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Start of funding 01.07.2004
Role of the Ets repressor METS/PE1 in the development of myeloid malignancies
PD Dr. Michael Rehli
University of Regensburg
Prof. Dr. Christopher K. Glass
University of California, San Diego
Department of Cellular und Molecular Medicine
The coordinate regulation of proliferation and differentiation is disturbed in aberrant proliferating tumor cells. Dr. Glass’s laboratory recently described a mechanism in which induction of the Ets repressor METS/PE1 links terminal differentiation to cell cycle arrest. The collaborative project aims at defining a putative role of the METS/DP103 disfunction in tumorigenesis. Due to its important role in terminal differentiation and cell cycle arrest, it is conceivable that disruption of METS/DP103 function could lead to myeloproliferation and could contribute to leukemogenesis. We have started to analyse METS/DP103 expression in normal human and myeloid leukemia cells and search for mutations in METS/DP103 genes that might correlate with loss/gain of function and aberrant proliferation.