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Article

Perturbation of base excision repair sensitizes breast cancer cells to APOBEC3 deaminase-mediated mutations.

eLife - 6 Jan 2020

Shen Birong, Chapman Joseph H, Custance Michael F, Tricola Gianna M, Jones Charles E, Furano Anthony V

Abstract excerpt

Abundant APOBEC3 (A3) deaminase-mediated mutations can dominate the mutational landscape ('mutator phenotype') of some cancers, however, the basis of this sporadic vulnerability is unknown. We show here that elevated expression of the bifunctional DNA glycosylase, NEIL2, sensitizes breast cancer cells to A3B-mediated mutations and double-strand breaks (DSBs) by perturbing canonical base excision repair (BER)....

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Identifiers

PMID: 31904337
DOI: 10.7554/eLife.51605
PMCID: PMC6961979

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Perturbation of base excision repair sensitizes breast cancer cells to APOBEC3 deaminase-mediated mutations.PMID 31904337Read ↗

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