{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T21:22:31Z","timestamp":1791408151145,"version":"4.3.3"},"reference-count":47,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2018,7,17]],"date-time":"2018-07-17T00:00:00Z","timestamp":1531785600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>The incidence of colorectal cancer (CRC) in younger patients is rising, mostly due to tumors in the descending colon and rectum. Therefore, we aimed to explore the molecular differences of left-sided CRC between younger (\u226445 years) and older patients (\u226565).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Subjects, Materials, and Methods<\/jats:title>\n                  <jats:p>In total, 1,126 CRC tumor samples from the splenic flexure to (and including) the rectum were examined by next-generation sequencing (NGS), immunohistochemistry, and in situ hybridization. Microsatellite instability (MSI) and tumor mutational burden (TMB) were assessed by NGS.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Younger patients (n\u2009=\u2009350), when compared with older patients (n\u2009=\u2009776), showed higher mutation rates in genes associated with cancer-predisposing syndromes (e.g., Lynch syndrome), such as MSH6 (4.8% vs. 1.2%, p\u2009=\u2009.005), MSH2 (2.7% vs. 0.0%, p\u2009=\u2009.004), POLE (1.6% vs. 0.0%, p\u2009=\u2009.008), NF1 (5.9% vs. 0.5%, p\u2009&amp;lt;\u2009.001), SMAD4 (14.3% vs. 8.3%, p\u2009=\u2009.024), and BRCA2 (3.7% vs. 0.5%, p\u2009=\u2009.002). Genes involved in histone modification were also significantly more mutated: KDM5C (1.9% vs. 0%, p\u2009=\u2009.036), KMT2A (1.1% vs. 0%, p\u2009=\u2009.033), KMT2C (1.6% vs. 0%, p\u2009=\u2009.031), KMT2D (3.8% vs. 0.7%, p\u2009=\u2009.005), and SETD2 (3.2% vs. 0.9%, p\u2009=\u2009.039). Finally, TMB-high (9.7% vs. 2.8%, p\u2009&amp;lt;\u2009.001) and MSI-high (MSI-H; 8.1% vs. 1.9%, p\u2009=\u2009.009) were more frequent in younger patients.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>Our findings highlight the importance of genetic counseling and screening in younger CRC patients. MSI-H and TMB-high tumors could benefit from immune-checkpoint inhibitors, now approved for the treatment of MSI-H\/deficient mismatch repair metastatic CRC patients. Finally, histone modifiers could serve as a new promising therapeutic target. With confirmatory studies, these results may influence our approach to younger adults with CRC.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1634\/theoncologist.2018-0117","type":"journal-article","created":{"date-parts":[[2018,7,17]],"date-time":"2018-07-17T16:16:10Z","timestamp":1531844170000},"page":"319-326","source":"Crossref","is-referenced-by-count":51,"title":["Impact of Patient Age on Molecular Alterations of Left-Sided Colorectal Tumors"],"prefix":"10.1093","volume":"24","author":[{"given":"Alberto","family":"Puccini","sequence":"first","affiliation":[{"name":"Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California, USA"},{"name":"Department of Medical Oncology, Ospedale Policlinico San Martino, Genova, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heinz-Josef","family":"Lenz","sequence":"additional","affiliation":[{"name":"Division of Medical Oncology, Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John L.","family":"Marshall","sequence":"additional","affiliation":[{"name":"Ruesch Center for The Cure of Gastrointestinal Cancers, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Arguello","sequence":"additional","affiliation":[{"name":"Caris Life Sciences, Phoenix, Arizona, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Derek","family":"Raghavan","sequence":"additional","affiliation":[{"name":"Levine Cancer Institute, Carolinas HealthCare System, Charlotte, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W. Michael","family":"Korn","sequence":"additional","affiliation":[{"name":"Caris Life Sciences, Phoenix, Arizona, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin A.","family":"Weinberg","sequence":"additional","affiliation":[{"name":"Ruesch Center for The Cure of Gastrointestinal Cancers, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kelsey","family":"Poorman","sequence":"additional","affiliation":[{"name":"Caris Life Sciences, Phoenix, Arizona, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arielle L.","family":"Heeke","sequence":"additional","affiliation":[{"name":"Ruesch Center for The Cure of Gastrointestinal Cancers, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip 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