Oncogenic KRAS drives radioresistance through upregulation of NRF2-53BP1-mediated non-homologous end-joining repair.
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DOI: 10.1093/nar/gkab871
Abstract: KRAS-activating mutations are oncogenic drivers and are correlated with radioresistance of multiple cancers, including colorectal cancer, but the underlying precise molecular mechanisms remain elusive. Herein we model the radiosensitivity of isogenic HCT116 and SW48 colorectal… read more here.
Keywords: end joining; nrf2 53bp1; radioresistance; homologous end ... See more keywords