An Overview of Multiple Myeloma

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EP: 1.An Overview of Multiple Myeloma

EP: 2.The Role of BCL-2 in Normal and Multiple Myeloma Cells

EP: 3.Venetoclax Monotherapy for the Treatment of Multiple Myeloma

EP: 4.Venetoclax plus Dexamethasone for Multiple Myeloma Treatment

EP: 5.Venetoclax for Multiple Myeloma: The Phase 3 BELLINI Trial

EP: 6.Venetoclax in Combination with Daratumumab for Multiple Myeloma Treatment

EP: 7.Venetoclax in Combination with Carfilzomib for Multiple Myeloma Treatment

EP: 8.Other Venetoclax-based Combination Regimens Being Evaluated in Multiple Myeloma

EP: 9.Other Investigational Agents Targeting BCL-2 Family Proteins for Multiple Myeloma Treatment

EP: 10.Where Does Inhibition of BCL-2 Family Proteins Fit into the Multiple Myeloma Treatment Landscape?

Shaji Kumar, MD: Hello, and thank you for joining this Targeted Oncology™ presentation titled, “BCL-2 Family Proteins as Therapeutic Targets in Multiple Myeloma.” I am Shaji Kumar, professor of medicine in the division of hematology at Mayo Clinic in Rochester, Minnesota. Joining me today is my esteemed colleague Dr Jonathan Kaufman. I would like to invite Dr Kaufman to introduce himself.

Jonathan Kaufman, MD: Hi, my name is Jonathan Kaufman. I am a professor of hematology and medical oncology at Emory University in Atlanta, Georgia. Thank you so much for joining me.

Shaji Kumar, MD: Although much progress has been made in the treatment of multiple myeloma, the majority of patients relapse after several lines of therapy, highlighting the need for new treatment strategies. In today’s Precision Medicine in Oncology® discussion, we will talk about the role of the BCL-2 family proteins in myeloma growth and progression and review the mechanism of action and current safety and efficacy data from the recent trials of agents that target the BCL-2 family proteins in patients with multiple myeloma. Let’s begin. I will start off this session with a question for Dr Kaufman in terms of where we with multiple myeloma, particularly in understanding the biology of the disease and the epidemiology.

Jonathan Kaufman, MD: As we know, myeloma is a malignancy of plasma cells, and the job of plasma cells is to make antibodies. The pathogenesis of myeloma comes from expected or common cytogenetic abnormalities. The most common ones occur with translocation of an oncogene downstream from the heavy-chain enhancer element. If you put an oncogene downstream from the heavy-chain enhancer element, that will transform the cell, leading initially to MGUS [monoclonal gammopathy of undetermined significance] and then ultimately, with subsequent cytogenetic abnormalities, to myeloma.

Myeloma is related to age. Median age of diagnosis is somewhere in the late 60s. While it is often diagnosed in older patients, we do see younger patients. Younger patients don’t necessarily have more high-risk disease. There is a slight male-to-female increase. There is an increase in the incidence in Black patients versus non-Black patients, and we do not understand the etiology of that difference. To date, myeloma is not a disease that we can cure, but it is a disease that we have become very good at treating.

Transcript edited for clarity.