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- W2896656693 abstract "Genetic variation conferring resistance and susceptibility to carcinogen-induced tumorigenesis is frequently studied in mice. We have now turned this idea to melanoma using the collaborative cross (CC), a resource of mouse strains designed to discover genes for complex diseases. We studied melanoma-prone transgenic progeny across seventy CC genetic backgrounds. We mapped a strong quantitative trait locus for rapid onset spontaneous melanoma onset to Prkdc, a gene involved in detection and repair of DNA damage. In contrast, rapid onset UVR-induced melanoma was linked to the ribosomal subunit gene Rrp15. Ribosome biogenesis was upregulated in skin shortly after UVR exposure. Mechanistically, variation in the ‘usual suspects’ by which UVR may exacerbate melanoma, defective DNA repair, melanocyte proliferation, or inflammatory cell infiltration, did not explain melanoma susceptibility or resistance across the CC. Instead, events occurring soon after exposure, such as dysregulation of ribosome function, which alters many aspects of cellular metabolism, may be important." @default.
- W2896656693 created "2018-10-26" @default.
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- W2896656693 date "2019-01-25" @default.
- W2896656693 modified "2023-10-16" @default.
- W2896656693 title "Different genetic mechanisms mediate spontaneous versus UVR-induced malignant melanoma" @default.
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- W2896656693 doi "https://doi.org/10.7554/elife.42424" @default.
- W2896656693 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6428585" @default.
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