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• W2981730489 abstract "Abstract Therapy-related and more specifically radiotherapy-associated acute myeloid leukaemia (AML) is a well-recognized potential complication of cytotoxic therapy for the treatment of a primary cancer. The CBA mouse model is used to study radiation leukaemogenesis mechanisms with Sfpi1/PU.1 deletion and point mutation already identified as driving events during AML development. To identify new pathways, we analysed 123 mouse radiation-induced AML (rAML) samples for the presence of mutations identified previously in human AML and found three genes to be mutated; Sfpi1 R235 (68%), Flt3-ITD (4%) and Kras G12 (3%), of which G12R was previously unreported. Importantly, a significant decrease in Sfpi1 gene expression is found almost exclusively in rAML samples without an Sfpi1 R235 mutation and is specifically associated with up-regulation of mir-1983 and mir-582-5p. Moreover, this down-regulation of Sfpi1 mRNA is negatively correlated with DNA methylation levels at specific CpG sites upstream of the Sfpi1 transcriptional start site. The down regulation of Sfpi1/PU.1 has also been reported in human AML cases revealing one common pathway of myeloid disruption between mouse and human AML where dysregulation of Sfpi1/PU.1 is a necessary step in AML development." @default.
• W2981730489 created "2019-11-01" @default.
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• W2981730489 date "2019-10-24" @default.
• W2981730489 modified "2023-10-16" @default.
• W2981730489 title "Kras mutations and PU.1 promoter methylation are new pathways in murine radiation-induced AML" @default.
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• W2981730489 doi "https://doi.org/10.1093/carcin/bgz175" @default.
• W2981730489 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7422620" @default.
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• W2981730489 hasPublicationYear "2019" @default.
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