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- W4385486996 abstract "Ionizing radiation (IR) is a risk factor for acute myeloid leukemia (rAML). Murine rAMLs feature both hemizygous chromosome 2 deletions (Del2) and point mutations (R235) within the hematopoietic regulatory gene Spi1. We generated a heterozygous CBA Spi1 R235 mouse (CBASpm/+) which develops de novo AML with 100% incidence by ∼12 months old and shows a dose-dependent reduction in latency following X-irradiation. These effects are reduced on an AML-resistant C57Bl6 genetic background. CBASpm/Gfp reporter mice show increased Gfp expression, indicating compensation for Spm-induced Spi1 haploinsufficiency. Del2 is always detected in both de novo and rAMLs, indicating that biallelic Spi1 mutation is required for AML. CBASpm/+ mice show that a single Spm modification is sufficient for initiating AML development with complete penetrance, via the “two-hit” mechanism and this is accelerated by IR exposure. Similar SPI1/PU.1 polymorphisms in humans could potentially lead to enhanced susceptibility to IR following medical or environmental exposure." @default.
- W4385486996 created "2023-08-03" @default.
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- W4385486996 date "2023-09-01" @default.
- W4385486996 modified "2023-10-17" @default.
- W4385486996 title "Spi1 R235C point mutation confers hypersensitivity to radiation-induced acute myeloid leukemia in mice" @default.
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- W4385486996 doi "https://doi.org/10.1016/j.isci.2023.107530" @default.
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