I t is estimated that 5%-6% of colorectal cancers are due to a hereditary cancer syndrome. 1,2 Genetic testing in at-risk relatives, known as cascade carrier testing, identifies those most likely to benefit from increased screening and preventive measures, leading to earlier detection and decreased cancer incidence. 3 The cost-effectiveness of broad panel genetic testing relies on uptake of targeted carrier testing and arguably on the effectiveness of hereditary cancer programs in general. 4-6 The most common hereditary colorectal cancer syndrome, Lynch syndrome, accounts for up to 5% of colorectal cancers. 2 People with Lynch syndrome have up to an 80% and 60% lifetime risk (up to age 80 yr) for colorectal and endometrial cancer, respectively. 7 In people with more rare hereditary colorectal cancer syndromes such as familial adenomatous polyposis and MUTYH-associated polyposis, there is up to a 100% colorectal cancer lifetime risk (to age 80 yr) without appropriate surveillance. 8 Given the substantially higher cancer risk among people with these syndromes than in the general population, identifying those at risk is an important health care priority. 9 Reports suggest variable carrier testing rates in clinic-based and cancer registry-based studies of at-risk relatives, ranging from 34% to 75%. 4,10-23 Most people who have received carrier testing for Lynch syndrome are satisfied in the long term with receiving testing, 11 as carrier testing enables them to make more informed decisions and to receive personalized health care. 24 Noncarriers also benefit from carrier testing, as

Purpose Referrals for Lynch syndrome (LS) assessment have traditionally been based on personal and family medical history. The introduction of universal screening practices has allowed for referrals based on immunohistochemistry tests for mismatch repair (MMR) protein expression. This study aims to characterize the effect of universal screening in a publicly funded healthcare system with comparison to patients referred by traditional criteria, from January 2012 to March 2017. Methods Patient files from the time of initiation of universal screening from 2012 to 2017 were reviewed. Patients were sorted into two groups: (a) universally screened and (b) referred by traditional methods. Mutation detection rates, analysis of traditional testing criteria met, and cascade carrier testing were evaluated. Results The mutation detection rate of the universal screening group was higher than the traditionally referred group (45/228 (19.7%) vs 50/390 (12.5%), P = .05), though each were able to identify unique patients. An analysis of testing criteria met by each patient showed that half of referred patients from the universal screening group could not meet any traditional testing criteria. Conclusion The implementation of universal screening in a publicly funded system will increase efficiency in detecting patients with LS. The resources available for genetic testing and counseling may be more limited in public systems, thus inclusion of secondary screening with BRAF and MLH1 promoter hypermethylation testing is key to further optimizing efficiency.