News Research

In vivo ablation of NFκB cascade effectors alleviates disease burden in myeloproliferative neoplasms

Study in Blood dissecting the role of NFκB signaling effectors in MPN disease biology

Stephen T. Oh, MD, PhD, Co-Chief and Associate Professor of Medicine, Division of Hematology, Department of Medicine, Washington University School of Medicine in St. Louis, and has been published in Blood.

Targeting NFκB pathway mediators ca alleviates myeloproliferative disease burden in vivo without toxicity to health tissue

The WashU group of researchers previously identified hyperactivation of NFκB pathway signaling in myeloproliferative neoplasms (MPNs). In this study we utilized genetic and pharmacologic approaches to comprehensively dissect the role of NFκB signaling components in MPN disease development.

Through these efforts the group found that abrogation of multiple different NFκB effectors consistently ameliorated MPN disease features including leukocytosis, splenomegaly, and bone marrow fibrosis. These findings highlight potential avenues for novel therapeutic approaches for MPN patients.

Stephen Oh, MD, PhD

This study provides clear evidence of the essentiality of NFκB pathway signaling in MPN disease pathogenesis, and I am very excited about the potential for translation of these concepts to the clinic

Stephen T. Oh, MD, PhD

Also involved in the research are Angelo Brunelli Albertoni Laranjeira, Tim Kong, Steven C. Snyder, Mary C. Fulbright, Daniel A.C. Fisher, from WashU and Daniel T. Starczynowski from Cincinnati Children’s Hospital Medical Center.