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Carbon-ion radiotherapy (CIRT) holds promise to treat inoperable locally-advanced non-small cell lung carcinoma (NSCLC), a disease poorly controlled by standard chemoradiotherapy using X-rays. Since CIRT is an extremely limited medical resource, selection of NSCLC patients likely to benefit from it is important; however, biological predictors of response to CIRT are ill-defined. The present study investigated the association between the mutational status of  EGFR  and  KRAS , driver genes frequently mutated in NSCLC, and the relative biological effectiveness (RBE) of carbon-ion beams over X-rays. The assessment of 15 NSCLC lines of different  EGFR / KRAS  mutational status and that of isogenic NSCLC lines expressing wild-type or mutant  EGFR  revealed that  EGFR- mutant NSCLC cells, but not  KRAS- mutant cells, show low RBE. This was attributable to (i) the high X-ray sensitivity of  EGFR -mutant cells, since  EGFR  mutation is associated with a defect in non-homologous end joining, a major pathway for DNA double-strand break (DSB) repair, and (ii) the strong cell-killing effect of carbon-ion beams due to poor repair of carbon-ion beam-induced DSBs regardless of  EGFR  mutation status. These data highlight the potential of  EGFR  mutation status as a predictor of response to CIRT, i.e., CIRT may show a high therapeutic index in  EGFR  mutation-negative NSCLC.

The EGFR mutation status affects the relative biological effectiveness of carbon-ion beams in non-small cell lung carcinoma cells