Homopolymer switches mediate adaptive mutability in mismatch repair-deficient colorectal cancer.

As a further control, we compared the frequency of homopolymer frameshift mutations in these genes to the proportion of all exonic length 8 C:G or A:T homopolymers mutated across the cohort and found highly significant enrichment of homopolymer frameshift mutations in the MSH6 C8 homopolymer (37.3% versus 23.4%, P = 1.9 × 10 −6 ) and the MSH3 A8 homopolymer (67.3% versus 9.9%; P < 2.2 × 10 −16 ).

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