Case 1: Refractory CP-CML With Multiple Comorbidities



James K. McCloskey II, MD:Thank you for joining us for thisTargeted Oncology Virtual Tumor Board®, which will focus on chronic myelocytic leukemia [CML]. In today’sTargeted Oncology Virtual Tumor Board®presentation, my colleagues and I will present 4 clinical cases. We will discuss an individualized approach to treatment for each patient, and we’ll discuss and review key trial data that impact our decisions.

I am Dr James McCloskey, interim chief of the Division of Leukemia at the John Theurer Cancer Center in Hackensack, New Jersey. Today I am joined by Dr Adam Bagg, director of hematology and professor of pathology and laboratory medicine at the Hospital of the University of Pennsylvania in Philadelphia, Pennsylvania; Dr Elias Jabbour, professor of medicine in the Leukemia Department at The University of Texas MD Anderson Cancer Center in Houston, Texas; Dr Michael Mauro, leader of the Myeloproliferative Neoplasms Program, member of the Memorial Sloan Kettering Cancer Center, and professor at Weill Cornell Medicine in New York, New York; and Dr Douglas Smith, professor of oncology, Division of Hematologic Malignancies at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins Medical Institute in Baltimore, Maryland.

Thank you for joining us, let’s get started on our first case.

James K. McCloskey II, MD:Dr Mauro, would you like to introduce our first case?

Michael J. Mauro, MD:Absolutely. Case 1 is refractory chronic phase CML with multiple comorbidities. The history of this patient would be a 62-year-old man who presents to his primary care physician with symptoms of fatigue, shortness of breath, and abdominal discomfort. The past medical history is significant in this case. This gentleman had a history of bacterial pneumonia with pleural effusion, hypertension, arrhythmia, and a supraventricular tachycardia, and he was noted to have some borderline QT prolongation and was managed on verapamil. In 2016, he was unfortunately also found to have renal insufficiency with phase IIIa changes in kidney function with a decreased glomerular filtration rate.

On physical examination, he’s got palpable splenomegaly. When we look at the laboratory presentation, we see the white count is elevated—as it should be for the diagnosis of CML—at 158,000 with a left shift, 4% metamyelocytes, 6% myelocytes, 4% basophils, and blasts at 8%. Hematocrit is 29%, platelets are at 135,000, and hemoglobin is 12. So if we calculate this, he’s got a higher Sokal score. As is appropriate, a bone marrow biopsy is done and shows a hypercellular marrow with the Ph chromosome in 20/20 metaphases. Based on BCR-ABL testing, it shows the transcript level is 75% of the International Scale.

So we have a diagnosis of chronic phase CML, but obviously a little bit more of a complicated patient. In this case, we see a patient who’s started on imatinib, 40 mg. At 3 months, his transcript level has reduced, but only to 26%. He’s followed subsequently and at 6 months, the transcript level is further reduced but only to 18%. A bone marrow biopsy is repeated and still shows Ph positivity with 10 out of 20 metaphases, consistent with a lack of a complete cytogenetic response. Sequencing is done and no known TKI [tyrosine kinase inhibitor] mutations are found. At this point, the CBC [complete blood count] looks much letter. Obviously, he’s in complete hematologic response with a white cell count of 5000, a normal differential, a hematocrit of 40%, platelets at 112,000, and a hemoglobin of 12.9.

Transcript edited for clarity.

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