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Lynch syndrome is an inherited cancer-susceptibility disorder caused by pathogenic germline variants in DNA mismatch repair (MMR) genes, including MLH1, MSH2, MSH6, and PMS2. Historically known as hereditary nonpolyposis colorectal cancer, this syndrome is associated with increased risk for a multitude of cancers, including colorectal, endometrial, ovarian, small bowel, urothelium, biliary tract, and stomach (1-3). Lynch syndrome affects 1 in 279 individuals, and is more common than Hereditary Breast and Ovarian Cancer Syndrome caused by BRCA1 and BRCA2 mutations (4, 5). Lynch syndrome is also inherited in an autosomal dominant fashion. Recent studies have suggested that breast cancer may be included in the spectrum of Lynch syndrome-associated cancers, but the evidence is controversial. Cohort studies have found significantly increased age-specific incidence rate ratios of breast cancer in Lynch patients (6, 7). Case series have also shown high prevalence of breast cancer in Lynch populations, with earlier age of diagnosis compared to the general population (8). Investigators have looked at microsatellite instability, immunohistochemistry and mismatch repair gene deficiency in breast cancers of Lynch syndrome patients, suggesting that patients with Lynch syndrome are more likely to exhibit microsatellite instability and MMR protein loss compared with sporadic breast cancers (9-11). However, other studies show no association and recommend that increased surveillance is not indicated for Lynch syndrome patients (1,12,13).Multigene panel testing has provided new insight, suggesting that individuals with MSH6 and PMS2 mutations may have a higher risk for breast cancer (14,15). A case-control study published by Couch showed that only MSH6 mutations were associated with a statisti-

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