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Summary: In this issue of Cancer Discovery, Poulin and colleagues apply structural, biochemical, and biological profiling of two mutants of KRAS, one found most frequently in all cancers (G12D) and one found nearly exclusively in colorectal cancer (A146T). They provide compelling evidence that specific mutations will impart different structural and biochemical consequences on KRAS function and that the same KRAS mutation displays tissue-distinct signaling and biological consequences. See related article by Poulin et al., p. 738.
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Hobbs et al. (2019) studied this question.
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