UCL Cancer Institute Seminar Series

The myeloid transforming gene EVI1 is aberrantly expressed in human AML with chromosome 3q26 abnormalities. EVI1 is essential for the growth of these leukemias. We recently uncovered the mechanism of aberrant expression of the gene in those leukemias. Furthermore, we obtained evidence that  disruption the EVI1 protein complex in the nucleus abrogates the differentiation block of transformed myeloid progenitors. The consequences for the treatment of this refractory AML subtype will be discussed. 

Hosted by: Tariq Enver and Beth Payne

Selected publications:

Eric M. J. Bindels, Marije Havermans, Sanne Lugthart, Claudia Erpelinck, Elizabeth Wocjtowicz, Andrei V. Krivtsov, Elwin Rombouts, Scott A. Armstrong, Erdogan Taskesen, Jurgen R. Haanstra,H. Berna Beverloo, Hartmut Döhner, Wendy A. Hudson, John H. Kersey, Ruud Delwel, and Ashish R. Kumar. EVI1 is critical for the pathogenesis of a subset of MLL-AF9–rearranged AMLs. Blood. 2012 Jun 14; 119(24): 5838–5849

Maria E. Figueroa, Sanne Lugthart, Yushan Li, Claudia Erpelinck-Verschueren, Xutao Deng, Paul J. Christos, Elizabeth Schifano, Jim Booth, Lucy Skrabanek, Fabien Campagne, Madhu Mazumdar, Bob Löwenberg, John M. Greally, Peter J.M. Valk, Ruud Delwel, and Ari Melnick. Epigenetic Signatures Identify New Clinically Relevant Subtypes in Acute Myeloid Leukemia. Cancer Cell .2010; 17(1):13-27

For more information, see http://www.erasmusmc.nl/MScMM/faculty/CVs/delwel_cv?lang=en

Location

UCL Cancer Institute
Paul O'Gorman Building 72 Huntley Street London WC1E 6DD

This seminar has been sponsored in part by Taconic Bioscience, the Biomedical Research Centre and Cancer Research UK