Dr. Treon on the Evolution of BTK Inhibitors in Waldenström Macroglobulinemia | OncLive

Dr. Treon on the Evolution of BTK Inhibitors in Waldenström Macroglobulinemia

July 14, 2020
Steven P. Treon, MD, PhD
Volume 2, Issue 1

Steven P. Treon, MD, PhD, discusses the role of BTK inhibitors in Waldenström macroglobulinemia.

Steven P. Treon, MD, PhD, director, Bing Center for Waldenström Macroglobulinemia, professor of medicine, Harvard Medical School, and senior physician, Dana-Farber Cancer Institute, discusses the role of BTK inhibitors in Waldenström macroglobulinemia.

The advent of BTK inhibitors has led to tremendous progress in the treatment of patients with Waldenström macroglobulinemia, says Treon.

BTK inhibitors were developed as a result of identifying MYD88 mutations, which are present in more than 95% of patients with Waldenström macroglobulinemia, explains Treon. MYD88 activates BTK through the hematopoietic cell kinase protein.

BTK inhibitors include ibrutinib (Imbruvica), acalabrutinib (Calquence), and zanubrutinib (Brukinsa), says Treon. Additionally, Japanese studies have shown that a fourth BTK inhibitor, tirabrutinib (Velexbru), has shown activity in this patient population.

Moreover, the agents have all demonstrated high overall response rates in the 90% range in patients with treatment-naïve, relapsed/refractory, or heavily pretreated Waldenström macroglobulinemia, concludes Treon.


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