A new paper in Cancer Cell from Ulrich Steidl, M.D., Ph.D., and colleagues at the Albert Einstein College of Medicine, identifies a key transcription factor that regulates hematopoiesis and has a role in leukemia. The transcription factor, H2.0-like Homeobox, or HLX, leads to increased proliferation of an abnormal population of hematopoietic progenitors. Hematopoietic stem cells (HSCs) give rise to red blood cells and immune cells. HLX appears to induce early differentiation of HSCs, but then prevents terminal differentiation into functional cells and causes these abnormal progenitors to proliferate indefinitely. Inhibiting HLX in leukemia cells leads to decreases in proliferation and increases in cell death and differentiation. Dr. Steidl studies acute myeloid leukemia (AML), a common form of blood cancer. Analyzing patient samples, Dr. Steidl’s group found that HLX is overexpressed in a majority of AML patients and high levels are associated with a more aggressive disease and a worse prognosis. Collectively these results suggest targeting HLX is a promising therapeutic strategy for the treatment of AML. This research was supported by a NYSTEM award to Dr. Steidl, C024350, and a Shared Facility award, C024172.
Kawahara M, Pandolfi A, Bartholdy B, Barreyro L, Will B, Roth M, Okoye-Okafor UC, Todorova TI, Figueroa ME, Melnick A, Mitsiades CS, Steidl U. H2.0-like Homeobox Regulates Early Hematopoiesis and Promotes Acute Myeloid Leukemia. Cancer Cell. 2012 Aug 14;22(2):194-208.