Oncology

Myelofibrosis

Expert Roundtables Podcast: Myelofibrosis – Frontiers and Future Directions

conference reporter by Gabriela S. Hobbs, MD; Andrew Kuykendall, MD; Lucia Masarova, MD

Overview

An improved understanding of genetics and disease mechanisms in myelofibrosis has spurred the development of newer therapeutic strategies. Promising research includes exploration of novel JAK2-specific approaches as well as mutant CALR-directed immunotherapy.

References

Masubuchi N, Yang Y, Imai M, et al. Loss of KDEL function from a calreticulin frameshift mutation drives expression of an immature, mutant calreticulin-dependent form of the thrombopoietin receptor MPL. Haematologica. Published online November 6, 2025. doi:10.3324/haematol.2025.287585

Reis ES, Buonpane R, Celik H, et al. Selective targeting of mutated calreticulin by the monoclonal antibody INCA033989 inhibits oncogenic function of MPN. Blood. 2024;144(22):2336-2348. doi:10.1182/blood.2024024373

Reynolds SB, Komrokji R, Kuykendall AT. The ongoing challenges of managing cytopenic myelofibrosis in 2025: The emergence of non-JAK inhibitor therapies. Blood Lymphat Cancer. 2025;15:181-192. Published 2025 Sep 24. doi:10.2147/BLCTT.S549533

Profile

Gabriela S. Hobbs, MD

Associate Professor, Medicine
Harvard Medical School
Clinical Director, Leukemia
Massachusetts General Hospital
Boston, MA

Profile

Andrew Kuykendall, MD

Associate Member, Department of Malignant Hematology
H. Lee Moffitt Cancer Center & Research Institute
Assistant Professor, Department of Oncologic Sciences
University of South Florida
Tampa, FL