The DOT1L inhibitor pinometostat reduces H3K79 methylation and has modest clinical activity in adult acute leukemia
Eytan M. Stein(Memorial Sloan Kettering Cancer Center), Guillermo Garcia‐Manero(The University of Texas MD Anderson Cancer Center), David A. Rizzieri(Duke Medical Center), Raoul Tibes(Mayo Clinic in Arizona), Jesús G. Berdeja(Sarah Cannon), Michael R. Savona(Vanderbilt University Medical Center), Mojca Jongen-Lavrenic(Erasmus MC), Jessica K. Altman(Northwestern University), Blythe Thomson(Epizyme (United States)), Stephen J. Blakemore(Epizyme (United States)), Scott R. Daigle(Epizyme (United States)), Nigel J. Waters(Epizyme (United States)), A. Benjamin Suttle(Epizyme (United States)), Alicia Clawson(Epizyme (United States)), Roy M. Pollock(Epizyme (United States)), Andrei V. Krivtsov(Dana-Farber Cancer Institute), Scott A. Armstrong(Dana-Farber Cancer Institute), Jorge DiMartino, Eric Hedrick(Epizyme (United States)), Bob Löwenberg(Erasmus MC), Martin S. Tallman(Memorial Sloan Kettering Cancer Center)
Cited by 456Open Access
Abstract
Key Points Pinometostat demonstrates first evidence of DOT1L target inhibition and clinical responses in a subset of MLL-r advanced leukemia patients. The observed safety profile of pinometostat shows potential for exploration of combination therapies in leukemia.