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- W3162617742 abstract "Anti-EGFR antibodies such as cetuximab are active against KRAS/NRAS wild-type colorectal cancers (CRCs), but acquired resistance invariably evolves. It is unknown which mutational mechanisms enable resistance evolution and whether adaptive mutagenesis (a transient cetuximab-induced increase in mutation generation) contributes in patients. Here, we investigate these questions in exome sequencing data from 42 baseline and progression biopsies from cetuximab-treated CRCs. Mutation loads did not increase from baseline to progression, and evidence for a contribution of adaptive mutagenesis was limited. However, the chemotherapy-induced mutational signature SBS17b was the main contributor of specific KRAS/NRAS and EGFR driver mutations that are enriched at acquired resistance. Detectable SBS17b activity before treatment predicted shorter progression-free survival and the evolution of these specific mutations during subsequent cetuximab treatment. This result suggests that chemotherapy mutagenesis can accelerate resistance evolution. Mutational signatures may be a new class of cancer evolution predictor." @default.
- W3162617742 created "2021-05-24" @default.
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- W3162617742 date "2021-05-20" @default.
- W3162617742 modified "2023-10-16" @default.
- W3162617742 title "Mutational signatures impact the evolution of anti-EGFR antibody resistance in colorectal cancer" @default.
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- W3162617742 doi "https://doi.org/10.1038/s41559-021-01470-8" @default.
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