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We aimed to assess the ability of PRS to refine CRC risk prediction in European-descendant individuals with LS.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      1465 individuals with LS (557\n                      <jats:italic>MLH1<\/jats:italic>\n                      , 517\n                      <jats:italic>MSH2\/EPCAM<\/jats:italic>\n                      , 299\n                      <jats:italic>MSH6<\/jats:italic>\n                      and 92\n                      <jats:italic>PMS2<\/jats:italic>\n                      ) and 5656 CRC-free population-based controls from two independent cohorts were included. A 91-SNP PRS was applied. A Cox proportional hazard regression model with \u2018family\u2019 as a random effect and a logistic regression analysis, followed by a meta-analysis combining both cohorts were conducted.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Overall, we did not observe a statistically significant association between PRS and CRC risk in the entire cohort. Nevertheless, PRS was significantly associated with a slightly increased risk of CRC or advanced adenoma (AA), in those with CRC diagnosed &lt;50 years and in individuals with multiple CRCs or AAs diagnosed &lt;60 years.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The PRS may slightly influence CRC risk in individuals with LS in particular in more extreme phenotypes such as early-onset disease. However, the study design and recruitment strategy strongly influence the results of PRS studies. A separate analysis by genes and its combination with other genetic and non-genetic risk factors will help refine its role as a risk modifier in LS.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/jmg-2023-109344","type":"journal-article","created":{"date-parts":[[2023,6,15]],"date-time":"2023-06-15T13:20:53Z","timestamp":1686835253000},"page":"1044-1051","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":12,"title":["Ability of a polygenic risk score to refine colorectal cancer risk in Lynch syndrome"],"prefix":"10.1136","volume":"60","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6624-3265","authenticated-orcid":false,"given":"Nuria","family":"Due\u00f1as","sequence":"first","affiliation":[{"name":"Hereditary Cancer Program, Catalan Institute of Oncology - ICO, L\u2019Hospitalet de Llobregat, Spain"},{"name":"Hereditary Cancer Group, Molecular Mechanisms and Experimental Therapy in Oncology Program, Institut 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