Molecular Testing for Newly Diagnosed CLL

EP: 1.CLL: Evolution of Treatment

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EP: 2.Molecular Testing for Newly Diagnosed CLL

EP: 3.Prognostic Factors in Chronic Lymphocytic Leukemia

EP: 4.CLL: Prognostic Markers

EP: 5.Long-Term Experience With Ibrutinib in CLL

EP: 6.BTK Inhibitors as Frontline Treatment for CLL

EP: 7.Safety and Efficacy of BTK Inhibitors in CLL

EP: 8.Mitigating Toxicities Associated With BTK Inhibitors

EP: 9.ALPINE Study: Zanubrutinib vs Ibrutinib in R/R CLL

EP: 10.BCL2 Inhibitors in Previously Untreated CLL

EP: 11.CLL Therapies: Novel Combinations

EP: 12.CLL: GLOW Trial Overview

EP: 13.CLL: BTK Inhibitors in the R/R Setting

EP: 14.High-Risk Patients With R/R CLL

EP: 15.CLL: Venetoclax in the R/R Setting

EP: 16.PI3K inhibitors for R/R CLL

EP: 17.Emerging Agents for R/R CLL

EP: 18.CLL: Final Thoughts

William Wierda, MD PhD: We’re going to talk about prognostic factors in detail in a minute. But Dr Atallah, can you give us some idea of what your standard work-up is for a patient with CLL [chronic lymphocytic leukemia]? Are you doing a prognostic factor work-up at initial presentation? Realizing that the indications for treatment haven’t really changed and aren’t dependent on the prognostic factors we test for.

Ehab Atallah, MD: Yes, the indications to treat have pretty much stayed the same. I still get prognostic factors—some patients want to know—although we can discuss later how much it makes a difference with the newer therapies we have. I make it clear, though, that if there’s no indication to treat and we do these prognostic factors, if they turn out good, then that’s great. If they turn out like having a higher-risk category, then it will just quadruple their anxiety for no good reason.

I spend some time discussing what we’re going to do with these tests when I order them. We still need to get a 17p deletions, cytogenetics, and FISH [fluorescence in situ hybridization]. It’s important to also get clonoSEQ testing for future follow-up, especially definition of MRD [minimal residual disease] on the blood initially for patients. Getting a TP53 mutation is also really important, because that might help guide us in choosing which treatment I’d start with, whether it’s a BTK inhibitor or a BCL2 inhibitor. That’s usually what I start with after having a conversation with the patient.

William Wierda, MD PhD: Is bone marrow necessary?

Ehab Atallah, MD: I don’t do a bone marrow. I used to do a bone marrow in the days of chemotherapy-immunotherapy to establish a baseline and make sure there’s no dysplasia or anything when I was planning on giving chemotherapy. With the current therapies, I don’t do a bone marrow. I consider a PET [positron emission tomography] scan if I have any suspicion for transformation. I would do a PET scan if there’s anything that looks different, but I don’t do a bone marrow.

William Wierda, MD PhD: I’d like to remark that transformation is exceedingly rare in previously untreated patients, so I wouldn’t imagine you do that very often. Maybe can you comment on CT scanning, because I do see a lot of referrals of patients who don’t have any palpable adenopathy but get a CT scan. I also see patients who are in watch-and-wait who have serial CT scans. Can you comment on initial CT scan and serial CT scans for monitoring?

Ehab Atallah, MD: I don’t do either unless there are symptoms that guide me toward doing that. If I’m suspicious of any internal organ involvement, that’s when I would do a CT scan. I don’t do serial CT scans for monitoring unless there are symptoms. Lots of radiation isn’t good, anyway.

TRANSCRIPT EDITED FOR CLARITY