Author/Authors :
Kovacic، نويسنده , , Boris and Stoiber، نويسنده , , Dagmar and Moriggl، نويسنده , , Richard and Weisz، نويسنده , , Eva and Ott، نويسنده , , René G. and Kreibich، نويسنده , , Rita and Levy، نويسنده , , David E. and Beug، نويسنده , , Hartmut and Freissmuth، نويسنده , , Michael and Sexl، نويسنده , , Veronika، نويسنده ,
Abstract :
Summary
mor 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.
