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- W1986384270 abstract "The NF1 tumor suppressor gene encodes neurofibromin, a GTPase-activating protein (GAP) for p21ras (Ras). Children with NF1 are predisposed to juvenile myelomonocytic leukemia (JMML). Some heterozygous Nf1 mutant mice develop a similar myeloproliferative disorder (MPD), and adoptive transfer of Nf1-deficient fetal liver cells consistently induces this MPD. Human JMML and murine Nf1-deficient cells are hypersensitive to granulocyte-macrophage colony–stimulating factor (GM-CSF) in methylcellulose cultures. We generated hematopoietic cells deficient in both Nf1 and Gmcsf to test whether GM-CSF is required to drive excessive proliferation of Nf1−/− cells in vivo. Here we show that GM-CSF plays a central role in establishing and maintaining the MPD and that recipients engrafted with Nf1−/−Gmcsf−/− hematopoietic cells are hypersensitive to exogenous GM-CSF." @default.
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- W1986384270 date "2000-01-01" @default.
- W1986384270 modified "2023-10-01" @default.
- W1986384270 title "Nf1 and Gmcsf Interact in Myeloid Leukemogenesis" @default.
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- W1986384270 doi "https://doi.org/10.1016/s1097-2765(00)80415-3" @default.
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