Global signatures of Ribonucleotide Excision Repair deficiency and its therapeutic vulnerabilities
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Ribonucleotide excision repair (RER) deficiency produces a distinct genome-wide mutational phenotype, and a new whole-genome classifier, RERDetect, detects RER-deficient tumors across cancer types. Applied to more than 11,000 primary and metastatic cancers, it found a recurrent subset of RER-deficient tumors, most lacking detectable RNASEH2 genetic alterations, with RNASEH2C promoter hypermethylation as a recurrent inactivation mechanism. RER-deficient cells were sensitive to EXO1 and FANCM inhibition, making RER deficiency a therapeutically actionable repair-deficient state.
Excerpted from biorxiv.org
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- biorxiv.orgGlobal signatures of Ribonucleotide Excision Repair deficiency and its therapeutic vulnerabilities
Ribonucleotide excision repair (RER) deficiency produces a distinct genome-wide mutational phenotype, and a new whole-genome classifier, RERDetect, detects RER-deficient tumors across cancer types. Applied to more than 11,000 primary and metastatic cancers, it found a recurrent subset of RER-deficient tumors, most lacking detectable RNASEH2 genetic alterations, with RNASEH2C promoter hypermethylation as a recurrent inactivation mechanism. RER-deficient cells were sensitive to EXO1 and FANCM inhibition, making RER deficiency a therapeutically actionable repair-deficient state.
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