MRE11

Overview

MRE11 (MRE11 Homolog, Double Strand Break Repair Nuclease) encodes a component of the MRN (MRE11–RAD50–NBN) complex, which is essential for homologous recombination (HR) DNA repair, DNA damage sensing, and checkpoint activation. MRE11 mutations can impair HR and may confer sensitivity to PARP inhibitors or other DNA damage-repair-targeting agents. In lung adenocarcinoma, MRE11 alterations are enriched in a specific clinical subgroup.

Alterations observed in the corpus

  • Enriched in the never/former-light smoker UMD (unmatched molecular driver) subset of a prospective LUAD cohort (860 patients, MSK-IMPACT); the paper uses the legacy symbol “MRE11A” but the current HUGO symbol is MRE11; specific mutation type and frequency not detailed in the primary alteration table PMID:28336552
  • Novel prostate-cancer-specific DNA-repair significantly mutated gene (SMG) in the MSK/PCF pan-prostate WES cohort (1,013 primary + 1,424 metastatic); truncating-biased mutation pattern supporting a tumor-suppressor role alongside PALB2. PMID:29610475

Cancer types (linked)

  • LUAD (Lung Adenocarcinoma): MRE11 alterations enriched in the never/former-light smoker UMD cohort alongside chromatin modifiers KMT2D, KMT2C, SETD2, and CREBBP; this subgroup lacked actionable matched therapy options under the study’s level 1–4 framework PMID:28336552

Co-occurrence and mutual exclusivity

Therapeutic relevance

  • MRE11 loss-of-function mutations may predict HR deficiency and sensitivity to PARP inhibitors; this study does not report matched PARP inhibitor therapy for MRE11-altered patients, though BRCA1/BRCA2-altered patients in the same cohort were flagged for olaparib eligibility PMID:28336552

Open questions

  • Frequency and specific mutation classes of MRE11 alterations in the LUAD UMD subset are not detailed; prospective evaluation of HR-deficiency–directed therapy in MRE11-mutated LUAD is not reported PMID:28336552

Sources

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