PMID:9697835

Citation	Traver, D, Akashi, K, Weissman, IL and Lagasse, E (1998) Mice defective in two apoptosis pathways in the myeloid lineage develop acute myeloblastic leukemia. Immunity 9:47-57
Abstract	Fas-deficient (Fas(lpr/lpr)) mice constitutively expressing Bcl-2 in myeloid cells by the hMRP8 promoter often develop a fatal disease analogous to human acute myeloblastic leukemia (AML-M2). Hematopoietic cells from leukemic Fas(lpr/lpr)hMRP8bcl-2 animals form clonogenic blast colonies in vitro and can transfer disease to wild-type mice. In vitro ligation of Fas on Fas+/+ hMRP8bcl-2 marrow cells depletes approximately 50% of myeloid progenitor activity, demonstrating that Bcl-2 can only partially block Fas-mediated death signals in myelomonocytic progenitors. In addition, Fas(lpr/lpr) marrow contains greatly increased numbers of myeloid colony-forming cells as compared to Fas+/+ controls. Taken together, these data suggest that Fas has a novel role in the regulation of myelopoiesis and that Fas may act as a tumor suppressor to control leukemogenic transformation in myeloid progenitor cells.
Links	PubMed
Keywords	Animals; Antigens, CD95/genetics; Antigens, CD95/physiology; Antigens, Differentiation/genetics; Apoptosis; Bone Marrow Cells; Calcium-Binding Proteins/genetics; Calgranulin A; Causality; Female; Granulocyte-Macrophage Colony-Stimulating Factor/metabolism; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology; Hematopoietic Stem Cells; Humans; Interleukin-3/metabolism; Interleukin-3/pharmacology; Leukemia, Myeloid, Acute/etiology; Leukemia, Myeloid, Acute/genetics; Lymphocyte Activation; Male; Mice; Mice, Inbred MRL lpr; Mice, Transgenic; Neoplasm Transplantation; Proto-Oncogene Proteins c-bcl-2/genetics; Proto-Oncogene Proteins c-bcl-2/physiology; Up-Regulation
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