Loss of the Tumor Suppressor BAP1 Causes Myeloid Transformation
Copyright policy )Loss of the Tumor Suppressor BAP1 Causes Myeloid Transformation
Identifying BAP1 Targets Inactivating mutations in the deubiquitinating enzyme BAP1 have been associated with cancer. Dey et al. (p. 1541 , published online 9 August; see the Perspective by White and Harper ) reveal molecular targets of the enzyme and show evidence for a role in leukemia. Mice specifically lacking the target of BAP1, HCF-1, in the bone marrow developed myeloid leukemia. BAP1 appears to be part of a complex that regulates modification of histones and gene expression important for normal hematopoiesis and tumor suppression.
- The University of Texas MD Anderson Cancer Center United States
- GENENTECH INC United States
- The University of Texas System United States
- Memorial Sloan Kettering Cancer Center United States
Mice, Knockout, Chromatin Immunoprecipitation, Embryonic Development, Leukemia, Myelomonocytic, Chronic, N-Acetylglucosaminyltransferases, Hematopoiesis, Mice, Cell Transformation, Neoplastic, Gene Expression Regulation, Myelodysplastic Syndromes, Animals, Humans, Genes, Tumor Suppressor, Myeloid Cells, Gene Knock-In Techniques, Promoter Regions, Genetic, Host Cell Factor C1, Gene Deletion, Myeloid Progenitor Cells, Bone Marrow Transplantation
Mice, Knockout, Chromatin Immunoprecipitation, Embryonic Development, Leukemia, Myelomonocytic, Chronic, N-Acetylglucosaminyltransferases, Hematopoiesis, Mice, Cell Transformation, Neoplastic, Gene Expression Regulation, Myelodysplastic Syndromes, Animals, Humans, Genes, Tumor Suppressor, Myeloid Cells, Gene Knock-In Techniques, Promoter Regions, Genetic, Host Cell Factor C1, Gene Deletion, Myeloid Progenitor Cells, Bone Marrow Transplantation
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