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Ruben A. Mesa, MD, discusses the impact of molecular biology on therapeutic development in myelofibrosis.
Ruben A. Mesa, MD, director of the Mays Cancer Center at UT Health San Antonio MD Anderson Cancer Center, discusses the impact of molecular biology on therapeutic development in myelofibrosis.
Researchers in the field of myeloproliferative neoplasms has developed a greater understanding of the molecular biology of myelofibrosis in recent years, Mesa says. For example, research shed light on the fact that myelofibrosis is a clonal disease that incorporates a leukemic clone with a secondary fibrotic process. Moreover, other research efforts led to the identification of driver mutations, such as JAK2, CALR, and MPL, as well as somatic mutations, such as ASXL1, EZH2, and IDH1/2. These markers have prognostic significance in myelofibrosis and the field is learning that they have clinical implications on therapeutic development, Mesa explains.
For example, molecular insight into a patient’s prognosis allows clinicians to consider moving forward with transplant early in the patient’s disease course, Mesa says. Additionally, targeted therapies, such as JAK inhibitors ruxolitinib (Jakafi), fedratinib (Inrebic), momelotinib, and pacritinib, IDH1/2 inhibitors, EZH2 inhibitors, are established or in clinical development in myelofibrosis. Moreover, agents including navitoclax, pelabresib, and PI3K inhibitors are being studied in ongoing clinical trials to expand upon targeted options in myelofibrosis, Mesa concludes.