| Literature DB >> 16843267 |
Boris Kovacic1, Dagmar Stoiber, Richard Moriggl, Eva Weisz, René G Ott, Rita Kreibich, David E Levy, Hartmut Beug, Michael Freissmuth, Veronika Sexl.
Abstract
The tumor suppressor STAT1 is considered a key regulator of the surveillance of developing tumors. Here, we describe an unexpected tumor-promoting role for STAT1 in leukemia. STAT1(-/-) mice are partially protected from leukemia development, and STAT1(-/-) tumor cells induce leukemia in RAG2(-/-) and immunocompetent mice with increased latency. The low MHC class I protein levels of STAT1(-/-) tumor cells enable efficient NK cell lysis and account for the enhanced tumor clearance. Strikingly, STAT1(-/-) tumor cells acquire increased MHC class I expression upon leukemia progression. These findings define STAT1 as a tumor promoter in leukemia development. Furthermore, we describe the upregulation of MHC class I expression as a general mechanism that allows for the escape of hematopoietic malignancies from immune surveillance.Entities:
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Year: 2006 PMID： 16843267 DOI： 10.1016/j.ccr.2006.05.025
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743