anticipated series will take an in-depth look at this disease. In this first episode, we discuss the basics, including staging, tumor markers, and microsatellite instability testing, before tackling the management of colorectal cancer in upcoming episodes.

Content:

What is the incidence of colorectal cancer (CRC) in the US?
How are CRC patients staged?
What is the role of CEA?
What are microsatellites and mismatch repair proteins, and how do they come into play for treatment purposes?
Who needs germline testing?
What is the TNM staging for CRC?
What are some high risk factors we need to pay attention to on the pathology report?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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With multiple options for frontline therapy in CLL, MRD has the potential to emerge as a factor that could be considered in our decision-making algorithm for sequencing treatment options. In this week’s episode, we dive into a deeper understanding of the role of MRD testing in CLL.

Content:

What is the role of MRD testing in CLL?
What are the techniques we use to evaluate for MRD?
What is the prognostic role of MRD testing?
Is there data to change treatment based on MRD testing?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we continue our discussion of treatment of CLL, this time focusing on the relapsed/refractory CLL. If you have not done so, we recommend checking out our prior episodes since we will be building on these conversations!

Content:

-If you suspect your patient has relapsed, what do you do?

-What is the approach to treatment in the relapsed/refractory setting?

What is Richter's transformation?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We continue on our journey through chronic lymphocytic lymphoma (CLL), this time focusing our attention to the treatment of CLL.

Content:

What are the indications for treatment?
Can I wait to treat and not impact OS?
What is our current approach to treatment ?
Fixed duration vs. indefinite treatment options?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we start a new series, this time all about the ins-and-outs of chronic lymphocytic leukemia (CLL) / small lymphocytic lymphoma (SLL)! Whether practicing general internal medicine, hospital medicine, or hematology/oncology, you will likely come across a patient with CLL. First, we go through initial diagnosis of this disease!

Content:

What is CLL? How is this different than SLL?
What is the approach to diagnosis?
Do you need a bone marrow biopsy? Imaging?
How do we prognosticate patients?
Are smudge cells always suggestive of CLL?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this week’s episode, we finish our series on hemolytic anemias with a discussion on cold agglutinin disease along with a few other causes of acquired hemolytic anemia.

Content:

What is "cold agglutinin disease"?
Why is it called "cold"?
How do we diagnose this disease?
How do we treat?
BONUS: What are some other examples of hemolysis?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Next in our heme consult series is all about the workup and management of warm autoimmune hemolytic anemia (wAIHA), a very scary situation! These patients can often be very sick and there can be a lot of underlying issues that may be causing this to occur. Rest assured- after this episode, you’ll be a pro at identifying this disorder and know how to manage it should you ever come across this.

If you have not done so already, we recommend you check out our initial episode about hemolytic anemias (Episode 091)

Content:

How do we work up warm autoimmune hemolytic anemia (wAIHA)?
Is it safe to transfuse patients with wAIHA? What about DVT prophylaxis?
What is the approach to initial treatment of wAIHA? How do manage patients once their hemolysis stabilizes?
How do we approach more refractory or relapsed cases?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In the next part of this heme consult series, we discuss several congenital causes of hemolytic anemias. These diseases are relatively rare, but in patients presenting with concerns for hemolysis on history and on labs, but with a negative DAT, it is important to have these in your differential diagnosis! We take you through how to think about these disorders, their diagnosis, and management.

If you have not done so already, be sure to check out Episode 091 where we discuss our initial approach to the diagnosis of hemolytic anemias. We also discuss the most common inherited cause of hemolytic anemia, G6PD deficiency, in that episode!

Content:

When should we suspect inherited causes of hemolytic anemia?
What are important examples of membranopathies that can cause hemolytic anemia?
What are important enzyme deficiencies that can cause hemolytic anemia?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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It’s time for another heme consult series, this time focusing on hemolytic anemias. In this multi-part series, we will go through our approach to thinking about concerns for hemolytic anemias. This is super high yield for anyone who cares for patients, especially those in hematology/oncology. It’s not uncommon to get a consult on the heme consult service for assistance with diagnosis and management of suspected hemolytic anemias!

Content:

What is "hemolytic anemia"?
When should we suspect hemolytic anemias?
What is the workup for acquired hemolytic anemias?
What is G6PD deficiency? When should we suspect this?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We made it to the end of another series. In our FINAL episode of the prostate cancer series, we turn our attention to metastatic castrate-resistant prostate cancer! We discuss treatment options, the data behind why we do what we do, and more targeted agents.

Content:

Approach to metastatic castrate-resistant prostate cancer
Refresher on what it means to be castrate-resistant
Role of bisphosphate therapy and denosumab
Treatment options and data surrounding sequencing of agents
Other options for prostate cancer (radium-223 and lutetium-177-PSMA-617)
Role of PARP inhibitors in BRCA-mutated disease

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we continue our discussion about metastatic castrate sensitive prostate cancer. Spoiler alert: there is not good guidance or biomarkers that help us pick one regimen over another. In this episode, we go through the data, our critical appraisal of the data, and some things to consider when selecting one regimen over another.

As a refresher, be sure to check out our Pharmacology Episode and our introductory episodes, as we will be building on these concepts.

Content:

Approach to metastatic disease
Who needs germline testing?
History of prostate cancer therapy
Selecting doublet vs. triplet therapy

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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As we continue our exploration of prostate cancer, we turn our focus to one of the earliest areas where medical oncologists are commonly involved: systemic therapy for non-metastatic prostate cancer. In this episode, we will review how to risk stratify localized prostate cancer, differences in FDA-approved prostate-specific PET tracers, how to evaluate for biochemical recurrence following surgical and radiation based treatments for localized prostate cancer, and when to consider utilizing systemic therapy in non-metastatic disease.

Content:

A refresher on how we think about systemic treatment options for localized prostate cancer
What role does imaging play?
Definition of biochemical recurrence after upfront surgery vs. radiation
What is castrate-sensitive vs. castrate-resistant disease?
What to do if someone is already on ADT at the time of recurrence?
The fundamental design behind the pivotal STAMPEDE trial and the role it plays in helping us care for our patients with localized prostate cancer

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Last, but not least, in our multidisciplinary discussions regarding the management of prostate cancer, we are thrilled to present a special episode featuring soon-to-be attending Radiation Oncologist Dr. Jacob Hall. Dr. Hall is a senior Radiation Oncology resident and Chief Resident at UNC-Chapel Hill. Today, he helps us better understand patient selection for radiation and helps define key terms.

As a reminder, we previously discussed the fundamentals of Radiation Oncology with Dr. Evan Osmundson in Episode 027!

Content:

-What information should we include when referring a patient to radiation oncology?

-How to counsel patients about effects of radiation oncology for prostate cancer

-What is brachytherapy?

-Is there a role for proton therapy?

-What is the role of radiation for metastatic disease?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In our next episode, we are joined by Dr. Sanjay Patel, a urologic oncologist from the Stephenson Cancer Center at the University of Oklahoma, who also happens to be Vivek’s older brother! We discuss the management of prostate cancer from the perspective of our urology colleagues. As medical oncologists, these are conversations and decisions that we are almost never a part of, as they are being had often before patients ever see us. It was so helpful to get to hear how Dr. Patel thinks about his patients!

Content:

What considerations go into determining if a patient is a good candidate for a prostate biopsy?

-What is the role of an MRI in the workup?

-What are the steps involved in a biopsy?

-When is additional imaging (such as PSMA PET) needed?

-How does he decide surgery vs. radiation referral in unfavorable intermediate risk patients?

-When is pelvic lymph node dissection recommended?

-What does active surveillance entail?

-What about management of high risk and very high risk localized prostate cancer?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we chat with Vineetha Thomas, PharmD, BCCCP, BCOP who is a clinical pharmacist specializing in genitourinary oncology at the Stevenson Cancer Center at the University of Oklahoma. In this episode, we discuss the ins-and-outs of how Dr. Thomas thinks about the various drugs available to treat prostate cancer and how she counsels her patients.

Thanks to our friends at the Pharmacy Podcast Network for connecting us with Dr. Thomas!

Content:

How do we pick one agent over another?
What are side effects of common drugs used for prostate cancer?
Why do we give prednisone with abiraterone?
What is the role of chemotherapy in the management of prostate cancer?
What is sipuleucel-T, radium-223, and lutetium-177?
Role of monitoring bone health in prostate cancer patients

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Prostate cancer is one of the common cancers diagnosed each year in males. In this new series, we will go through the ins-and-outs of this disease. As medical oncologists, there is so much more to prostate cancer than we see. In our future episodes, we will also highlight the important role of pharmacists, radiation oncologists, and urologists in disease management!

Content:

What is the incidence of prostate cancer?
What are the screening guideline recommendations?
How do we diagnose prostate cancer?
How do we risk stratify patients with prostate cancer?
What additional imaging, if any, is needed as part of our workup of prostate cancer?
What is the overview regarding treatment of prostate cancer?
What is the overview about what to expect after surgery or radiation for prostate cancer?
What are key terms we need to know in prostate cancer?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In the final episode in our reboot of Pharmacology 101, we sit down with Renee McAlister, PharmD, BCOP to learn more about the nuances of pharmacology from an expert that does this day in and day out.

Content:

How to manage extravasation accidents?
Pharmacy operations
What is "ideal body weight" vs. "AUC"
Why do we give G-CSF
Supportive care tips and tricks

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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As we prepare for another round oncology series in the weeks to come, we thought we would pause and go back to to the basics. We continue on our Pharmacology 101 series this week. This is such a high yield episode for anyone who cares for patients receiving therapy for their cancer!

Content:

What is an irritant? How is it different than a vesicant?
Does my patient need central access?
Overview of side effects of chemotherapy

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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As we prepare for another round oncology series in the weeks to come, we thought we would pause and go back to to the basics. We previously released this episode as Episode 020. This episode is a must-listen for anyone who talks to patients about chemotherapy!

——

Picture this: it's day 1 of fellowship and your attending needs you to "get consent for treatment." Huh? How do you educate your patient? We share our tips!

In this episode, we discuss the fundamentals and some of our favorite resources.

Content:

How do you know what regimens to use?
What are options for patient education?
What are the basics of terminology used when describing cancer care?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We started this conversation last week! This week, we focus on how to approach warfarin and enoxaparin failure! Be sure to check out Episode 079 for part 1!

Content:

What do you do about "wafarin failure"?
What about lovenox failure?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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It’s time for another Heme Consult series, this time focusing on another common question we see in the hospital and in clinic: “is this anticoagulation failure?”

In this two-part series, we break down how we approach the workup to determine exactly this. In this episode, we discuss "DOAC failure".

Content:

How to approach a "DOAC failure" situation
When to consider warfarin

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this FINAL episode of our DLBCL series, we build on our conversation from last week, focusing on the management of relapsed DLBCL. If you have not done so already, we recommend you check out Episode 077!

Content:

Treatment with selective antibodies against CD19
How to approach relapsed disease after CAR-T
Use of BiTE therapy
Role of allo?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In our last episode, we discussed our approach to primary refractory DLBCL. This week, we start our conversation about relapsed DLBCL! This is an important and complex discussion, so we have split it into two episodes to help you follow along.

If you have not done so already, we recommend you check out episode 076 for a discussion about the primary refractory setting.

Content:

Approach to relapsed disease (after 12 months)
How to approach relapse with CNS involvement
Role of CAR-T vs. autologous transplant in this setting
How to approach treatment in patients who are poor candidates for auto or CAR-T

** This episode is sponsored by HemOnc.org

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we pick up on our discussion about management of DLBCL, focusing on the primary refractory setting. A big part of this discussion is the role of CAR-T therapy. If you have not done so already, we highly recommend you check out episode 075 for the fundamentals of CAR-T before proceeding with this episode!

Content:

Definitions for "primary refractory" vs. "relapsed" disease
How do we approach patients with primary refractory disease?
What are the treatment regimens for patients with primary refractory disease?
What is the role of CAR-T therapy?
How do we "bridge" patients to CAR-T therapy?
How do we monitor patients post CAR-T?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this week’s episode, we pause from our discussion about DLBCL to talk about the fundamentals of CAR-T, BiTE and autologous transplants, which will lay the foundation for subsequent discussions about DLBCL. These therapies are the talk of the town and have changed/will continue to change our approach to hematologic malignancies - definitely an episode you don’t want to miss.

Content:

What is CAR-T?
How are CAR-T cells manufactured?
What are commercially available CAR-T cell products?
What are side effects of CAR-T?
What is BiTE therapy?
What is the role of autologous transplants in lymphoma?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we continue our conversation about DLBCL, this time focusing our attention on the management of early stage disease.

In this week’s episode, we delve into the management of advanced stage DLBCL.

If you have not done so, we highly recommend you listen to our hemepath series before proceeding with this episode. Furthermore, if you have not listened to the introduction to DLBCL episode (https://www.thefellowoncall.com/tfocpodcast/dlbclintro) or our early stage DLBCL episode (https://www.thefellowoncall.com/tfocpodcast/dlbclearlystage), we highly recommend doing so, as we will be building on these basics this week.

Content:

Reminders about diagnosis and staging
Treatment approaches to advanced staged diffuse large b-cell lyphoma
Management of double hit/high grade B-cell lymphomas
Links to important trials

**This episode is sponsored by HemOnc.org

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we continue our conversation about DLBCL, this time focusing our attention on the management of early stage disease.

If you have not done so, we highly recommend you listen to our hemepath series (https://www.thefellowoncall.com/rotationguide-intro-to-hematopathology) before proceeding with this episode. Furthermore, if you have not listened to the introduction to DLBCL episode (Episode 072; https://www.thefellowoncall.com/tfocpodcast/dlbclintro), we highly recommend doing so, as we will be building on these basics this week.

Content:

What is the role of PET/CT in diagnosis of DLBCL?
What is the Deauville score?
How do we approach treatment to early stage DLBCL?
What are options without radiation?
What are treatment options for older patients with early stage DLBCL?

**This episode is sponsored by HemOnc.org

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we kick off a new series focusing on diffuse large B-cell lymphoma. In this first episode, we discuss the basics that everyone needs to understand before diving into the management of this disease.

We highly recommend listening to our hemepath series before proceeding with this DLBCL series: https://www.thefellowoncall.com/rotationguide-intro-to-hematopathology

Content:

Approach to workup for a patient with suspected lymphoma
FNA vs. Core vs. Excisional biopsy for diagnosis
Use of PET/CT for staging
How to risk-stratify patients
"Double hit" vs. "double expressor"

**This episode is sponsored by HemOnc.org

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We revisit a topic covered previously as part of our “Heme/Onc Emergencies” series: heparin-induced thrombocytopenia (HIT) in Episode 017. As part of our return, we dive deeper into the pathophysiology, principles of diagnosis, and management of HIT to help you to better understand how to approach the question of “is this HIT?” as a Hematology consultant and, more importantly, how to guide management based on your index of suspicion.

Content:

What is the pathogenesis of HIT?
What are risk factors for HIT?
How do we diagnose HIT?
What are the assays that we use to make this diagnosis and how do the assays work?
Practical points about management of HIT/HITT

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week in our hematological consultation series, we continue our discussion on von Willebrand disease (vWD), this time focusing on the type 2 subtypes and we also discuss management.

In case you missed it, we recommend checking out episode 069 for Part I of this vWD series, covering taking a bleeding history and about Type 1 and Type 3 disease.

Content:

What testing do we send for suspected vWD (refresher)
What to do if type 2 vWD is suspected?
What are the different subtypes of Type 2 vWD?
What is "platelet-type vWD"?
What is the approach to perioperative management?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We resume our hematological consultation series with an overview of von Willebrand disease, the most common inherited bleeding disorder. In this episode, we talk about the initial steps we should take to evaluate suspected von Willebrand disease (vWD) and how to differentiate the various subtypes. We will focus on vWD type 1 and 3! Be sure to tune in next week as we discuss vWD type 2 and management.

Content:

Taking a bleeding history
What is von Willebrand factor?
What tests should we order for diagnosis?
What are the different types of vWD?
What is the DDAVP challenge?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we complete our breast cancer series, focusing on triple-negative breast cancer (TNBC). The last few months have been quite the journey! Please continue to refer to our shownotes to help navigate this complex disease treatment paradigm.

Content:

What is the data about recurrence of disease of TNBC?
The history of how we got to our current standards of care
Important trials to support our current treatment paradigm

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We are not yet done with our breast cancer series, but we could not wait to share this incredibly personal conversation with a patient with a recent breast cancer diagnosis. This week, we sit down with Kaele Leonard, who herself is a Pulmonary/Critical Care fellow at Vanderbilt University Medical Center who was diagnosed with breast cancer in her early 30s.

As physicians, we don’t always get to hear what the journey through diagnosis, treatment, and follow up looks like from a patient’s perspective. We are so grateful to Dr. Leonard for opening up about this with us.

Content:

The patient experience of finding out results and subsequent management
Importance of discussing fertility preservation
Financing fertility preservation
Role of “cold caps” for our patients (https://www.breastcancer.org/treatment-side-effects/hair-loss/cold-caps-scalp-cooling)
The “post-cancer crash”

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we continue our discussion about metastatic breast cancer, focusing on HER2+ disease.

Content:

What is the data about recurrence of disease of different breast cancer subtypes?
The history of how we got to our current standards of care
Important trials to support our current treatment paradigm

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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After several weeks of covering localized disease, this week, we shift our discussion to metastatic breast cancer, focusing first on ER+ disease.

Content:

Importance of taking a biopsy at time of disease progression
What endocrine therapy backbone do we choose in metastatic ER+ disease?
What agents can we add to endocrine therapy for metastatic ER+ disease?
What is "visceral crisis"?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week, we round out our discussion on the early stage breast cancer, turning our attention to the triple negative subtype. Once again, there are a lot of trials and data, but be sure to check out the show notes for the highlights!

Content:

What is TNBC?

-What is the data to support the use of neoadjuvant therapy in this disease?

What is "pathologic CR" and how is different than "residual cancer burden"?
Can we ever omit neoadjuvant therapy?
What are our options for chemotherapy regimens in neoadjuvant and adjuvant setting?

** This episode has been sponsored by HemOnc.org

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We continue on our journey through early stage breast cancer, this time turning our attention to HER2+ disease. There is a lot of data in this episode, as you will both hear and see. To make this easier, we highlight key takeaways to make understanding this even easier.

Content:

What is HER2?
Discovery of trastuzumab
Data for use of trastuzumab in adjuvant and neoadjuvant setting
Data for use of pertuzumab in adjuvant and neoadjuvant setting
Data and use of trastuzumab emtansine (TDM-1) in the adjuvant setting
Management of HER2+ stage I breast cancer
Highlights of key trials that shape the paradigm of management
Our approach to management

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week’s episode is part 4 of 5 of a joint mini-series with our friends Two Onc Docs. In today’s episode, we will be recapping the current treatment of resectable NSCLC and discussing KEYNOTE 671, which was presented at ASCO 2023, looking at neoadjuvant chemo+immunotherapy followed by adjuvant immunotherapy. We also discuss the use of the “interaction test,” “multiplicity,” and it’s important role in understanding subgroup analyses.

Content:

A quick recap of the current standard of care for resectable lung non-small cell lung cancer
A discussion about KEYNOTE 671 presented at ASCO 2023
We define the "interaction test"
We discuss "multiplicity"

Want to read the abstract for yourself? Click here!

Episode list:

Episode 1 covering covering rectal cancer & the PROSPECT Trial, as well as non-inferiority trials (released by Two Onc Docs): https://podcasts.apple.com/us/podcast/updates-from-asco23-rectal-cancer-the-prospect-trial/id1616541733?i=1000616604349

Episode 2 covering classical hodgkin’s lymphoma & SWOG 1826 as well as “p-values” and what it means when trials say “the median was not reached.” (released by The Fellow on Call): Episode 061: “Paging Heme/Onc: Updates from ASCO 2023” - Classical Hodgkin’s Lymphoma and SWOG 1826

Episode 3 covering mRCC & the CONTACT03 Trial, as well as subgroup analysis (released by Two Onc Docs): https://podcasts.apple.com/us/podcast/updates-from-asco23-mrcc-the-contact03-trial/id1616541733?i=1000617519386

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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This week’s episode is part 2 of 5 of a joint mini-series with our friends Two Onc Docs. In today’s episode, we recap the current treatment of classical hodgkin’s lymphoma and then dive into the the SWOG 1826 plenary session abstract from the ASCO 2023 annual meeting. We also cover the concept of “p-values” and what it means when trials say “the median was not reached.”

Content:

A quick recap of the current standard of care for classical hodgkin's lymphoma
A review of the recent SWOG 1826 trial presented at ASCO 2023
A discussion about "p-values"
A discussion about what it means when "the median was not reached"

Want to reach the abstract yourself? Click here: https://ascopubs.org/doi/abs/10.1200/JCO.2023.41.17_suppl.LBA4?af=R

Have you checked out Episode 1? See link here for this episode released by Two Onc Docs: https://podcasts.apple.com/us/podcast/updates-from-asco23-rectal-cancer-the-prospect-trial/id1616541733?i=1000616604349

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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We are taking a small pause from our breast cancer series to discuss an important topic that is so critical to understand for clinical practice, no matter what discipline of medicine you are in: the fundamentals of transfusion medicine. This topic often shows up quite frequently on board exams, as well. In this episode, we talk about terms such as “type and screen” and more.

Content:

What is a "type and screen"?
What does this process entail?
What is the difference between this and crossmatching?
When do we see discrepancies in the antibody screen?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Surprise! The teams at Two Onc Docs and The Fellow on Call are teaming up for his special series!

Each episode will focus on a single abstract, poster, or oral presentation from ASCO 2023, and will feature a quick review of any guidelines and management pointers relevant to the disease state under study, followed by an overview of the study design and findings, and finally a discussion of the implications of the research on clinical practice.

We expect to release episodes on June 12, 14, 19, 21, and 26. Episodes will be released alternating between our two podcasts, so make sure you’re subscribed to both!

Follow Two Onc Docs on Twitter: www.twitter.com/twooncdocs

Subscribe to Two Onc Docs on Apple Podcasts: https://podcasts.apple.com/us/podcast/two-onc-docs/id1616541733

Follow The Fellow on Call on Twitter: www.twitter.com/thefellowoncall

Subscribe to The Fellow on Call on Apple Podcasts: https://podcasts.apple.com/us/podcast/the-fellow-on-call-the-heme-onc-podcast/id1602921628

Subscribe to The Fellow on Call on Spotify: https://open.spotify.com/show/3LFKY3jlU2T0MpvKwkvMvl?si=acca1fa9413a4f60&nd=1

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This week, we continue discussing the management of early stage ER+/HER2- breast cancer. If you have not done so already, be sure to check out Episode 057 for the first part of this discussion.

Content:

Who warrants chemotherapy?
Who benefits from gene expression assays?
What are important gene expression assays used clinically?
Post-treatment surveillance and survivorship
Targeted agents in the adjuvant setting

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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After several weeks of incredible discussions with our special guests, it’s time that we dive into the medical oncology regarding breast cancer. We start our discussion with the first of our two-part discussion on early stage (AKA non-metastatic) ER+/HER2- breast cancer.

Content:

What information do we need to consider in patients with HR+ breast cancer?

-What is the role of chemotherapy?

-If chemotherapy is indicated, what are the treatment options? Why?

-Anti-estrogen therapy selection and duration

-Is there a role in ovarian suppression in HR+ disease?

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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So much incredible progress has been made in the management and treatment of breast cancer, largely thanks to advances in available therapies and drugs. A good understanding of pharmacology is key to selecting the correct regimen and providing counseling to your patients. This week, are so fortunate to be joined by special guest Dr. Danielle Roman, PharmD, who is an Oncology Clinical Pharmacy Specialist at West Penn Allegheny Oncology Network in Pennsylvania, as she helps us navigate breast cancer pharmacology.

Content:

A discussion about different anti-estrogen therapies
Counseling about anti-estrogen therapy side effects
An overview of regimens used in ER+, HER2+, triple negative disease
Highlighting key trials related to the approval of these agents
Supportive care for breast cancer patients

** This episode is sponsored by HemOnc.org!

**Thank you to our guest, Dr. Danielle Roman

** Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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Surgery plays a pivotal role in the management of breast cancer, particularly in early stages of disease. This week, we are joined by special guest Dr. Carla Fisher, Associate Professor and Medical Director of Breast Surgical Oncology at Indiana University School of Medicine

Content:

When to perform breast conservation surgery
When is additional imaging required?
Timing of neoadjuvant/adjuvant therapy in relation to breast surgery
What is a sentinel lymph node biopsy?
A discussion about breast reconstruction surgery
When is prophylactic mastectomy performed?
Role of surgery in inflammatory breast cancer

** Thank you to our guest, Dr. Carla Fisher!

**Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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The language of breast cancer can be confusing and very technical. In this episode, we help you learn and understand so many important words and phrases that have important implications on diagnosis and management. Understanding these will not only help you learn more about breast cancer, but it will also ensure you are better able to communicate the lingo to your patients!

Content:

Definitions of important terms and phrases pathologists include on their reports
Important terminology to understand
Fundamentals of TNM staging for breast cancer
Important buzzwords to know when reading clinical trials in breast cancer

** Help us as we continue to grow our show by filling out this BRIEF survey! Link: https://forms.gle/KBhDRTGBqRJ1CgnK7

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A critical part of breast cancer management is often the incorporation of radiation therapy. This week, we sat down with our special guest, Dr. Ryan Miller, who is a radiation oncology resident at Thomas Jefferson University Hospital in Philadelphia who shared some super high yield points about how he approaches radiation planning in his patients with breast cancer.

Content:

General guidance for counseling patients about radiation oncology in breast cancer management
What is a "radiation boost"?
What is "regional nodal irradiation" and when is this indicated?
Can you give radiation treatment concurrently with systemic therapies?
Role of radiation in partial mastectomy/lumpectomy vs. mastectomy
Can radiation be omitted?
What is role of radiation in DCIS?

** About our Guest: A huge thank you to Dr. Ryan Miller from Thomas Jefferson University Hospital for joining us!

** Help us as we continue to grow our show by filling out this BRIEF survey! Link: https://forms.gle/KBhDRTGBqRJ1CgnK7

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The workup and management of breast cancer is complex! In this next series, we will dissect this topic inside and out. We will are so excited to be kicking off this series with special guest, Dr. Yasha Gupta to shed light on the role of our friendly breast radiologists and the very important role they/their team plays in the initial diagnosis and workup for a patient with a breast mass.

Content:

Fundamentals of breast cancer screening
Difference between screening and diagnostic mammogram
What is "BI-RADS"?
Workup of a concerning breast mass
What are marker clips? How do we use these clinically?
Role of tomosynthesis
How are the axillary lymph nodes assessed?

** About our Guest: A huge thank you to Dr. Yasha Gupta from Memorial Sloan Kettering for joining us!

** Help us as we continue to grow our show by filling out this BRIEF survey! Link: https://forms.gle/KBhDRTGBqRJ1CgnK7

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We are kicking off our intermittent “Heme Consults Series” with a great overview of the approach to leukocytosis, a common question we get on the wards. In this episode, we talk about the initial steps we should take to triage these cases and what we should be thinking about in regards to next steps.

Also - a huge shoutout to one of our listeners who had emailed us and said this is a common question that puzzles them in their work as a hospitalist! If there is something that you’d like to hear us cover in this series, definitely reach out!

Content:

A refresher on the cell differentiation pathway
What are the key elements of the history and physical exam?
What labs should we order?
A breakdown of the approach to next steps based on the predominant type of WBC

** Help us as we continue to grow our show by filling out this BRIEF survey! Link: https://forms.gle/KBhDRTGBqRJ1CgnK7

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The Fellow on Call is thrilled to partner with so many of our podcasting friends be a part of #NephMadness 2023 this year. In today’s episode, we welcome three incredible guests to our show, Dr. Matthew Abramson, Dr. Timothy Yau, and Dr. Scott Stockholm, to talk about the two very critical topics in hematology/oncology. The first is a discussion about immune checkpoint inhibitor-related AKIs. The second is a discussion about hypomagnesia in our patients. To learn more about NephMadness and to cast your votes, be sure to check out: https://ajkdblog.org/tag/nephmadness2023/. We’d love to see Onconephrology snag that #1 spot :)

Content:

What is the mechanism of immune checkpoint inhibitor-associated AKIs?
What is the etiology of ICI-related AKIs?
How do we work these up?
How do we treat? Steroids? Do we biopsy?
Can we re-trial ICI in someone who had ICI-related AKI?
How do we use ICI in patients with kidney transplants?
What are symptoms of hypomagnesemia?
A refresher on magnesium homeostasis
How do we manage hypomagnesemia?
What drugs are associated with hypomagnesemia?

**A huge thank you to Dr. Joel Topf and the team at NephMadness for the invitation to be a part of this podcrawl, helping to collect resources, and create a show outline

** A huge thank you to our guests!

** Help us as we continue to grow our show by filling out this BRIEF survey! Link: https://forms.gle/KBhDRTGBqRJ1CgnK7

Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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It’s been a long road, but incredibly educational journey, through our Myeloma Series. We finish off our series with a bang by sitting down with Multiple Myeloma Superstar, Dr. Manni Mohyuddin. In this episode, Dr. Mohyuddin takes us through his approach to complex decisions in the care of patients with myeloma, highlighting that myeloma treatment is an art in which we take imperfect data and try to make the best decisions for our patients. Trust us, folks, you do NOT want to miss this episode!

Content:

How does Dr. Mohyuddin approach treatment of myeloma?
How does he approach maintenance?
What is the role of transplant in patients with myeloma?
Is there a role of MRD testing?
What is his approach to relapsed/refractory setting?
What about the use of agents like venetoclax or VDT-PACE?
A discussion about role of CAR-T therapy
Approach to bridging strategies

** A huge THANK YOU to our guest, Dr. Manni Mohyuddin!

** This episode has been sponsored by Primum. To sign up for a free account, check out: tfoc.primum.co

** Help us as we continue to grow our show by filling out this BRIEF survey! Link: https://forms.gle/KBhDRTGBqRJ1CgnK7

Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In episode 046, we discussed the fundamentals of transplant in the treatment of patients with multiple myeloma. This week, we sit down with two incredible hematologists who specialize in transplant to discuss the real-life decision-making that goes into evaluating each patient. We are so excited to welcome two special guests this week, Dr. Shonali Midha and Dr. Amar Kelkar, joining us from the Dana-Farber Cancer Institute in Boston!

Content:

What goes into determining if a patient is transplant eligible?
What counseling is provided to patients?
Approach to melphalan dosing
How does apheresis work?
What agents are used to help mobilize stem cells?
How many stem cells do we need to collect?
Does how much therapy one has received affect their collection?
Is there still a role for transplant in today's world?
Is there a role for an "MRD-adapted" approach to treatment?
Is there a role for a second transplant in patients who have relapsed?
Is there a role for allogeneic stem cell transplants in myeloma?

A huge THANK YOU to our guests, Dr. Shonali Midha and Dr. Amar Kelkar, both of the Dana-Farber Cancer Institute!

Help us as we continue to grow our show by filling out this BRIEF survey! Link: https://forms.gle/KBhDRTGBqRJ1CgnK7

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We continue our myeloma series, transitioning our discussion from autologous stem cell transplant to maintenance therapy for myeloma.

Content:

Why do we use revlimid (lenalidomide) maintenance?
What about in high risk patients?
What is the role of MRD testing?
What about daratumumab in the maintenance setting?

This episode has been sponsored by Primum. To sign up for a free account, check out: tfoc.primum.co.

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In this continuation of our myeloma series, we discuss all the key principles and data surrounding autologous stem cell transplant in myeloma. We provide a succinct summary of key trials in this space that will give you a deep understanding of the field.

Content:

What are all these cooperative groups in the studies?
What are some of the important trials that show us the benefit of autologous stem cell transplant?
Should transplant be done early or should it be delayed? What does it matter?
We translate the data/guidelines into what this means for patients in real-life
How do we approach transplant in high risk patients in myeloma and what are the guidelines about tandem transplant?

This episode has been sponsored by Primum. To sign up for a free account, check out: tfoc.primum.co.

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In this episode, we start with a little bit of story time about the history of myeloma treatments and how we got to the present day. We then finish off the episode with how this information helped us treat transplant ineligible patients.

Content:

What is the history of myeloma treatment? How did we get to where we are today?
How do we approach treatment in transplant ineligible patients?
What are the key trials that every fellow needs to know?
Links to key trials

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In this continuation of our myeloma series, we build on our prior discussion about myeloma pharmacology, this time discussing how to select the optimal regimen for treatment of our patients.

Content:

What are the phases of multiple myeloma treatment?
How do we determine transplant eligibility?
What does doublet, triplet, and quadruplet therapy mean?
What categorizes "high risk" myeloma?
What are the current standards of care for transplant eligible patients?
Where does "CyBorD" fit in for treatment?
When do we consider adding daratumumab?
Links to key trials

This episode has been sponsored by Primum. To sign up for a free account, check out: tfoc.primum.co.

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In this continuation of our myeloma series, we begin our discussion about treatment options for multiple myeloma, focusing first on pharmacology. We are so thrilled to have a special guest, Kathryn Maples, PharmD, BCOP who is a clinical pharmacy specialist in Multiple Myeloma at the Winship Cancer Institute of Emory Healthcare in Atlanta, Georgia!

Content:

What are common drugs we use in "triplet regimens"? "quadruple therapy"?
What considerations must we take into account when prescribing commonly used medications in myeloma?
How should we counsel our patients?
What about supportive care?
How and when do we make dose adjustments?
This episode is SO eye-opening about the "behind the scenes" of myeloma care that physicians do not see

Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this continuation of our myeloma series, we discuss the progression of MGUS & smoldering myeloma to multiple myeloma. We also outline how to risk stratify a patient with multiple myeloma and gauge their response to treatment.

Content:

-What is the natural progression from MGUS to smoldering myeloma to multiple myeloma?

How do we risk stratify patients with a new myeloma diagnosis?
What is the role of FISH/karyotype in risk stratification in myeloma?

-How do we gauge disease response in myeloma?

How do we define disease progression?
How do we define treatment response?
What is the role of minimal residual disease (MRD) in myeloma?

Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In today’s episode, we continue our myeloma series, this time we’ll delve deeper into the spectrum of plasma cell dyscrasias, including defining MGUS, discussing surveillance of MGUS, defining smoldering myeloma (SM). We are slowly inching our discussion towards the diagnosis of Multiple myeloma (MM)!

Content:

Defining MGUS
Discussing risk of progression of MGUS to MM
How to interpret free light chains in renal failure
How do we monitor MGUS patients?
When do we do additional testing in MGUS?
What is smoldering myeloma?
What are myeloma defining events?
How do we risk stratify SM patients?
How do we monitor SM patients?

Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In the first episode in our highly-anticipated multiple myeloma series, we begin our discussion about introduction to testing/workup for plasma cell dyscrasias and having our initial discussion about monoclonal gammopathy of undetermined significance (MGUS).

Contents:

What is a plasma cell ?
What is a plasma cell dyscrasia?
What is an "SPEP"?

-What is "immunofixation"?

-What are "serum free light chains"?

-Checking UPEP

-Does everyone need a bone marrow biopsy and/or additional workup?

-What is MGUS?

Want to review the show notes for this episode and others? Check out our website: https://www.thefellowoncall.com/our-episodes

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In this episode, we discuss the acute management of the bleeding patient with acquired hemophilia.

Prior to starting this episode, we highly recommend you listen to Episode 036 to review:

Approach to Hemophilia (physical exam, workup)
Review coagulation cascade

When to suspect acquired hemophilia?

For a suspected acquired hemophilia, want to ensure you are looking at prior coagulation studies (if available); suspect if patient has spontaneous bleeding with abnormal coags (with prior coags normal)

Case presented in this episode (helps to better understand below):

75M with PMHx HTN, HLD, CLL who was lost to follow up for CLL (but never required treatment). Had presented to ED with bilateral back pain with significant bruising. He also had ROS +SOB, fatigue. Exam notable for flank bruising. Labs concerning for severe anemia and elevated PTT

Since there is an abnormal PTT, proceed with mixing study.

In acquired hemophilia, mixing study will not correct
Why? An antibody is interfering with the function of one of the proteins in the coagulation pathway.
What does “correct” mean? It needs to go to normal range.
In inherited hemophilia, recall that patient’s activity levels will correct
Putting this in clinical context, the patient who is bleeding with an abnormal coagulation assay you need to suspect as having acquired hemophilia
Once again, check factor activity levels to assess which protein’s function is interfered with

-Most often factor VIII is most affected

What are Bethesda Units and why are they important?

This is a unit of measure to quantify how “strong” the inhibitor is
Based on the idea of reciprocal dilutions of the patient’s plasma with control plasma and then testing factor activity
The Bethesda assay result that we want is the reciprocal of the dilution at which 50% of factor activity is observed
Example:

Patient presents with spontaneous bleeding of the thigh. They have no prior history of spontaneous bleeding and a normal family history. PTT is abnormal and does not correct with mixing study.

You check factor VIII activity level was 6%, and so now you are suspicious of an inhibitor.

Perform 1:2 dilution → let’s say 21% activity

Perform 1:5 dilution → let’s say 50% activity

Perform 1:10 dilution → let’s say 75% activity

So here, the 1:5 dilution resulted in 50% activity; so the reciprocal of ⅕ is 5, therefore we would say the inhibitor titer is 5BU

Why does this matter?

Bethesda units in acquired vs. congenital hemophilia are slightly different
Congenital: Recall that patients can form inhibitors to factor replacement in congenital hemophilia

**Patients with <5BU often have their inhibitors disappear spontaneously

**Patients with BU > 5 have “high responding inhibitors”. These can become undetectable overtime, but many times, these will rise 4-7 days after factor is given in future events (amnestic response)

Acquired: A means of assessing “what’s ahead of us” and also a way to measure if “eradication therapy” is working to get rid of the auto-antibody.

How do we treat patients with acquired hemophilia?

-How do we stabilize the acute bleed?

**The patient is bleeding so we need to force a clot

**Consider use of bypassing agent

***Since often FVIII is the protein targeted, use recombinant factor VIIa to bypass the intrinsic pathway

****Has short half life

***Also can consider use of FEIBA (factor eight inhibitor bypassing agent)

How do we treat the underlying cause?
Suppress the immune system:

** Steroids or rituximab (anti-CD20 antibody)

** Oral cyclophosphamide + steroids (better outcomes in EACH2 Registry when compared to steroids alone or rituximab based regimens)

If there is an underlying malignancy (such as CLL), treat the underlying cause

** Likely will be a prolonged course of steroids

References:

https://pubmed.ncbi.nlm.nih.gov/30396835/ : Review on treatment of acquired hemophilia A

https://pubmed.ncbi.nlm.nih.gov/22517903/ : Results of the EACH2 registry which showed improvements in inhibitor eradication with cyclophosphamide + steroids than steroids alone or with rituximab based regimens.

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In this episode, we discuss the acute management of the bleeding patient with hemophilia including factor replacement.

Some patients with a history of hemophilia and spontaneous bleeding have factor replacement at home and can treat themselves to 100% factor activity level.

*For Hemophilia A, 1 unit/kg of factor 8 replacement will increase the factor level activity by 2%. So, 50 units/kg will raise the factor activity from 0% to 100%

*For Hemophilia B, 1 unit/kg of factor 9 replacement raises factor level activity by 0.75%. So, 130 units/kg raises the factor level from 0% to 100%.

**If the patient does not know their baseline factor levels, assume factor level activity is less than 1%. Replace to 100% for a major, life-threatening bleed.

**Give factor replacement BEFORE you get imaging.

When do you give more factor replacement?

The goal is to keep the patient in the normal range of 50-150% factor activity level. The half-life of the factor replacement is about 12 hours. So, this means that if you replace to 100%, 12 hours later, you’ll need another 50% replacement dose. Get trough levels q24 hours before the morning dose.

Remember that trough levels are not useful in patients taking Emicizumab. Emicizumab is the bispecific monoclonal antibody that binds to factor 9 & 10 activating the latter. This essentially replacing the role of factor 8, which is missing in hemophilia A.

If the patient has an inhibitor, you can overwhelm the coagulation system with activated factor 7, which bypasses the intrinsic pathway to form a clot.

Particularly for mucosal bleeding, you can use an antifibrinolytic agent (tranexamic acid, aminocaproic acid) which stabilizes the clot and prevents the breakdown of fibrin mesh.

Another treatment for patients with milder forms of hemophilia is DDAVP, which release stores of Factor 8 and Von Willebrand Factor from the blood vessel endothelium. Side effects include hyponatremia and fluid retention.

If you are in a hospital with no specific factor replacement, you can use cryoprecipitate, which contains fibrinogen, factor 8, factor 13, & Von Willebrand Factor.

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In this episode, we discuss the fundamentals and approaches to chronic management and treatment for patients with known inherited hemophilia.

What is hemophilia?

As name suggests, tendency to bleed
Two types: genetic and acquired

Inherited hemophilia:

Genetic: sex-linked, meaning males will express it, females will, by and large be carriers
Main ones to be worried about: Hemophilia A and Hemophilia B

** Hemophilia A: deficiency in factor VIII (1:5000 men)

** Hemophilia B: deficiency in factor IX (1:30,000 men)

** Thousands of underlying mutations

We grade the severity of hemophilia using the factor activity levels:

** Severe: <1% activity

** Moderate: 1-5% activity

** Mild: 5-50% activity

Patients will often have objective severity and separate phenotype (someone with moderate severity may have phenotype of someone who is severe) - need to individualize

Treatment:

GOAL: Want to start patients on treatment after their first bleed – goal is to prevent bleeding + avoid joint damage
Prophylaxis (not in acute bleed; acute bleeds to be discussed in a future episode):
Factor Replacement:

** Typically started for patients with >1 bleed into the joints for patients with severe hemophilia (goal is to keep levels >1%)

** In patients with moderate or mild can do intermittent dosing

*Hemophilia A/Factor VIII replacement (many options; here is what we use at Rouleaux):

**Recombinant factor concentrates: Advate

**Plasma-derived concentrates: Humate-P

Factor IX replacement:

** Recombinant factor concentrates: BenefIX

*Bypassing agents: For patients with inhibitors (to be discussed in a future episode) or can be used for Hemophilia A or B

*Options:

** Novoseven (activated recombinant factor VII): Activates the extrinsic pathway to bypass the need for factors VIII or IX

** FEIBA (factor eight inhibitor bypassing agent): Activated prothrombin complex concentrate (FIIa, VIIa, Xa)

Emicizumab (Hemlibra): bispecific monoclonal antibody that binds factor activated IX and X → essentially doing the job of factor VIII and leads to activation of the downstream common pathway

** Note that it binds activated factor IX not inactivated factor IX and this is why you won’t just constantly form clots by forcing down the common pathway like you would by giving a bypassing agent

cannot be used in Hemophilia B because it relies on the presence of factor IX

Several new therapies have been introduced in recent years

References:

https://www.uptodate.com/contents/hemophilia-a-and-b-routine-management-including-prophylaxis?search=hemophilia%20treatment&source=search_result&selectedTitle=2~150&usage_type=default&display_rank=2: UpToDate article on current management of Hemophilia

DOI: 10.1055/s-0042-1756188: “The More Recent History of Hemophilia Treatment.” Semin Thromb Hemost. 2022.

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In this episode, we break down the initial approach to the evaluation of a patient with a suspected bleeding disorder, particularly in regards to hemophilia, including standardized bleeding assessment tools, the basics of the coagulation cascade, and mixing studies.

The first step is taking a thorough bleeding history:

The Fellow on Call Bleeding Assessment:

Mucosal bleeding working from nose down: epistaxis (did they need cauterization), gum bleeding, bleeding with tooth pulling, hematochezia, hematuria, menorrhagia or excessive post-partum bleeding
Skin: Bruising, petechiae, telangiectasias
“Ortho bleeding”: spontaneous joint or muscle hematoma (raises concern for hemophilia)
Prior surgical or family history?
Medications?

Always clarify: are these issues lifelong?

The International Society for Thrombosis and Hemostasis scoring tool is useful for standardizing bleeding symptoms, and it can help you determine the likelihood that a patient has an underlying bleeding disorder.

Physical exam: Pay particular attention to:

Assess skin for bruising or petechiae
Assess the fingertips
If having epistaxis, may need to have help to assess nostrils for anatomical issues (vessels)
Assess mucosal surfaces for telangiectasias which could point to a diagnosis of Hereditary Hemorrhagic Telangiectasia, a mimicker of bleeding disorders
Assess thighs and flanks for obvious signs of bruising/bleeding

We sort bleeding disorders into two large buckets:

Platelet dysfunction → minor bleeding (i.e., mucosal bleeding, epistaxis)
Factor deficiency → major bleeding (i.e., joint effusions, spontaneous ICH)

The basic workup includes:

CBC - to assess for low platelets
Peripheral smear - rule out schistocytes (DIC)
CMP - to check for liver dysfunction or severe renal dysfunction/uremia which leads to platelet dysfunction
PT/INR, aPTT, fibrinogen
Von Willebrand Panel

Coagulation Cascade:

PT → measures the extrinsic pathway → factor 7 (lucky)
PTT → measures the intrinsic pathway → factors 12, 11, 9, 8 (TENET)
Intrinsic and extrinsic pathway feed into the common pathway → factors 10, 5, 2, 1 (All dollar bills less than $20)

If a patient has an abnormal PT/PTT, you must ask: is it a lack of a necessary clotting factor or something interfering with the time it takes a clot to form? You assess this with a mixing study.

A mixing study combines equal parts of the patient’s plasma with control plasma.
Mixing study corrects → deficiency of a coagulation factor
Mixing study does not correct → antibody interfering with assay or the function of the factors in the coagulation cascade

**To correct, the time must be in the normal range for the assay, not just slightly improved!

**The mixing study is assessed at time points 0 hr, 1 hr, 2 hr; the presence of an inhibitory may improve the time initially, but can then become longer again at time points 1hr and/or 2hr

After the mixing study, then you also need to know which of the factors is the issue! How to do this:

Functional assays can be ordered to measure individual coagulation factor function.
Factor 11 – Hemophilia C
Factor 9 – Hemophilia B
Factor 8 – Hemophilia A
Understanding the coagulation cascade allows you know quickly know what to order

References:

https://bleedingscore.certe.nl: ISTH/SCC Bleeding Assessment Tool

https://ashpublications.org/ashclinicalnews/news/2436/How-I-Teach-the-Coagulation-Cascade: “How I Teach the Coagulation Cascade” by Dr. Alice Ma at University of North Carolina

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We strongly recommend you listen to our previous episodes metastatic lung cancer (Episodes 0032 and 0033) to better be able to follow along with this conversation. Key trials mentioned in this episode include:

CHECKMATE 227

KEYNOTE 024

Q:Do you send molecular testing (PDL1 and NGS) on the biopsy, peripheral blood or both?

Yield is highest from the tissue sample
Peripheral blood (circulating DNA) samples are dependent on the burden of disease and so often the yield is lower

** One of the benefits is that it can be sent quickly and having a fast turn-around; Tissue samples are dependent on being able to schedule a biopsy

Dr. West says he definitely sends this on a non-smoker with non-squamous lung cancer, as they are more likely to have molecular targets
Dr. West has not personally adopted the idea of sending peripheral and tissue samples for NGS testing for everyone

Q: Do you ever use Ipi/Nivo in patients with PDL1 <50% (ref: CHECKMATE 227)?

There are a lot of other options so he does not use this, as it is harder to predict the side effects with therapy like this
“Chemo-free does not mean side-effect free”

Q: We understand there is a lack of randomized trial data on the use of consolidative radiation after IO based treatment in the metastatic setting. If patients have a good response to systemic treatment, when do you consider using consolidative radiation for cure?

A systemic therapy that is effective that leaves you with oligo-residual disease, radiation can be considered for the right patient

** We need to balance what a radiation oncologist says he/she can radiate vs. what is actually the right thing to do

** Sometimes, it’s best to give the cancer some time to “declare itself”.

A nuanced discussed, but it may be worth considering especially in patients who have disease that is

** (a) growing at a clinically meaningful rate

** (b) in patients with a few sites of disease, but otherwise great control

This is much more effective in patients with driver mutations being treated with TKIs with oligo-residual disease

Q: Do you ever give chemo along with IO in patients with PDL1 >50%?

KEYNOTE 024: First study to show that IO was superior to chemo in high PDL1 patients lead to an instant change in our approach
More recent data suggests that there are differences between patients with PDL1 90% vs. someone at like 50, 60, or 70% (not all PDL1 >50% is created equal!)
If there is a patient with a lot of cancer burden, a lot of symptoms, and rapid progression of disease, you don’t want to miss an opportunity to do what is best for the patient. There is always a chance that IO may not work as monotherapy. This is a case-by-case discussion, but in cases like this, he discusses with his patient about using chemo + IO

** Essentially attacking the cancer from multiple angles

Q: In patients with positive driver mutations who are initially stable on treatment, but then progress, do you repeat molecular testing at the time of progression? Do you ever treat with two TKIs at the same time?

Dr. West referenced recent abstract at ESMO 2022 by Dr. Julien Mazieres from CHU de Toulouse in France who presented data regarding the use of MET inhibitor tepotinib with osimertinib:

** In the study, when screening for MET amplification, about 36% of patients were positive; at 9 months, the response rate was 54%

** One limitation of this study is that every company that tests for MET amplification has a different definition of what constitutes “amplification”

Otherwise, there is mixed data about this
Molecular testing is often done on repeat biopsies in many academic centers, but that is not universally true and not the standard of care

Q: TKIs have great CNS penetration. Let’s say a patient achieved a CR of CNS metastasis, but has progression of disease elsewhere. Do you continue the TKI?

He prefers, in general, to continue TKI given great CNS penetration while adding chemotherapy for other systemic metastatic sites

** This is more expert opinion, not well-studied

Flare phenomenon can happen, meaning that abruptly stopping TKI may allow a clone of the cancer to begin rapidly growing if this subset of disease is responsive of treatment
Remember: Not all mutations are created equally

** You DO NOT want to give EGFR and/or ALK IO even if they have a high PDL1

** On the other hand, patients with KRAS and BRAFV600E do respond to IO treatment

About our guest:

Dr. Jack West is an internationally-renowned Thoracic Oncologist. Associate Professor in the Department of Medical Oncology & Therapeutics Research at City of Hope Comprehensive Cancer Center. He is also the Clinical Executive Director of AccessHope. He completed his medical education at Harvard Medical School, and then trained at Brigham and Women’s Hospital before heading to Fred Hutchinson at the University of Washington. Twitter: @JackWestMD

References:

https://www.nejm.org/doi/full/10.1056/nejmoa1606774 - KEYNOTE024

https://www.nejm.org/doi/full/10.1056/nejmoa1910231 - CHECKMATE227

https://oncology.medicinematters.com/esmo-2022/non-small-cell-lung-cancer/insight-2-tepotinib-osimertinib-advanced-nsclc/23480600 - ESMO 2022 abstract on tepotinib with osimertinib

https://www.thefellowoncall.com/tfocpodcast/jt7mmp342rn85wy - Episode 032

https://www.thefellowoncall.com/tfocpodcast/jt7mmp342rn85wy-stczg - Episode 033

Please visit our website (TheFellowOnCall.com) for more information

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Lung cancer is one of the most commonly diagnosed type of cancer and so it is fitting that we start the first of our disease-specific oncology series with this diagnosis. This week, we begin to round out our NSCLC series with the first of two episodes where we interview Dr. Jack West from City of Hope!

We strongly recommend you listen to our previous episodes on early stage lung cancer (Episodes 026 and 029) to follow along in this discussion. Key trials mentioned in this episode include:

ADAURA Trial

IMPOWER010

CHECKMATE816

Q: We’ve previously discussed that adjuvant cisplatin doublet chemotherapy is used for tumors > 4cm and/or nodal involvement. Given that PD-L1 status and EGFR status can also potentially change adjuvant therapy choices, how do you employ these tests in your practice?

Different approaches at every center/with different thoracic oncologists.
Dr. West does NOT recommend sending broad NGS testing on everyone if it is not going to change management.
It it may influence management, at the very least, PDL1 and EGFR should be performed because of implications on adjuvant treatment options (See Episode 026 for treatment discussions):

** ADAURA Trial: Adjuvant Osimertinib x3 years for EGFR+ patients

** IMPOWER010: In patients with PDL1 >50%, patients did better with 1 year of immunotherapy (atezolizumab) after adjuvant therapy

In patients with higher risk disease, can consider sending broad NGS, particularly looking for ALK and other mutations; remember that EGFR and ALK+ patients do NOT respond to immunotherapy well. This is important because we don’t want to give someone side effects that they would not otherwise had (these patients are getting treatment adjuvantly AKA after their disease is already resected!)

Q: What are limitations of the ADUARA Trial?

The ADUARA suggested disease-free survival advantage with use of osimertinib, but we don’t know final overall survival data yet.

*Limitations:

** Three years of therapy

** Very expensive drug

** More data presented at ESMO 2022 on efficacy; Dr. West stated that there appears to be drop off in survival after stopping drug. Overall survival data not yet available

Just because patients can get osimertinib does NOT mean that they are not eligible for chemotherapy

**Adjuvant chemotherapy for patients provides long-term benefit

** JBR.10 Trial: Older trial, but showed that patients who got adjuvant treatment (in this case vinorelbine plus cisplatin) had prolonged disease-free and overall survival in early-stage non–small-cell lung cancer.

** Follow up study suggested that EGFR+ patients trended towards longer survival

Q: What are your thoughts on Checkmate 816 with the use of neoadjuvant nivolumab in addition to the platinum doublet? Do you think pathologic CR was an appropriate surrogate endpoint for the trial?

Complete path CR is a new end-point, but it does correlate with PFS. We cannot always for traditional endpoints, such as overall survival data, to mature because doing so may result in us withholding therapy that may be very beneficial.
Biggest benefit to neoadjuvant treatment is that more patients are able to get the full regimen. Many have complications after surgery and never are able to then get/benefit from chemotherapy. Supported by data from NATCH trial

Q: What are your thoughts on induction chemoradiation vs. chemotherapy alone?

Dr. West prefers to not use radiation pre-operatively, with some exception (for instance, pancoast tumor)

Tune in next week for part 2 of this discussion!

About our guest:

References:

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)02098-5/fulltext - IMPOWER 010 Trial

https://www.nejm.org/doi/full/10.1056/NEJMoa2027071- ADAURA Trial

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4032958/ - NATCH Trial

https://www.nejm.org/doi/pdf/10.1056/NEJMoa043623 - JBR.10 Trial

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033998/ - Follow up to JBR.10 Trial looking at influence of EGFR status on chemotherapy response

https://www.nejm.org/doi/10.1056/NEJMoa2202170 - CHECKMATE 816

https://www.thefellowoncall.com/tfocpodcast/episode-001disclaimer-wfhgf-ml3b6-9m66a-8rrc4-k8w87-x7xdd-wrzye-4xg8x-t73gt-cxc5s-nmg8f-cfyd6-hgs35-5pcwx-tf6dh-trggt-xzkt7-923gg-rpjzx-6s36p-hk27n-bbpgx-jymml-9lfam-76m4s - Episode 026

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Lung cancer is one of the most commonly diagnosed type of cancer and so it is fitting that we start the first of our disease-specific oncology series with this diagnosis. This week, we continue our discussion on metastatic non-small cell lung cancer, focusing on NSCLC with driver mutations.

The approach to treatment of a patient with widespread metastatic NSCLC (mNSCLC) is very different than a patient without distant disease, which highlights why we do what we do:
Important to complete staging (discussed in prior episodes) to determine the extent of disease
Important to check molecular testing (looking for mutations in the cancer cells) and IHC for tumor proportion score (TPS) helps determine treatment options
If your molecular testing is identified in a driver mutation gene, there are targeted options for this!

*Driver mutations are predictive of response to an oral therapy and a LACK of response to immune therapy (particularly in EGFR and ALK mutated patients)

EGFR Mutation:
Pay attention to the types of mutation in EGFR (not all are the same):

-- Exon 19 deletion

-- Exon 19 L858R

-- Exon 21 T790M

-- Exon 20 Insertion (Osimertinib [see below] cannot be used for this mutation)

Osimertinib is first-line standard of care for patients with EGFR

-- Used to be a second-line agent. Many patients with EGFR mutations receiving earlier generation TKIs would develop resistance and when these tumors were sequenced, they would have Exon 21 T790M mutations. Osimertinib was effective even with this mutation and had superior overall survival data compared to chemotherapy (AURA3 Trial)

--Now it is used in first-line setting for patients with EGFR mutation based on the FLAURA trial

--- In this study, patients received osimertinib as first line vs. older generation EGFR-targeting TKIs (erlotinib or gefitib) and Osimertinib had better outcomes:

---- Showed that the median OS was 38.6 months with Osi vs. 31.8 months; also improved brain penetration!

---- Also effective in patients with metastatic disease to the brain:

----- Only 6% of patients had CNS progression with Osi vs. 15% with others

What if a patient is on Osi and later develops new brain mets?

-- If there is progression within just the brain (and good control in other sites of the body) you can refer patient to Radiation Oncology for SRS

-- Remember, based on discussion with Dr. Osmundson in our RadOnc lectures (Episode 028), it is important to HOLD Osimertinib if patient is going to get radiation to minimize the side effects

What is patient had progression of disease in several sites throughout the body?

-- Management is less straightforward.

-- In many of these cases, you can consider:

--- Consolidative radiation - If small amounts of disease

--- Changing therapy - If there has been widespread progression; likely would change to chemotherapy (without IO, since lower predictive response to IO with EGFR mutation)

---- No clear guidelines if you should continue the TKI

---- Remember that IO + TKIs can cause increased risk of side effects, such as pneumonitis and hepatitis. DO NOT DO THIS!

ALK Mutation:
There are many options for ALK mutations

-- The first generation drug is crizotinib

--- Lots of side effects —> “It is crazy to start with crizotinib”

--- Studies for later generation TKIs were compared to crizotinib

-- Many people today will use third generation ALK-inhibitor alectinib (Important trials: ALEX Trial and J-ALEX Trial)

--- With alectinib, PFS 34.8 months, RR 83%, less CNS progression (12% vs 45%)

--- 5 year OS rate 62.5%

What to do with disease progression while on ALK inhibitor?

-- In ALK, you can actually switch to another ALK inhibitor and many will respond well

--- Of course, with each change, you may expect not as great of a response

Lots of other mutations!
TFOC recommends just looking these up!

-- Link to NCCN Guidelines on NSCLC; Page 41 has full list!

Another way to think about this, when do we NOT do TKIs as first line:

-- KRAS G12C

-- EGFR Exon 20 Insertion

-- HER2

How do you counsel a patient when considering/starting a TKI?

-- Patients with highest chance of having a targeted mutation are younger non-smokers with adenocarcinoma

-- Set expectations: great outcomes overall, but still not a cure.

-- Remembering the drugs: All TKIs usually end in “-nib”

-- In general, the way we recommend remembering this: “Fatigue, GI, Derm (skin/nail changes)”; rarely pneumonitis

References:

AURA3 Trial - https://www.nejm.org/doi/full/10.1056/NEJMoa1612674

Established osimertinib was better than chemo for patients with EGFR mutation and acquired Exon 21 T790M resistance mutation

FLAURA Trial - https://www.nejm.org/doi/full/10.1056/nejmoa1713137

Established osimertinib as first-line agent for patients with EGFR mutation

ALEX Trial - https://www.nejm.org/doi/full/10.1056/nejmoa1704795

Helped establish alectinib as superior for ALK mutations compared to crizotinib

J-ALEX Trial - https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)30565-2/fulltext

Helped establish alectinib as superior for ALK mutations compared to crizotinib

NCCN Guidelines on NSCLC - https://www.nccn.org/guidelines/guidelines-detail?category=1&id=1450

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Lung cancer is one of the most commonly diagnosed type of cancer and so it is fitting that we start the first of our disease-specific oncology series with this diagnosis. This week, we start our discussion on metastatic non-small cell lung cancer, focusing on NSCLC without driver mutations.

The approach to treatment of a patient with widespread metastatic NSCLC (mNSCLC) is very different than a patient without distant disease, which highlights why we do what we do:
Important to complete staging (discussed in prior episodes) to determine the extent of disease
Important to check molecular testing (looking for mutations in the cancer cells) and IHC for tumor proportion score (TPS) helps determine treatment options
Choosing a treatment is based on:
Histology - cannot use pemetrexed or bevacizumab in squamous cell
Platinum - Carboplatin is usually used (as opposed to our prior discussions about using Cisplatin because of LACE pooled analysis data)

-- Why is Cisplatin not a great idea? Cisplatin should not be used if patients have (high yield to know cisplatin eligibility criteria!!):

--- Poor performance status

--- Patients with eGFR <60

--- If a patient has baseline hearing loss

--- If a patient has baseline neuropathy

--- Patients with NYHF class III+

--If patient is getting “palliative” / non-curative setting, you want to spare patients these terrible potential side effects

-Immunotherapy - All patients with mNSCLC should have IO considered for treatment, unless they have contraindications. Considerations include:

-- Patients with EGFR and ALK mutations - patients with these mutations do NOT respond well to IO so should not use

-- TPS score:

--- Patients with score >50% can get IO monotherapy (spared chemotherapy)

---- KEYNOTE 024: approval for pembrolizumab monotherapy in patient with PDL1>50%

----- Study compared pembro to platinum doublet

----- OS 70% vs. 50% at one year

---- IMPOWER110: approval for atezolizumab monotherapy

----- Study compared atezo to chemotherapy

----- OS 64.9% vs 50% at 12 months

--- Patients with score <50% can get IO + chemotherapy

---- KEYNOTE 189: Showed that the addition of Pembrolizumab to carboplatin/pemetrexed followed by pembro/pemetrexed maintenance in mNSCLC with adenocarcinoma histology had impressive benefits

---- Carbo/taxol/pembro for squamous histology

--- Lots of other trials, check out NCCN for a comprehensive list

Putting this all together:
In PDL1 >50% WITHOUT SYMPTOMS: IO alone
In PDL1 >50% WITH SYMPTOMS: Chemo + IO
In PDL1 <50%:

-- Lots of options, but usually some combination of chemotherapy + IO

-- Many people use Pembro, as it was first to market

Management of mNSCLC to the brain:
Recommend discussion with radiation oncology about role of SRS

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Lung cancer is one of the most commonly diagnosed type of cancer and so it is fitting that we start the first of our disease-specific oncology series with this diagnosis. This week, we sit down with Thoracic Surgeon, Dr. Jane Yanagawa to discuss surgical considerations in treatment of NSCLC.

How do you choose what type of surgical resection to do?
Considerations:

--Lung anatomy

--Location of the nodule within lung

--Lymph node involvement

-Options:

--Pneumonectomy: removal of whole lung

--Lobectomy: remove a whole lobe

--Segmentectomy/sublobar resection: part of a lobe

What does “adequate margins” mean? And how do you know if it’s enough?
If you’re removing the whole lobe, it does not matter as much
If you’re doing a segmentectomy, you want to have samples evaluated while in the OR because if there is signs of more disease that initially thought, you would take this one step further and do a lobectomy.
Need to consider the patient’s situation - how good is their status
Why does preoperative workup matter?
Pulmonary function tests: Surgeons are looking at the %FEV1 and %DLCO to then predict what their function would be AFTER surgery. After surgery, they want to ensure patient has %FEV1 or %DLCO >40%.
Lung anatomy: In patients with COPD and endobronchial lesions, sometimes they also get V/Q scans to evaluate ratio
Cardiac echo: Important in pneumonectomy where removal of lung tissue will also remove a significant amount of blood vessels. Want to rule out pulmonary hypertension pre-operatively.
Pulmonary hypertension can also affect someone’s survival while they’re ventilating with only one lung during the procedure (“single lung ventilation”).
Smoking status: Smoking can increase complications by ~60%.
Pre-habilitation: Encouraging patients to be fit prior to surgery with walking, nutrition, +/- pulmonary rehabilitation
What is “VATS”?
VATS stands for video-assisted thoracoscopic surgery; it is not, in itself, a procedure. But a VATS allows for minimally invasive surgery through the use of a camera.
It involves three incisions (axilla, lowest part of mid-axillary line, one posterior)
In what scenario is a mediastinoscopy warranted?
Needed after EBUS if there is still high index of suspicion for cancer involvement in lymph nodes, even if lymph nodes are negative from EBUS
What is “systematic lymph node sampling”?
An organized way to sample lymph nodes, including all lymph nodes that are along the way, not just the ones that may be involved
As a surgeon, how do you determine if a patient is okay for surgery if the mass is invading another structure?
Need to take the anatomy into consideration - are there major blood vessels or nerves there, for instance, which can impact outcome and recovery.
When should we consider induction chemotherapy from a surgeon’s perspective?
Lots of changes in this sphere coming; lots of discrepancy between institutions when there is N2 disease
In Dr. Yanagawa’s opinion, anyone with N2 disease should get neoadjuvant therapy
If there is neoadjuvant chemoradiation given, how does that effect your surgery?
Radiation increases scar tissue in the lung tissue. But what is worse is that radiation neoadjuvantly may make wound healing more difficult. She does not prefer radiation pre-operatively
Chemotherapy also adds scar tissue

*How does neoadjuvant IO therapy affect scar tissue formation?

The hilum and lymph nodes are more swollen, but does not translate to more complications
She has even seen patients who had gotten IO for another cancer and then get lung cancer, she can still appreciate swollen nodes!
How long after surgery is it safe to start adjuvant therapy?
If patient has a complication from surgery, would not start right away. It is important to discuss with the surgeon about when it is okay to proceed with adjuvant therapy.
If patient has good recovery/without complications, okay to start about 4 weeks after
There is no good guidance yet about when it is safe to start IO after surgery

About our guest: Jane Yanagawa, MD is an Assistant Professor of Thoracic Surgery at the UCLA David Geffen School of Medicine and the UCLA Jonsson Comprehensive Cancer Center. She completed medical school at Baylor College of Medicine, after which she went to UCLA for her surgical residency. She went onto Memorial Sloan-Kettering for her Thoracic Surgery Fellowship. In addition to her practice as a thoracic surgeon at UCLA, Dr. Yanagawa also sits on the NCCN NSCLC guidelines committee! We are so grateful she was able to join us despite her very busy schedule!

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If you’ve been with us since the beginning, thank you! But we've had a lot of new friends join the party so we thought we'd interrupt our regular programming to re-introduce ourselves! So if you’re new here, welcome to the Fellow on Call! We are so glad you’re here.

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Lung cancer is one of the most commonly diagnosed type of cancer and so it is fitting that we start the first of our disease-specific oncology series with this diagnosis. This week, we round out our discussion of early stage lung cancer treatment!

When deciding if a patient can get surgery upfront or not, remember the three “Fellow on Call” criteria for early stage lung cancer:
Mass invading other structures or mediastinum
Central lymph nodes (single digit)
Tumor >7 cm
If surgery is NOT an option at this time, where do we go from here?
Treat with upfront concurrent definitive chemoradiation
Treat with “induction” chemotherapy or induction concurrent chemoradiation

If surgery is/may be possible

*What are the goals of “induction” treatments?

Eradicate microscopic disease
Improved local control, possibly shrinkage
Adding radiation may allow you to downstage tumor or lymph nodes to have a possible improvement in surgical outcomes
What sorts of discussions are being had a thoracic tumor board in patients with newly diagnosed early stage NSCLC?
Is the patient a surgical candidate?
If the patient is not a surgical candidate, then what are the options:

--Definitive concurrent chemoradiation (usually) followed by immunotherapy

---Pearl 1: Always choose this if surgeon thinks the patient is unresectable in general even with an induction approach

---Pearl 2: Always choose this if 2 out of 3 criteria we discussed above are met

---Pearl 3: Always choose this if N3 disease

“Induction” regimen with either chemotherapy alone or concurrent chemoradiation followed by surgery
What’s the idea behind “induction” chemo or chemoradiation?
There is a chance that patients with these high risk features may already have micrometastatic disease, so treatment upfront can help address that
There is a chance that after surgery, patient may suffer deconditioning, which may preclude the use of chemo +/- radiation (up to 90% of patients are often eligible for chemoradiation before surgery; this drops to ~60% after surgery)
Local disease control to achieve the best possible surgical outcome (R0 resection) and also prevent any microscopic residual disease from then having the opportunity to spread systemically, especially in areas where the mass may be adjacent to many blood vessels or lymph nodes
What to treat with in the neoadjuvant setting?
Platinum containing regimens (“platinum doublets”):

-- Carboplatin + paclitaxel

-- Cisplatin + etoposide

-- Cisplatin + gemcitable

-- Cistplain + pemetrexed

Can combine this with radiation
How does the data about chemotherapy+IO in the neoadjuvant setting fit in here (CHECKMATE 816)?
In patients with Stage IIB to IIIA (8th edition) WITHOUT EGFR or ALK mutation, treatment with NEOADJUVANT chemotherapy q3w x3 cycles (most got cisplatin based therapy) + nivolumab 360mg q3w x3 cycles resulted in improved event free survival (31.6 months vs. 20.8 months) AND pathological complete response was 24.0% vs. 2.2%
Current NCCN guidelines state that if nivolumab is used in neoadjuvant setting, it should not be used in adjuvant setting
There is still uncertainty about how this fits into treatment compared to “traditional” neoadjuvant approaches with chemo+/-radiation

*So after neoadjuvant treatment, does everyone go to surgery?

Always re-assess the status of the disease; if there is progression of disease, then will go to definitive chemoradiation
Discuss with surgeons to confirm if the patient is still a surgery candidate
If patient undergoes surgery, then what?
If patient got neoadjuvant therapy and an R0, then they are done with treatment
If R0 resection was not able to achieved, then either radiation “boost” to the area (if they previously got radiation), a course of radiation (if they just got induction chemo) or re-resection
We discuss the adjuvant setting in more detail in Episode 026 (https://www.thefellowoncall.com/tfocpodcast/episode-001disclaimer-wfhgf-ml3b6-9m66a-8rrc4-k8w87-x7xdd-wrzye-4xg8x-t73gt-cxc5s-nmg8f-cfyd6-hgs35-5pcwx-tf6dh-trggt-xzkt7-923gg-rpjzx-6s36p-hk27n-bbpgx-jymml-9lfam-76m4s)

If surgery is not possible

If patient cannot go through to surgery Definitive chemoradiation:
Same chemotherapy agents as above, but treatment course is longer.
For instance, for NSCLC, total 60Gy in 2Gy divided fractions (5 days/week, 6 weeks of treatment) with chemotherapy
Additional therapy after chemoradiation (PACIFIC Trial)
Found that “consolidation” durvalumab 44% PFS 18 months vs 20% 5year survival benefit 40% vs. ~30% without treatment

References:

https://www.nccn.org/guidelines/guidelines-detail?category=1&id=1450 - NCCN Lung Cancer guidelines

https://www.nejm.org/doi/full/10.1056/nejmoa1709937 - PACIFIC Trial (NEJM 2017)

https://www.nejm.org/doi/10.1056/NEJMoa2202170 - CHECKMATE 816 (NEJM 2022)

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Lung cancer is one of the most commonly diagnosed type of cancer and so it is fitting that we start the first of our disease-specific oncology series with this diagnosis. An important component of treatment in lung cancer (and many other cancers) is the use of radiation. This week, we continue our discussion about the fundamentals of Radiation Oncology with our guest, Dr. Evan Osmundson.

*We hear the terms “hypo-fractioned” and “hyper-fractionated” radiation. What do those mean?

Fractionation, that is breaking up the total dose of radiation into smaller ones, has allowed patients to tolerate the radiation better. The repeat exposure allows the healthy tissue to repair, whereas the tumor is not able to heal as well
Standard fractionation involves keeping the maximum dose per session at 1.8-2Gy/fraction.
Hyper-fractionation is when a patient gets multiple doses per day, each less than 2Gy. This is important in small cell lung cancer, where the standard dose of radiation is 1.5Gy twice daily
Hypo-fractionation os when larger doses are given in each session, typically larger than 2.5-3Gy, often 4-5Gy per fraction. This is analogous to SBRT.

*With regards to SBRT, how do you determine the number of sessions?

Typically 3-5 sessions, and this is based on data run through their computer algorithm that allows the dose to be tumoricidal.
More sessions (more likely 5 sessions) if central tumor (<2cm central proximal bronchial tree) or ultra-central tumor (directly abutting bronchial tree/major vessel) or abutting the chest well. Poor outcomes in some studies with fewer sessions; 5 sessions seem to work well in central tumors, based on recent data.
Logistically speaking, five sessions is also typically the maximum that insurance will pay for.

*What’s the max size of the tumor that is amenable to SBRT?

Most clinical trials have limited size to 5cm or less, but he has done SBRT to larger tumors. This is a case-by-case basis.
How do you calculate the duration of treatment when we are going to do concurrent chemo-radiation?
Treatment is usually 5 days a week, with the weekends off for patients
In NSCLC, total 60Gy appears to be the standard of care, based on RTOG 0617 study. (J Clin Oncol 2020 Mar 1;38(7):706-714. doi: 10.1200/JCO.19.01162. Epub 2019 Dec 16.); practically this means about 6 weeks of treatment.
In SCLC, Target 45Gy broken up into 1.5Gy TWICE daily OR 66Gy broken up into 2Gy ONCE daily is the standard of care based on CONVERT trial (Lancet Oncol. 2017 Aug;18(8):1116-1125. doi: 10.1016/S1470-2045(17)30318-2. Epub 2017 Jun 20.)
What is your guidance to avoid brain toxicity, for instance with using SRS to the brain for a brain met?
There is a risk of brain necrosis from the synergism between certain chemotherapies/targeted agents that penetrate the blood-brain barrier with SRS that can cause radiation necrosis to the brain. This is particularly an issue with TKIs, such as osimertinib. Dr. Osmundson recommends holding TKIs about 5-7 days, if possible.

*What is proton therapy and how does it differ than “traditional” radiation therapy?

With x-rays/photon therapy, the beam is attenuated and there is an exit dose that can affect the neighboring tissues.
With proton beams, there is a “Bragg-Peak” effect, whereby you can specify how deep you want to radiation to deposit with little exit dose.
Per Dr. Osmundson, we are not currently in a position to recommend proton therapy AT THIS TIME, but this may be changing. Research is being done to better be able to maneuver the beam angles.
Proton therapy is also very expensive at this time

A special thank you to our guest, Evan Osmundson, MD, PhD, Associate Professor in the Department of Radiation Oncology and serves as the Medical Director of Radiation Oncology at Vanderbilt University Medical Center in Nashville, TN!

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Lung cancer is one of the most commonly diagnosed type of cancer and so it is fitting that we start the first of our disease-specific oncology series with this diagnosis. An important component of treatment in lung cancer (and many other cancers) is the use of radiation. Here, we discuss the fundamentals of Radiation Oncology with our guest, Dr. Evan Osmundson.

Basic vocabulary:

Fraction/Fractionation: The total dose of radiation divided into smaller doses
Grey: Unit of measure of radiation being delivered in each session
Bragg-Peak effect: Specific to proton therapy (as opposed to photon therapy). It describes the sharp increase in concentration of the energy when hitting the tumor, while minimizing the effects to surrounding tissue.
Radiosensitizing chemotherapy: small doses of chemotherapy used to make the cells more responsive to the deleterious effects of radiation

Fundamentals of radiation oncology:

*When we make a referral to RadOnc, what happens then?

Send over any available imaging that is available
Team reviews the imaging to ensure that staging is completed
Simulation scan: Uses a CT scan to “simulate” the treatment; specifically map out the tumor and the surrounding organs/structures. Multidisciplinary team reviews the scan to maximize the dose to the tumor and minimizes damage to surrounding structures.
Based on the scans, they test run the treatment on a model to ensure that the simulation on the computer is able to be replicated on a model.
The above is why it can take a while for treatment planning to take place

*What sorts of imaging modalities are important to have for patients prior to getting to Rad Onc?

Send prior CT imaging
If planning for radiation to the brain, should get thin-sliced MRI w/ and w/o contrast
If prostate cancer, also consider getting MRI

*Many patients express concern about the “mask fitting” - what is that?

To ensure that the same dose of radiation is administered each time, it is important for the patient to remain very still and/or the same position every session. The mask is custom fit to ensure patient is in the correct position.

*How do you determine the “maximum dose” of radiation in the mediastinal area is?

The maximum dose tolerance is dependent on the structure in question. A structure “in series” such as the bronchial tree would have profound effects if tissue is injured compared to lung parenchymal tissue (If you damage some, there is plenty more that is able to compensate)
Always concern for spinal cord when radiating the mediastinum

*What are side effects you counsel patients on, specifically in thoracic radiation?

Fatigue (usually not debilitating), radiation esophagitis, pericarditis (rare)
Radiation pneumonitis (usually 6-8 weeks, but can be up to one year), presents with cough, shortness of breath; likelihood of this is dependent on duration of treatment, dose of radiation, location

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How do we think about treatment of lung cancer?

Recap on staging (see Episode 025)

Pro-tip: Highly recommend that you “forget” about the actual staging and focus more on the individual T, N, and M status
Tumor size:

**T1a <1 cm

**T1b <2 cm

**T1c <3 cm

**T2a <4 cm

**T2b <5 cm

**T3 5-7 cm

**T4 cm

*Nodal status:

**Double digit nodes = hilar or intrapulmonary (peripheral) = N1

**Single digit nodes = mediastinal (central ) = N2

**Contralateral nodes or supraclavicular = N3

*Sites of metastatic disease

Approach to treatment in a stepwise approach:

*Goal: Whenever feasible, we want to consider getting the patient to surgery to remove the cancer.

*Surgery or no surgery?

**How do we decide if someone is appropriate for surgery:

***Do they want surgery?

***Do they have the pulmonary reserve if they were to get surgery ?

***Do they have the cardiac reserve to withstand surgery?

***Is the tumor size too big? (Usually >7cm)

***Is the tumor invading other structures?

****If invading other structures, surgery may not be possible; highly consider tumor board discussion

***Mediastinal lymph node involvement?

****Central lymph node involvement usually requires definitive chemotherapy + radiation (not surgery up-front)

***Supraclavicular lymph node or contralateral lymph node?

****This would be treated with chemotherapy and radiation

Speaking of surgery, what are the options for types of surgeries for lung cancer?

*Sub-lobar:

**Wedge (smallest resection)

**Segmentecomy - ideally we want to do at least a segmentectomy

*Lobar resection:

**Lobectomy

**Pneumonectomy

What if a patient’s tumor is amenable to surgery, but the patient’s underlying co-morbid conditions preclude him from getting a surgical intervention?

*This is where we consider using radiation for treatment, specifically Stereotactic body radiation therapy (SBRT)

Characteristics of surgical report?

*The “R” status is if there is residual tumor after the surgery. This is a combination of evaluation by a pathologist AND by gross inspection by the surgeon

**R0: No evidence of disease

**R1: Microscopic sites of disease

**R2: Macroscopic sites of disease (visible tumor)

*Why does this matter?

**If there is residual disease, there may be a role for further resection and/or systemic therapy

*When a tumor is >4cm, patients are higher risk for recurrence, even without nodal disease or metastatic disease. We will give these patients chemotherapy in the adjuvant setting.

Approach to adjuvant chemotherapy:

*In NSCLC, it is often a two-drug regimen, including a platinum-based therapy

*Cisplatin is important

**Based on LACE Pooled Analysis (https://ascopubs.org/doi/10.1200/jco.2007.13.9030)

***Cisplatin-based adjuvant therapy vs. placebo showed >5% improvement in survival when using cisplatin-based therapy

***For adenocarcinoma:

****Give cisplatin with pemetrexed

****ALWAYS start patient on B12 and folate at least 1 week before starting pemetrexed and continue this throughout treatment, up to and including 3 weeks after their treatment course

***For squamous cell caricnoma:

****Give cisplatin with gemcitabine OR docetaxol (taxotere)

*Nodal involvement (N1): Give two-drug regimen, as noted above

*Additions to two-drug regimen:

**IMPOWER 010 Trial: In patients with PDL1 >50%, patients did better with 1 year of immunotherapy (atezolizumab) after adjuvant therapy (https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)02098-5/fulltext; https://ascopost.com/issues/november-10-2021/impower010-adjuvant-atezolizumab-improves-disease-free-survival-and-nsclc-relapse-in-patients-whose-tumors-express-pd-l1/)

**Mutations matter! ADAURA Trial: EGFR with exon 19 deletion or L858R can get osimertinib, which had an improved outcomes (https://www.nejm.org/doi/full/10.1056/NEJMoa2027071)

References:

https://ascopubs.org/doi/10.1200/jco.2007.13.9030 - LACE Pooled analysis

https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)02098-5/fulltext - IMPOWER 010 Trial

https://www.nejm.org/doi/full/10.1056/NEJMoa2027071- ADAURA Trial

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Lung cancer specialized testing in NSCLC:

What do we do if we biopsy a suspected metastatic lesion?

Immunohistochemistry (IHC):

**Confirm if it is metastatic NSCLC

**Confirms the histology of the NSCLC (such as adenocarcinoma vs. squamous cell)

**Used to determine the type of chemotherapy that can be administered for treatment

*PDL1 testing:

**PDL1 is a protein expressed by certain cancer cells allowing them to evade the immune system (“fake mustache analogy”).

**Also confirmed by IHC

**This protein is targetable!

**Often measured as:

***Total protein expression (TPS): The number of positive tumor cells divided by the total number of viable tumor cells multiplied by 100%

***Composite protein expression (CPS): The number of positive tumor cells, lymphocytes and macrophages, divided by the total number of viable tumor cells multiplied by 100%

*Molecular testing:

**We discuss this in detail in Episode 005

**Genetic information from the tissue sample

**Always better to get sample from soft tissue than from bone

**Why is this important?

***To be able to identify “driver mutations”

****What is it? Important mutations that may be “driving” oncogenesis

****Many of these have drugs that directly target these mutations

Prognostic vs. predictive biomarkers:

*Prognostic biomarkers: Mutations or changes that give information about the cancer’s overall outcome regardless of therapy

*Predictive biomarkers: Mutations that provide information about how a cancer may respond to a particular drug

Cell-free DNA (AKA “liquid biopsy”):

*Special tests that can detect microscopic amounts of cancer cell DNA within the patient’s blood which may also be used to find prognostic/predictive biomarkers

*Ongoing studies to see if this can be used to find relapse of disease

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Lung Cancer Histology and Staging

*Workup for a nodule that is concerning:

**Ensure there is a dedicated CT scan of the chest to evaluate

**Try to obtain old imaging; the rate of change is important

**Can get PET, but even if a lesion if not FDG-avid, but growing quickly we should consider biopsy anyway

**Referral to pulmonary medicine, who can assist with biopsy and also regional lymph node evaluation (important – more below)

**PFTs are often ordered because it provides information about lung function in anticipation of possible surgery for treatment

Lung Cancer Histology:

*Non-small cell lung cancer (NSCLC)

**Umbrella term for a variety of cancers

**Increased risk in smokers

**More common types:

***Adenocarcinoma (~50% of all lung cancers)

****Most common overall; cancer of the mucus producing cells

****IHC: TTF-1, NapsinA, CK7 positive

***Squamous Cell Carcinoma (22.7%)

****More often seen in patients with a smoking history

****IHC: p63 positive and cytokeratin pearls

***Remaining ~15% are the other types of lung cancer / mixed histologies

**Small cell lung cancer (SCLC)

***Neuroendocrine tumor with very different pathology

***Much more aggressive than NSCLC

***Oncologic emergency

***IHC: Chromogranin and synaptophysin positive

IHC pearls: TTF-1 usually means lung cancer (but can be negative in squamous cell lung cancer). This will be important in the future (we promise :])

*Staging for NSCLC:

**Nodal evaluation: lymph node evaluation is part of the workup for NSCLC

**Single digit = central/mediastinal nodes (higher risk)

**Double digit = peripheral/hilar/intrapulmonary lymph nodes (lower risk)

**“R” vs. “L” is direction

*Pearl: Why is this important? If there is nodal involvement, systemic therapy is going to be necessary

*Putting it all together:

**T: Tumor size: T1-4

**N: Nodal involvement

***N0: no nodal involvement

***N1: Nodes closest to the primary tumor (double digits)

****Ipsilateral peribronchial, hilar, intrapulmonary

***N2: Further away (single digit)

****Ipsilateral mediastinal and/or subcarinal LN

***N3: Contralateral any node or supraclavicular LN

**M: Metastasis – in lung cancer, patients with certain patterns of metastatic disease are still curable!

***M0: no mets

***M1a: Contralateral lobe, pleural effusion or pericardial effusion à these are generally still curable!

***M1b: single site of metastatic disease à these are generally still curable!

***M1c: multiple sites of metastatic disease à these are generally not curable

*Staging for SCLC:

**Limited stage - meaning it can fit in “one radiation field”

**Extensive stage - does not fit in “one radiation field”

*Once lung cancer is diagnosed:

**Go to NCCN to learn the flow of ongoing management

**Complete staging (if not already done):

***CT C/A/P (don’t necessarily need if a PET scan is done)

***PET Scan

***MRI brain à in general this is needed, but there are some exception to this (see NCCN)

**Referral to pulmonary for nodal evaluation

References:

NCCN.org

https://doi-org.proxy.library.vanderbilt.edu/10.1016/j.semcancer.2017.11.019-Article about IHC markers for lung cancer

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Lung cancer is one of the most commonly diagnosed type of cancer and so it is fitting that we start the first of our disease-specific oncology series with this diagnosis.

This week, we sit down with guest pulmonologist Dr. Greta Dahlberg to discuss how she thinks about and works up lung nodules concerning for malignancy.

Lung nodules:

For discussions about incidental lung nodules and lung cancer screening, check out Episode 197 from our friends, The Curbsiders (link: https://thecurbsiders.com/podcast/197)
Nodule vs. mass:

** “Micronodule” is <3mm

** “Nodule” is <3 cm

** “Mass” is anything bigger

*Characteristics of “benign” vs. “malignant” nodule

** Most important thing is change over time; therefore always good to have old imaging if possible.

** If growing overtime, even if slowly, that should raise red flags for malignancy

** Volume doubling time (link: https://radcalculators.org/volume-doubling-time-vdt-calculator-for-pulmonary-nodules-volume-based/)

*** If doubling time <20 days, it’s often infectious

*** Average lung cancer doubling times is 100 days

Benign:

** Smooth

** Calcifications (diffusely or popcorn calcifications)

** Internal fat appearance

What about a spiculated nodule?

** This is when there are nodules with “little hairs” coming off, often thought to be malignant

** Dr. Dahlberg reports that odds ratio of it being malignant is 2.5, so it is high, but not that high. So spiculated does NOT necessarily mean malignant.

Workup before referring to Pulmonary:

** Dedicated CT scan of the chest

** Obtain old imaging

** PET CT

*** Expert tip: If growing, whether it’s hot or not, it warrants a biopsy

*** PET can help identify spread and/or nodal involvement

Biopsy approaches (we don’t know approach which one is better … There are studies ongoing!):

** Transthoracic biopsy (CT guided):

*** Performed by IR

*** Major risk: pneumothorax (20-25% have one after procedure!)

*** Benefit: Does not need general anesthesia

**Transbronchial biopsy:

*** Performed by Pulmonary

*** Requires general anesthesia and paralyzing

*** Options while doing biopsy:

**** EBUS

**** Fluoroscopy

*** Major risks: Pneumothorax (1.5% have one, less than half need chest tube)

*** Benefit: You can also do EBUS to stage mediastinum. Remember- we always look to upstage a cancer and by looking at the mediastinum, this helps to accomplish that

What if someone has two lung nodules on contralateral sides?

** Likely both will be sampled

** If PET has one nodule that is more FDG-avid than the other, they will go after that first. But they can sample both if safe.

Does PET help with bronchoscopy?

** It can help, but appearance during bronchoscopy is more important

When is something NOT amenable to bronchoscopy?

** The middle third of the lung is hardest and most technically challenging

** Lower lobes of lungs, made difficult by atelectasis

** Contrary to common belief, peripheral lesions are easier due to anatomy of the lungs

About our guest: Dr. Greta Dahlberg (link: https://medicine.vumc.org/person/greta-dahlberg-md) is a pulmonary/critical care fellow at Vanderbilt University Medical Center in Nashville, TN. Thank you so much for joining us!

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We have now covered the fundamentals of pharmacology. This week, we sit down with Renee McAlister, PharmD, BCOP to learn more about the nuances of pharmacology from an expert that does this day in and day out.

*The products/resources we share are our OWN opinions. Naming of resources are not endorsements. We are not sponsored by any of these entities.

Pharmacology Capstone:

Irritant vs. Vesicant:

** For extravasation, what to do?

*** Not a great general source; would recommend checking institutional guidelines.

*** Different drugs may require a cold vs. warm compress.

*** Some drugs have antidotes - it is best to just look this up when it happens

Why is there a “cut off time” to get in chemotherapy orders?

** Many hospital pharmacies are not 24 hours, therefore need prep time.

** Many drugs take a long time to prepare!

** A lot verification goes into ensuring that the drugs are correctly ordered, prepared, and handled. Therefore this requires adequate staff to do this safely.

What does "ideal body weight” mean?

** Calculated by the patient’s sex, height, and the calculated body weight based on this information

** Helps with drug-dosing to ensure that drugs are not over/under-dosed

What does “AUC” mean?

** Incorporates renal function and the amount of exposure you want the patient to have to the drug. Based on the Calvert equation.

** It is important to re-calculate each time with a new Cr to ensure that this is updated.

** Example: https://reference.medscape.com/calculator/169/carboplatin-auc-dosing-calvert

What is the role of granulocyte colony-stimulating factor (GCSF)?

** Helps to prevent the risk of infection, especially from endogenous bacteria.

** GCSF helps to minimize the window of neutropenia related to treatment with chemotherapy

** NCCN guidelines (www.nccn.org) provides guidelines about febrile neutropenia risk. A risk >20% means that we build in GCSF administration into the treatments.

*** If risk 10-20% with certain risk factors, we may consider adding GCSF

*** Always look at the paper that was what the approval of the regimen was based off of - they will comment on if/how GCSF was used during the study.

*** If patient develops neutropenic fever during a cycle, if even the drug is not traditionally one that we consider GCSF for, it would be appropriate to consider GCSF for future cycles to decrease the risk of febrile neutropenia.

What are the different “types” of GCSF?

** Examples:

*** Filgrastim (“Neupogen”) - daily dosing, short-acting GCSF

*** Pegylated-filgrastim (“Neulasta”) - don’t have to give daily dosing; one time shot because it lasts for longer

*** On-body injector (OBI) - a device put on the arm that delivers pegylated- filgastrim at approximately 26 hours after chemotherapy

** Dosing: Very different dosing for all of these medications; pay attention to the dosing!

Supportive care:

** How do you decide what anti-emetics to include?

*** NCCN supportive care guidelines is a great place to start

*** Regimens with >90% emetic potential should get at least three agents (for example: ddACT, cisplatin based regimens)

**** Example: 5-HT3 receptor antagonists, dexamethasone, olanzapine, and aprepetant

*** Moderate emetic potential (30-90%), add at least 2 drugs

**** Example: 5-HT3 receptor antagonists and dexamethasone

*** Lower risk (30%): usually one one drug

**** Example:5-HT3 receptor antagonists

** If patients have refractory nausea in a cycle, add another agent. When adding drugs, always ensure you are incorporating the patient’s other medical history AND drug-drug interactions

Pharmacists are an amazing source of information! Please reach out with questions!

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Picture this: it's day 1 of fellowship and your attending needs you to "get consent for treatment." Huh? How do you educate your patient? We share our tips!

In this episode, we discuss important considerations, including “does my patient need a port?”, “what if drugs extravasate?”, “how do I keep side effects of drug classes straight?!”

*The resources we share are our OWN opinions. Naming of resources are not endorsements. We are not sponsored by any of these entities.

Pharmacology 101:

Irritant vs. Vesicant:

** Each drug is deemed one of these based on the degree of tissue damage that can result if drug extravasates under skin.  

** Vesicant: needs central access 

** Irritant: can be given peripherally  

Does my patient need a port/picc?

** If vesicant; for continuous infusions over several days (e.g. 5-FU); some patients with difficult access may request.  

*Advantages of ports:

** Easy access for labs 

** Easy access for chemotherapy/fluids 

Disadvantages:

** Risk of infection 

** Risk of thrombosis  

General overview of chemotherapy side effects:

** Going to target the fastest growing cells in the body, which includes cells that line the GI tract, skin, hair/nails, and blood cells 

** Therefore side effects are related:

*** GI: nausea/vomiting, diarrhea (sometimes constipation), decreased appetite, taste changes 

*** Low blood counts

**** WBC nadir ~10-14 days (generally), and recover 21-28 days after chemo 

What about unique side effects of chemotherapy classes? How do we keep them straight?

** We love keeping “Chemoman” from the USMLE study days in mind! 

Anthracycline

*** MOA: Topoisomerase inhibitors 

*** Ends in “rubicin” 

*** You might hear people call doxorubicin the “red devil” 

*** Used in lots of cancers 

*** Hair loss occurs with this one 

*** Known to cause cytopenias and associated with higher nausea potential  

*** Unique side effects:

**** Heart failure (always get baseline echo!) 

**** Development of MDS and leukemia  

Alkylating agents

** MOA: Drugs add alkyl group to the guanine base of the DNA molecule, preventing linking of strands 

** End in “fosfamide” 

** fosfamide or cyclophosphamide (AKA cytoxan) 

** Used in lots of cancers 

** Known to cause cytopenias and hair loss 

** Unique side effects:

*** Secondary MDS or leukemia possible  

*** Ifosfamide = neurotoxicity = methylene blue antidote 

*** Cyclophosphamide = hemorrhagic cystitis due to acrolein byproduct accumulation = prevent by giving mesna to protect bladder 

Antimetabolites

** MOA: Purine analog, pyrimidine analog, folate antagonists; therefore prevent production of base pairs or binds instead of normal base pairs 

** End in “abine” - capecitabine, cytarabine, gemcitabine, cladribine, fludarabine 

** Also 5-FU and 6-MP in this category so “number followed by dash” 

** Unique side effects:

*** Think bone marrow suppression in this category  

Platinum agents

** MOA: Believed to cause cross-linking of DNA 

** End in “platin” 

** Associated with high risk of neuropathy  

** Unique side effects:

*** Cisplatin:

**** Nephrotoxicity  

**** Ototoxicity  

**** High risk of nausea; need special prophylaxis  

*** Carboplatin: cytopenias 

*** Oxaliplatin: higher rates GI side effects  

Microtubule agents

** MOA: Impair microtubule function, therefore impacting cell division 

** End in “taxel” or vincristine/vinblastine (“V-stine”) 

** Unique side effects: Neuropathy 

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Picture this: it's day 1 of fellowship and your attending needs you to "get consent for treatment." Huh? How do you educate your patient? We share our tips!

In this episode, we discuss the fundamentals and some of our favorite resources.

*The resources we share are our OWN opinions. Naming of resources are not endorsements. We are not sponsored by any of these entities. *

1) How do you know what regimen to use for a disease?

www.NCCN.org :

** National Comprehensive Cancer Network

** Free resource, but need to make an account!

** Provides stepwise approach to workup, choosing a regimen, and surveillance information, treatment for refractory disease

www.HemOnc.org :

**Organized by disease type with long lists of treatment options

** Provides a breakdown of regimen, but also provides the primary literature that lead to the regimen’s approval for use!

**We cannot highlight how important it is to remember to check out the primary literature!

2) Patient education: Use these to drive discussion; you still want to walk your patients through these

www.Oncolink.org : Ronak’s favorite resource
www.Chemocare.com : Vivek and Dan’s favorite resource

3) Basic Terminology:

Cycle: The number of days between one round of treatment until the start of the next; abbreviated with “C”
Days: Counts the actual days within a cycle; abbreviated with “D”
Example: C1D1: Cycle 1 of a regimen, day 1 of this cycle

4) Dosing:

Always have updated height and weight for patients

** Many drugs are dosed based on body surface area (BSA)

** Other drugs use area under the curve (AUC)

Always get a CMP and CBC prior to giving treatment

5) General categories of cancer therapies:

Cytotoxic: Kills cells in the body

** Analogous to antibiotics killing bacteria

** Relatively non-specific in terms of what cells they target; but they’re often specific for parts of the cell replication cycle

Immune therapy: Harness the immune system to attack cancer

** More specific than cytotoxic agents

Targeted therapy: Drugs made specifically for known mutations

** A cancer with a distinct mutation in a protein is then a target for this drug

** In general:

***“Mab”- antibody targeted for phenotypic expression

***“ib”- small molecule for driver mutation

** Targeted cytotoxic chemotherapy: a monoclonal antibody specific for a mutation linked to very potent chemotherapy

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further.

In this episode, we’ll talk about one of the key hematologic malignancies that you’ll encounter as a fellow, one that requires immediate action to reduce mortality: acute promyelocytic leukemia (APL or APML)

Acute Promyelocytic leukemia (APL or APML):

**Stay tuned for our upcoming “part two” and “chemotherapy basics” episodes for more information on non-acute management of this disease

**APL is a true hematologic emergency! Although this is a very curable form of leukemia, it is associated with high rates of severe DIC and high mortality in the period immediately following diagnosis

***Untreated, can see pulmonary or cerebrovascular hemorrhage in up to 40% of patients

***10-20% incidence of hemorrhage-related mortality in the initial period

***Statistically significant increase in mortality at 30 days with just a 12-hour delay in initial hematologist consultation

Disease basics:

** Rare subtype of AML( <10% of cases)

** Driven by translocations involving the retinoic acid receptor alpha (RARA) on chromosome 17, classically with the promelocytic leukemia gene (PML) on chromosome 15 [i.e. t(15;17)]

***Other non-classical translocations exist, but nearly all involve RARA

**Because of this driver mutation, treatment with a specific isoform of vitamin A: all-trans retinoic acid (ATRA) forces promyelocytes to differentiate and ultimately apoptose

Initial work up:

**Standard CBC with differential, CMP

** Review smear for characteristic features:

** Large nuclei and scant cytoplasm

** “Folded” appearance to nuclei (like a peach emoji 🍑)

** Auer rods (which tells you blasts are myeloid lineage)

** Heavily granulated cytoplasm (hypergranular form - most common)

***Also a “hypogranular variant,” so like always, make sure to discuss any findings with your friendly neighborhood hematopathologist

**Stat DIC labs:

**PT/aPTT

**Fibrinogen

**Stat PML-RARA FISH (see next section) to look for classic driver mutation and clinch diagnosis

** “Tumor lysis syndrome (TLS) labs”

***LDH

*** Uric acid

**Peripheral flow cytometry

***CD33+, CD 117+

***CD34-, HLA-DR-, CD11a/b/c-

*** Increased side scatter (esp in hypergranular type)

Acute Management

** Start ATRA: immediate treatment is so important in this disease, and side effect profile is minimal enough that empiric treatment when disease is on the differential is standard of care

**Correct coagulopathies as you detect them

***Keep fibrinogen > 110 mg/dL

*** Keep INR < 2.0

*** Keep plt > 30k/uL

References:

Gulam Abbas Manji, Samira Khan Manji, Sheetal Karne, and Jeff Chao “Time to ATRA in suspected newly diagnosed acute promyelocytic leukemia and association with early death rate at a non-cancer center institution: Are we meeting the target?” Journal of Clinical Oncology 2012 30:15_suppl, 6615-6615 - impact of treatment delay on 30-day mortality

Eytan M. Stein, Neerav Shukla, Jessica K. Altman “Chapter 20: Acute Myeloid Leukemia” section on acute promyelocytic leukemia ASH SAP 7th Ed pp588-590. DOI: 10.1182/ashsap7.chapter20

Warrell RP Jr, de Thé H, Wang ZY, Degos L. Acute promyelocytic leukemia. N Engl J Med. 1993 Jul 15;329(3):177-89. doi: 10.1056/NEJM199307153290307. PMID: 8515790. - Great review of the basics in NEJM from the early 2000s

Sanz MA, Fenaux P, Tallman MS, Estey EH, Löwenberg B, Naoe T, Lengfelder E, Döhner H, Burnett AK, Chen SJ, Mathews V, Iland H, Rego E, Kantarjian H, Adès L, Avvisati G, Montesinos P, Platzbecker U, Ravandi F, Russell NH, Lo-Coco F. Management of acute promyelocytic leukemia: updated recommendations from an expert panel of the European LeukemiaNet. Blood. 2019 Apr 11;133(15):1630-1643. doi: 10.1182/blood-2019-01-894980. Epub 2019 Feb 25. PMID: 30803991. - Updated treatment guidelines (more on this in “Part 2” to come)

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our fourth hematologic emergency: thrombotic thrombocytopenic purpura (TTP).

Thrombotic thrombocytopenic purpura (TTP):

Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!
New anemia and thrombocytopenia should raise concerns for TTP!

Workup:

Peripheral smear - concern for schistocytes. Look at this first! Example of these cells from ASH image bank here
ADAMTS13 level - always draw ASAP before any intervention
Repeat CBC
Reticulocyte count - will have elevated retic count
Citrated platelet count
CMP
PT, PTT, INR
Fibrinogen
Haptoglobin
LDH
Viral serologies

Clinical manifestations:

Fever, Anemia, Thrombocytopenia, Renal (AKI), Altered Mental Status
If you see this - the patient is in bad shape

Mechanism:

Tiny blood clots form in the body, causing platelet shearing
Loss of ADAMTS13 - This protein normally is responsible for chopping up von Willebrand’s factor (vWF)
In the absence of ADAMTS13, vWF multimers are extra long, therefore interacting with platelets/collagen more and causing activation of platelets and clotting system
This causes red blood cell shearing due to small vessel microthrombi (brain, kidneys, heart)
Cytokine release causes fevers

Management:

Do not reflexively transfuse platelets; can make situation worse
PLASMIC Score: helps to stratify likelihood of TTP; MDCalc link (https://www.mdcalc.com/plasmic-score-ttp)

Treatment:

Plasma exchange: replacing ADATMS13-deficient plasma with ADAMTS13-rich plasma
This is different than plasmapheresis, where we replace plasma with albumin
Steroids: 1mg/kg prednisone daily to stop auto-antibody (against ADAMTS13) production
Confirm with ADAMTS13 levels; if <10%, this is confirmatory. This is why this is the FIRST step that we just send off as soon as TTP is suspected
IF YOU DON’T HAVE ACCESS TO PLASMA EXCHANGE: can administer FFP until you can get them to a center than can do plasma exchange
Caplacizumab: reserved for patients with severe neurological dysfunction, stroke, or myocardial infarction. Check out the NEJM paper on this (below)!

Microangioathic hemolytic anemia (MAHA):

Umbrella term for red blood cells shearing in the small blood vessels; TTP is one example of a MAHA

References:

https://ashpublications.org/blood/article/129/21/2836/36273/Thrombotic-thrombocytopenic-purpura - great review article from ASH on TTP

https://www.nejm.org/doi/10.1056/NEJMoa1806311 - NEJM paper on caplacizumab

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our third hematologic emergency: heparin-induced thrombocytopenia (HIT)!

Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!

HIT:

Any time a patient with heparin exposure and now with a new thrombotic event, you need to think about HIT!

What is HIT?

Type 1: a transient drop in platelets after heparin is started
Type 2:

**The scary one! Antibody-mediated process

**Heparin molecules bind to platelet-factor 4 (PF4)

**This complex activates platelets, which then further releases more PF4 from the platelets

What is the difference between HIT and HITT?

HITT is when there is also thrombosis (HIT + Clot)

Why is this more common in the cardiac ICU?

It is believed that IgM interacts with ultra-long complexes, which heparin is
Lots of heparin is required for cardiac surgery
Therefore lots of exposure to heparin increases likelihood, increasing likelihood for IgM to IgG class-switching; HIT is IgG-mediated process

** Remember - since this is antibody-mediated, therefore it takes a few days for the antibodies to form in patient with a new diagnosis of HIT!

How to stratify?

4-T score (MDCalc Link: https://www.mdcalc.com/4ts-score-heparin-induced-thrombocytopenia)

Workup:

Sent HIT ELISA test in patient with high suspicion
ELISA just suggests if the HIT antibody is present
If ELISA positive, then do confirmatory assay, i.e., is this antibody actually doing anything, is the "serotonin-release assay”
Send 4 extremity dopplers to look for thrombosis
STOP heparin/heparin-derived products and SWITCH anticoagulant, such as argatroban, fondaparinux, bivalirudin (do not wait for a positive test if your suspicion is high enough!)

If HIT positive:

Add heparin to their allergy list
Continue anticoagulation until platelets are recovered (>150K)
Continue anticoagulation for 3-6 months for patients with HITT

Words of wisdom: If patient comes from outside hospital and starts having decreasing platelets, consider HIT in your differential!

References:

https://ashpublications.org/blood/article/119/10/2209/29530/How-I-treat-heparin-induced-thrombocytopenia- great review article from ASH on HIT

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our second hematologic emergency: disseminated intravascular coagulation (DIC) with an added bonus of an intro to thrombotic microangiopathic anemias (TMAs).

Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!

Disseminated intravascular coagulation (DIC):

Workup:

CBC

CMP

PT, PTT, INR

Fibrinogen

Peripheral smear - concern for schistocytes. Example of these cells from ASH image bank: https://imagebank.hematology.org/image/60306/schistocytes?type=upload#:~:text=A%20schistocyte%20is%20present%20in,angles%20and%2For%20straight%20borders.

Basic mechanism of DIC is consumption of clotting factors leading to coagulopathy

Need to be weary of thrombotic microangiopathy: Small blood clots forming in the small vessels leading to endothelial damage, which cause shear stress on the RBCs, which then break down into a schistocyte (AKA triangulocyte or helmet cell)

Examples: thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS)

Management (our opinion!):

Repeat coags q4-6 hours initially (but base interval based on patient) NOTE: INR Is NOT a good assessment of “clotting status” in these situations
Repeat fibrinogen q4-6 hours initially (but base interval based on patient); keep fibrinogen >100 with cryoprecipitate in more stable patients; consider higher thresholds for more acutely ill patients (such as >150)
Repeat CBC q6-8 hours initially; can provide platelets if low, especially if they are bleeding
Workup and treatment for trigger of DIC (infection, trauma, medications, etc.)

How does cirrhosis affect data interpretation?

Use clinical context to determine if labs are acutely abnormal or if they have signs/symptoms to suggest underlying liver dysfunction
In the acute setting, always just replace what is missing!

How can you tell the difference between nutritional deficiencies vs. consumption (as in with DIC?)

Factor activity levels! Consider checking: Factor 8 (made in endothelium), Factor 5 (Vit K independent), Factor 7 (vitamin K dependent)
If all down, then consider DIC
If Vit K-dependent low, then nutritional deficiency

Reference:

https://ashpublications.org/blood/article/131/8/845/104418/How-I-treat-disseminated-intravascular-coagulation - Great How I Treat article from Blood

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our first hematologic emergency: immune thrombocytopenic purpura (ITP).

Immune thrombocytopenic purpura (ITP):

Be sure to check out episode 009 on thrombocytopenia for a general approach and differential!

Specific instances where there may be close to undetectable platelet count:

Lab artifact (clumping)
Very severe DIC
Thrombotic thrombocytopenic purpura - though usually higher platelets in these cases
Heparin induced thrombocytopenia (in very severe cases) - though usually higher platelets in these cases
ITP

ITP: Diagnosis of exclusion

How to confirm it is ITP?

Post-transfusion CBC - a repeat CBC 30-60 mins after a platelet transfusion. In ITP, the platelet count will likely not budge. (Not perfect test!)
Immature platelet fraction (if available) - this will be elevated if mature platelets are being destroyed. (Again - not a perfect test)

Treatment in acute cases:

IVIG 1g/kg daily x2 days + Dexamethasone 40mg daily x4 days

Reference:

https://ashpublications.org/blood/article/106/7/2244/21649/How-I-treat-idiopathic-thrombocytopenic-purpura - Great How I Treat article from Blood

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our third oncologic emergency: new brain mets.

Cord compression:

If someone has a pathologic fracture, think about the following differential as underlying etiologies:
Females: rule out breast cancer
Males: Prostate cancer
Others: multiple myeloma, lymphoma, lung cancer, renal cell carcinoma, bladder
If cord compression, administer steroids; may require radiation to help with shrinking; also may need involvement of neurosurgery if there is lack of spine stability.

Role of radiation in cord compression:

-MRI is beneficial to help with radiation planning

-Where is the disease in proximity to the spinal cord? In the bone? In the epidural space? Or pushing against the spinal cord +/- blocking CSF?

-Is the spine stable? Use SINS scoring (https://radiopaedia.org/articles/spinal-instability-neoplastic-score-sins-2?lang=us)

-If good spine stability (low SINS) or is not surgical candidate or radio-sensitive tumor: radiation up front

-If poor spine stability (high SINS) then may need surgery up front

Radiosensitive tumors examples:

Lymphoma

Germ cell tumors

Small cell lung cancer

Radio-resistant tumor examples (resistant does not mean that radiation cannot be used, however):

Melanoma

Colorectal

Renal cell

Continue steroids as they are undergoing radiation to prevent flare up from inflammation and acute worsening from the mass on the spinal cord

Role of neurosurgery:

What is a reasonable time that we can wait before operating for a new cord compression?
As noted above, cord compression has various degrees
Questions to ask: What neurologic symptoms? Over what time period?
Asymptomatic: You have time! Perhaps investigate why mass may be there.
Progressive over a couple of weeks: You have a little bit of time (a few days to get them to surgery)
Acutely having symptoms: You should intervene.
Spinal stability: are the weight-bearing components (ligaments) intact? Assessed via upright X-rays
If the tumor is radio-sensitive, may opt for radiation first (if diagnosis is known)

A HUGE thank you to our special guests:

Ryan Miller, MD, MS: PGY5 in Radiation Oncology at Thomas Jefferson University Hospital, Philadelphia, PA

Joshua Lowenstein, MD, MBA: Neurosurgery Attending, REX Neurosurgery and Spine Specialists, Raleigh, NC

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about our second oncologic emergency: new brain mets.

Brain mets:

Strongly consider steroids, particularly with the presence of vasogenic edema associated with brain mets

Stereotactic radiosurgery (SRS): use of high dose radiation delivered in a single treatment (“fraction”) that is delivered focally to the area of disease seen on imaging (typically MRI); great option for brain mets; can be performed by radiation oncology

What to do to expedite Rad Onc planning:

Thin-cut MRI

Start patient on steroids

Interpreting MRI imaging:

T1 post-contrast sequence: to look for brain mass

T2 sequence: looking for vasogenic edema surrounding brain mass

Midline shift is an issue more so when it is acute; this is very different than slow changes over time

Who to operate on? Functional status prior to surgery; not in an area that can cause other harm; no other good alternative treatment options

What to tell your NSGY colleague during a consult:

A quick neuro exam (consciousness, strength, sensation, focal neurologic issues)

Brief cancer history

Underlying organ dysfunction

Antiplatelet/anticoagulants

A HUGE thank you to our special guests:

Ryan Miller, MD, MS: PGY5 in Radiation Oncology at Thomas Jefferson University Hospital, Philadelphia, PA

Joshua Lowenstein, MD, MBA: Neurosurgery Attending, REX Neurosurgery and Spine Specialists, Raleigh, NC

Please visit our website (TheFellowOnCall.com) for more information

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Emergencies happen in hematology and oncology. This is a fact. But how do we manage these emergencies? Look no further. In this episode, we talk all about first oncologic emergencies: superior vena cava (SVC) syndrome.

Superior vena cava syndrome:

Important: although we focus on a possible malignant mass in this discussion about SVC, other things can also cause SVC syndrome.

How do you know about the chronicity of someone’s possible SVC syndrome? Compare to a recent picture!

Image of patient with collateralization with SVC syndrome: DOI: 10.1056/NEJMicm1311911

Workup:

Need to determine the etiology; imaging is important:

CT of chest (CT venogram)

Consider ultrasound to rule out thrombosis

Get biopsy (eventually) if this is malignancy

DDx of mediastinal masses:

5Ts:

Thymoma

Terrible lymphoma (B or T-cell)

Testicular cancer

Teratoma

Thyroid malignancies

Central line (causing occlusion) +/- clot

So now what?

Yes, an answer to what is causing the issue is important, but we need to ensure that patient has a stable airway and temporize the situation

Often requires input of specialists, such as Interventional Radiology or Radiation Oncology

How to treat patients with SVC syndrome?

Chemotherapy: Important in chemo-responsive tumors (ex. germ cell tumors, lymphomas, small cell lung cancer); This can take a while to work

-Placement of stents: Provides more immediate relief, but more invasive

-Radiation treatment: Not always possible

Laryngeal edema/cerebral edema: steroids for life-threatening complications; Can affect diagnostic yield of sample and affect diagnosis, but may be required in emergent situations

When is more emergent treatment indicated and consultants definitely need to be called (TELL YOUR CONSULTANT IF ANY OF THESE ARE SEEN!):

Hemodynamic instability

Worsening respiratory status

Worsening neurological status

Final decision for what to do is often a multi-disciplinary discussion

Stents:

Provides quick relief

Does not prohibit a diagnosis and curative treatment for the underlying malignancy

Radiation:

Takes several days or weeks; depending on underling histology

If they have received prior radiation, they may not be eligible for more radiation

A HUGE thank you to our special guests:

Ryan Miller, MD, MS: PGY5 in Radiation Oncology at Thomas Jefferson University Hospital, Philadelphia, PA (https://www.jefferson.edu/university/jmc/departments/radiation_oncology/education/residency/residents/miller.html)

Rupal Parikh, MD: PGY6 in Diagnostic/Interventional Radiology at the Hospital of the University of Pennsylvania, Philadelphia, PA (https://www.pennmedicine.org/departments-and-centers/department-of-radiology/education-and-training/residency-programs/current-residents/ir-integrated-residents/ir-dr-fifth-year/rupal-parikh-md)

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In our final stop in our Cytopenias series, we discuss the ins and outs of neutropenia. This is another very commonly seen issue in the clinic and in the hospital so most definitely high yield!

Why is neutropenia dangerous?

Prone to infections, especially gut translocation of bacteria

Definition of neutropenia:

NORMAL: WBC 4400-11000 cells/microL; neutrophils make up 40-70% of that

Neutropenia defined by ANC: WBC (cells/microL) x percent (PMNs + bands) ÷ 100

Breakdown:

Neutropenia: ANC <1500 cells/microL

Mild: ANC ≥1000 and <1500 cells/microL

Moderate: ANC ≥500 and <1000 cells/microL

Severe: ANC <500 cells/microL

Agranulocytosis: ANC <200 cells/microL

Approach to workup: HISTORY IS KEY!

Medications; examples of common culprits-

Chemotherapy

Methimazole

Clozapine

Infections

Any infections due to bone marrow suppression

Toxins

Less common causes:

Congenital

Severe congenital neutropenia:

Diagnosed in childhood; used to be fatal, but now patients living longer because of G-CSF support

10-30% risk of AML in lifetime

Mutations in neutrophil elastase (ELANE) gene or mitochondrial HAX1 gene

Cyclic neutropenia:

Self-limiting neutropenia that occurs every 2-5 weeks

Spectrum of symptoms: none or oral ulcers/mild infections

Constitutional/ethnic neutropenia:

Mild neutropenia (ANC >1000)

No history of infections

More common in people of Mediterranean and African descent

Duffy Antigen Receptor Complex (DARC) gene mutations in patients of African origin

Benign Familial:

Mild neutropenia

Not linked to particular ethnic group

Unclear underlying etiology

Autoimmune

Primary autoimmune neutropenia rare in adults

Typically secondary autoimmune neutropenia

Due to underlying autoimmune disorder

Seen with SLE and can worsen with flare of disease

Typically mild, seldom needs treatment unless ANC <500

Felty syndrome:

Rheumatoid arthritis, splenomegaly, and neutropenia

Neutropenia improves with treatment of RA

Malignancy

Large granular lymphocyte (LGL) leukemia:

Often associated with RA and shares features of Felty syndrome (RA, splenomegaly)

Caused by monoclonal population of large granular lymphocytes

In contrast, in Felty’s: polyclonal or oligoclonal

T-cell LGL is more commonly associated with neutropenia

Requires treatment with methotrexate or cyclophosphamide

Dietary

B12 and folate rarely cause isolated neutropenia

Copper deficiency (gastric bypass): Zinc excess can cause copper deficiencies – ask about denture creams in your history!

Workup:

History:

Prior CBCs

History of recurrent infections (pneumonia, sinusitis, skin/soft tissue, dental caries)

Ethnic background

Family history

Social history

Dietary history

Surgical history (gastric bypass)

Physical exam:

Adenopathy

Splenomegaly

Skin findings suggesting recent ulcers

Aphthous ulcers

example: https://en.wikipedia.org/wiki/Aphthous_stomatitis

Testing:

CBC with differential

CMP – assess liver and renal function

Peripheral smear

HIV, Hepatitis serologies

Special scenarios

ANA – if autoimmune disease expected

RF – if autoimmune disease expected

ESR – if autoimmune disease expected; probably not great for inpatient workup

CRP – if autoimmune disease expected; probably not great for inpatient workup

Flow cytometry for LGL

Bone marrow biopsy – mainly for unexplained neutropenia to rule out neoplastic process, such as leukemia, lymphoma, myeloma; if longstanding, likely negative

Management:

Treat the underlying cause

Autoimmune neutropenia –

When to suspect? Workup is negative, but their counts still continue to worsen

Treatment if they have serious complications

Treat with rituximab

LGL-

Responds to low dose methotrexate or cyclophosphamide

Do you give G-CSF?

For patients with recurrent/severe infections or mucosal erosions

Do not treat based on the number alone

Takes time for the growth factors to work

References:

https://doi.org/10.1182/blood-2014-02-482612 - Great “How I Treat” article from Blood!

https://www.uptodate.com/contents/approach-to-the-adult-with-unexplained-neutropenia - UpToDate article written by same author as Blood article

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We continue on our cytopenias journey, this time talking all about anemia. This is a high yield topic for anyone who sees patients, as this is something we will all see.

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One of our most common consults in hematology is teams seeking guidance for workup and management of thrombocytopenia. In this episode, we cover our approach to this hematologic conundrum.

Major Points Covered:

Thrombocytopenia is defined as a platelet count <150K

Mild: 100-150K
Moderate: 50-100K
Severe: <50K
We get really worried when <20K (risk of spontaneous bleeding)

What to ask in history and in chart review:

How quickly did the platelets drop - this is just as important as the absolute number; platelets may still be “normal” but have dropped significantly!
Mucosal bleeding? Menstrual bleeding?
Rashes?
Infections/Meds/Toxins?
Constitutional symptoms
Weight loss

Our approach to a differential diagnosis - analogous to everyone’s favorite approach to renal AKI: “pre”, “intra,” and “post”:

Pre: Infections/Meds/Toxins

1st: HIV, Hepatits
2nd: EBV, CMV, Histoplasmosis

Intra: Primary bone marrow failure

Post: Destructions/consumption/splenomegaly (Cirrhosis, too)

DIC
ITP
TTP
Platelet clumping

Workup:

Smear - helps to quickly rule in or rule out a lot of the post-BM issues that are emergencies!
Citrated platelet count (to rule out platelet clumping)
Repeat CBC
Coags (PT/PTT/INR)
Fibrinogen
HIV serologies
Hepatitis B/C serologies
+/- Haptoglobin (note: in liver disease, you can have low haptoglobin)
Don't send SPEP/IFE!
If there is no abdominal imaging, consider abdominal ultrasound to evaluate for cirrhosis and/or splenomegaly

References:

https://www.sciencedirect.com/topics/medicine-and-dentistry/hypersplenism (Textbook of Gastrointestinal Radiology, 3rd edition 2008)- 90% of platelets in spleen at one time

https://pubmed.ncbi.nlm.nih.gov/29978544/ (J Thromb Hemostasis 2018)- Platelet threshold for bleeding risk

https://www.bjanaesthesia.org/article/S0007-0912(18)30753-0/fulltext#fig1 (British Journal of Anesthesia 2019)- Perioperative thrombocytopenia (Look at Figure 1)

https://ashpublications.org/blood/article/131/8/845/104418/How-I-treat-disseminated-intravascular-coagulation (Blood 2018) - DIC with normal fibrinogen (Look at case 1, Table 2 shows good diagnostic criteria)

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Not to be confused with “carcinoma of unknown primary,” in this episode of metastatic disease of “origin TBD”, we discuss the workup of a mass noted incidentally on imaging. This is a very high yield topic often faced on solid oncology consults!

Major Points Covered:

Mass found incidentally on imaging → we need to stage always

Initial Workup:

Reasonable to get CBC, CMP, UA, PSA (if male)

Low blood counts, maybe marrow involvement

Cr elevated concern for obstruction possibly

LFTs elevated concern for mass in the biliary/pancreas region

UA w/ hematuria → maybe bladder

But bottom line you’re gonna get a scan, which scan to get though?

Recommend referencing NCCN guidelines to determine additional staging scans

Create an account on nccn.org and look at guidelines by tumor type

Not all cancers require a PET/CT scan

There are newer modalities for imaging other than FDG PET including PSMA PET (prostate), Auxumin PET (prostate), and DOTATE PET (neuroendocrine)

Certain cancers can be diagnosed on imaging alone (RCC and HCC)

Some cancers require Brain MRI for staging

What to biopsy?

FNA often adequate for solid tumors but may need core if non diagnostic

Need core or ideally excisional if highly concerned for lymphoma

Always try to biopsy the site that will upstage

Distant lymph nodes or other metastatic sites

What about tumor markers?

We use this for treatment monitoring, not for diagnostic purposes

Important to establish a baseline to follow, special circumstances for diagnostic purposes to consider below:

PSA in male if concerned about prostate cancer

AFP helpful if concerned for HCC → liver masses in a cirrhotic

AFP and b-HCG if concerned for testicular → young or middle aged male with mediastinal mass

Molecular testing not necessarily needed at the time of biopsy

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Heme Path Capstone Pt. 2 Pearls

In this episode, we continue our conversation with guest, Dr. Emily Mason, hematopathologist at Vanderbilt University Medical Center (Nashville, TN), as we apply all that we have learned in our Heme Path series. This time, we talk about a patient with a new leukocytosis, fevers, and easy bruising; and our approach to workup and management.

Reminder: While these episodes may seem a little more in-depth than the prior Heme Path episodes, simply break down the conversation into the components we have discussed already and you will be amazed at how much you actually know - we promise!

ELN Risk Stratification: https://www.researchgate.net/figure/ELN-2017-risk-stratification-of-AML-by-genetic-abnormalities-Adapted-from-Dohner-et_fig1_334634713

original paper: https://dx.doi.org/10.1182%2Fblood-2016-08-733196

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Heme Path Capstone Pt. 1 Pearls

It’s time to put all you have learned in our Heme Path series to the test! Listen in as our guest, Dr. Emily Mason, hematopathologist at Vanderbilt University Medical Center (Nashville, TN) sits down with us to discuss the approach to diagnosis and workup of a new enlarged lymph node.

While these episodes may seem a little more in-depth than the prior Heme Path episodes, simply break down the conversation into the components we have discussed already and you will be amazed at how much you actually know - we promise!

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Molecular Testing Pearls

In Part 4 of our Heme Path series, we thoroughly examine the details of molecular testing and how it relates to hematologic and oncologic malignancies

I. Molecular Testing Basics

A. Provides a means of assessing patient’s genotypes, specifically at smaller changes in the genetic information

B. How is it performed?

Polymerase chain reaction (PCR)-based testing, which involves using a specific primer that is complementary to the area of interest on the patient’s DNA
PCR can allow for both amplification and quantification of gene of interest

C. Can look for either single gene mutations (faster) or a panel of mutations (slower but more information) also known as NGS

II. Clinical Utility of Molecular Testing

A. Very useful in risk stratification based on the mutations noted (some mutations are unfavorable and some are favorable)

B. Certain genetic mutations have drugs that are effective against them, therefore provides information about targeted therapeutic options

C. In hematologic malignancies, can be used to also assess response to treatment

You can determine minimal residual disease or MRD
Can look for a gene mutation that was present in the original cancer clone and see if there is any amount of residual cancer left over on the order of 1 in a million cells

D. In solid cancers, used to determine presence of genetic changes that have prognostic and targeted treatment implications

BRAF V600E mutation in melanoma → BRAF inhibitor pill treatment
EGFR mutation in lung cancer → EGFR inhibitor pill treatment

III. How is molecular testing different than FISH?

A. Both require choosing probes and understanding what you are looking for before running the test

B. FISH (discussed in part 3!) reports out of 200 cells and provides information about only larger kilobase sized genetic changes (translocations, inversions, deletions)

C. Molecular testing analyzes a much larger number of cells and can detect changes at the single base pair level. Much more detailed and microscopic evaluation of genetic changes

IV. Single Gene Molecular Testing

A. Look for a specific gene mutation (i.e. EGFR for lung cancer, BRAF for melanoma, FLT3-ITD for AML)

B. Pros:

Faster turnaround time
Has a higher resolution and effective for detecting MRD

B. Cons:

Only looks for one genetic mutation as opposed to a panel like in NGS
Some diseases ideally require understanding of multiple mutations not just one for prognostication and treatment planning

V. Next Generation Sequencing (NGS)

A. Allows to sift through a larger part of the genome to identify a panel of mutations

B. Panel of mutations chosen is based on the clinical context

For example: NGS for acute myeloid leukemia is much different than NGS testing for lung cancer as each cancer has a much different genetic mutation profile

C. Overview of technical aspects of running NGS

Massively parallel sequencing meaning that many tiny primers are used and the areas that primers encode may be overlapping
A computer takes all of the smaller pieces and puts them together to determine the correct sequence

D. Pros:

Gives us an understanding of many different mutations present based on the panel chosen
Again, this has both prognostic and predictive treatment implications

E. Cons:

May find mutations of undetermined significance meaning we currently do not understand how these mutations will affect prognosis and treatment decisions
Very time consuming (~2-4 week turnaround time)
Costly

References:

https://jamanetwork.com/journals/jamaoncology/fullarticle/2734828 - Quick overview of NGS
https://ashpublications.org/blood/article/125/26/3996/34323/Minimal-residual-disease-diagnostics-in-acute - Look at table 1 to see the difference in sensitivity for MRD testing
https://www.oncotarget.com/article/27602/text/ - Emphasizes prognostic relevance of EGFR mutations in NSCLC
https://www.nejm.org/doi/full/10.1056/NEJMoa1612674 - Phase 3 trial showed that targeted treatment for EGFR mutation in NSCLC was superior to chemotherapy
https://www.nejm.org/doi/full/10.1056/nejmoa1614359 - Phase 3 trial showed that targeted treatment of FLT3 mutation in AML improved outcomes

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Immunohistochemistry Pearls

In Part 3 of our Heme Path series, we break down the basics of immunohistochemistry (IHC)

What is Immunohistochemistry?

A. A molecular technique that utilizes fluorescently-labeled probes or chromogenic reporter stains to identify populations of cells. The goal being to help identify clonality

B. Procedure entails taking thin slices of tissue and then using the probes to look for the presence (or absence) of cells specific to that probe

C. Helps to identify specific proteins, the pattern and distribution of which can help identify what it is that we are looking at

Pros of IHC:

A. Can be performed on fixed specimen (vs. flow cytometry, which requires live cells)

B. Provides an idea of micro-architecture of the sample (diffuse distribution of cells vs. clusters) in context

Cons of IHC:

A. More labor intensive than flow, therefore can take longer to result

B. Need to have an index of suspicion for what you are looking for. Your search is only as good as the probes you use!

Examples of utility:

A. Diagnosis of acute leukemia: For instance, staining for CD34, which is expressed on blasts, can help you determine the “blast percentage.” That is, you count up number of cells that stain for CD34 probe then divide by total number of cells in the sample, which gives blast percentage.

B. Diagnosis of plasma cell dyscrasias: These disorders result in “sticky” bone marrows, such that it is hard to get a good aspirate. This means on flow, you may not get an accurate percentage. Using IHC helps you better estimate the numbers.

C. Diagnosis of lymphoma: Staining for specific markers (for example CD20, CD19 for B-cell lymphomas) can help in diagnosis. Can also use IHC to determine KI67, which is the proliferation index.

D. Diagnosis of metastatic cancers: For instance, if you see a lung mass but also note axillary lymphadenopathy, so you sample the lymph node because less invasive. How you do you know if the cells in the lymph node are representative of metastatic lung cancer cells? Use IHC to stain them!

E. PDL-1 status: This is believed to be important marker to predict response to immunotherapy.

References

https://www.abcam.com/content/immunohistochemistry-the-complete-guide - Great description of process and images to showcase what IHC staining looks like (not endorsement of product)

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Flow Cytometry Pearls

In Part 2 of our Heme Path series, we get into the details of cytogenetics (conventional karyotype and FISH)

“Cytogenetics” is the analysis of chromosomal changes in a cell, which includes additions, deletions, inversions, and translocations of important regions of genetic information.
We typically use cytogenetic information to help in disease diagnosis, decide treatment options, determine prognostic information, and, historically, assess response to treatment.
Two different techniques fall under this umbrella: conventional karyotype and fluorescence in situ hybridization (FISH)
Conventional karyotype:

A. What does this mean?:

i. Assessment of large changes in chromosomes (Megabase sized)

ii. Bone marrow specimen is arrested in metaphase with microtubule inhibitors, stained with Giemsa stain, and then cells are analyzed; a total of 20 cells are analyzed

iii. The changes seen provide genetic and prognostic information

iv. Example is in chronic myelogenous leukemia (CML), with pathognomonic t(9;22) which encodes the Philadelphia chromosome (ASH Image Bank example: https://imagebank.hematology.org/image/60150/t922-karyotype)

B. Pros:

i. Provides important information regarding diagnosis, treatment options, and prognosis particularly for MDS and acute leukemia.

B. Cons/caveats:

i. Can only be run on actively dividing cells (cannot be run on peripheral blood)

ii. Very labor intensive, therefore slower turnaround time

Cannot detect smaller genetic changes

FISH

A. What does this mean?

i. More sensitive and targeted technique compared to conventional karyotype (Down to kilbased sized changes)

ii. Uses fluorescently-labeled probes that target DNA regions that are pathognomonic for the suspected disease. Therefore, which probes are used is based on the clinical context

iii. Example is in acute promyelocytic leukemia (APL), with pathognomonic t(15;17) which encodes PML-RARA gene (ASH Image Bank example: https://imagebank.hematology.org/image/61450/fish-showing-t1517q24q21-pmlrara-translocation)

iv. Can also be run on fixed specimens. For example, FISH probes are used to determine presence of HER2 for breast cancer or for high risk rearrangements for DLBCL (MYC, BCL-2, BCL-6).

B. Pros:

i. Can be run on peripheral blood, marrow, or fixed specimen

ii. Much faster than karyotype, which is useful when a diagnosis is needed quickly

C. Cons:

i. You need to have an index of suspicion for what you are looking for

ii. Does not give full analysis of chromosomal changes, therefore you still need the karyotype

References:

https://www.nature.com/articles/nrg1692 - Nature review article about overview of cytogenetics

https://www.ashclinicalnews.org/spotlight/demystifying-the-lab/demystifying-lab-cytogenetics/ - ASH overview on Cytogenetics

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Major Points Covered:

In Part 1 of our Heme Path series, we break down the logistics and applications of flow cytometry.

Take aways:

Cancer = cells that clone themselves uncontrollably due to mutations.
Purpose of flow cytometry is to assess phenotype of the cell by characterizing cell surface markers (CD markers for example). For blood cells, this is called the “immunophenotype”.
Testing requires live cells in suspension and can’t be fixed. Remember to keep all lymph node biopsies in suspension when sending for flow cytometry.
Flow tells us that if cells share the same abnormal expression of cell surface markers, they are clonal and therefore raise concern for cancer.
Flow tells us if cells have specific cell surface markers that we can target for treatment. For example, expression of CD20 can be targeted by the drug Rituximab.
If a clone is identified at diagnosis, flow cytometry can be used to sift through thousands of cells to see if a single clone with the original abnormal phenotype is left over. This is called minimal residual disease (MRD) testing and is a great way to monitor response to treatment and identify if any tiny amount of cancer is left over.
There are a variety of indications to send flow cytometry but the bottom line to remember is that we are trying to find an abnormal clonal population of cells. You may not see anything abnormal in the peripheral blood because those cells are living in the bone marrow.
Blasts reported on the CBC w/ diff is done based on visual inspection of morphology by a hematology lab scientist or pathologist; but can only confirm if it is truly a blast with flow cytometry.
Always send bone marrow biopsy aspirate samples for flow cytometry.
We use flow cytometry as one piece of the larger puzzle to prove clonality and make a diagnosis. Other uses are for determination of targeted treatments based on cell surface markers and to identify any amount of residual disease (MRD testing by flow cytometry).

References:

https://ashpublications.org/blood/article/111/8/3941/24550/Flow-cytometric-immunophenotyping-for-hematologic - ASH review article on use of flow cytometry to diagnose heme malignancies.

https://onlinelibrary.wiley.com/doi/10.1002/cyto.b.20365 - Bethesda International Consensus Guidlines for Flow Cytometry in 2006

https://www.bloodresearch.or.kr/journal/view.html?uid=2357&vmd=Full& - Minimal residual disease testing in ALL as an example of another clinical use of flow cytometry

http://www.cyto.purdue.edu/archive/flowcyt/research/pdfs/encyclopedia_2004.pdf - Good article explaining the complexities of the flow cytometry technique

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Thank you so much for checking out The Fellow on Call: The Heme/Onc Podcast. In this intro episode, learn more about our show and what you can expect.

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