STAT1 acts as a tumor promoter for leukemia development.

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.
Authors	Boris Kovacic, Dagmar Stoiber, Richard Moriggl, Eva Weisz, René G Ott, Rita Kreibich, David E Levy, Hartmut Beug, Michael Freissmuth, Veronika Sexl
Journal	Cancer cell (Cancer Cell) Vol. 10 Issue 1 Pg. 77-87 (Jul 2006) ISSN: 1535-6108 [Print] United States
PMID	16843267 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	DNA-Binding Proteins Histocompatibility Antigens Class I Oncogene Proteins v-abl Oncogene Proteins, Fusion Rag2 protein, mouse STAT1 Transcription Factor Stat1 protein, mouse TEL-JAK2 fusion protein, mouse Interferon-gamma
Topics	Animals B-Lymphocytes (metabolism, pathology) Cell Line, Tumor Cell Proliferation Cell Survival (genetics) Cell Transformation, Neoplastic (genetics) DNA-Binding Proteins (genetics, metabolism) Disease Progression Genotype Histocompatibility Antigens Class I (immunology, metabolism) Interferon-gamma (genetics, metabolism) Killer Cells, Natural (immunology, metabolism) Leukemia, Experimental (genetics, metabolism, pathology) Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Oncogene Proteins v-abl (genetics, metabolism) Oncogene Proteins, Fusion (genetics, metabolism) Phenotype STAT1 Transcription Factor (deficiency, genetics, physiology) Stem Cells (metabolism, pathology) Survival Analysis

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.

Realize the full power of the drug-disease research graph!