{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,13]],"date-time":"2026-08-13T00:27:34Z","timestamp":1786580854715,"version":"build-2736575974"},"reference-count":58,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T00:00:00Z","timestamp":1785456000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,8,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Molecular underpinnings and clinical characteristics of ERBB2\/HER2-mutated colorectal cancers (CRCs) remain poorly understood. We aimed to comprehensively characterize the genomic landscape and clinical features of ERBB2\/HER2-mutated CRC and to compare them with those of ERBB2\/HER2-amplified CRC.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Patients and methods<\/jats:title>\n                    <jats:p>We analyzed cBioPortal data from 4348 CRC patients with available ERBB2\/HER2 profiling. Clinicodemographic features, microsatellite instability (MSI), tumor mutational burden, and alterations in 94 cancer-associated genes were evaluated using chi-square\/Fisher\u2019s exact test, Kruskal\u2013Wallis test, and hierarchical clustering.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>ERBB2\/HER2 putative driver mutations were identified in 95 patients (2.2%), amplifications in 87 (2.0%), and wild-type status in 4166 (95.8%). In the overall cohort, ERBB2\/HER2-mutated tumors demonstrated significant KRAS enrichment (50.5%) compared to wild-type (37.7%; P\u2009=\u2009.014) and amplified tumors (18.4%; P\u2009&amp;lt;\u2009.001), alongside MSI enrichment (37.2% vs 1.6%; P\u2009&amp;lt;\u2009.001), elevated tumor mutational burden, and right-sided predominance. ERBB2\/HER2-mutated tumors also showed broad driver co-alterations largely reflecting their MSI background. In contrast, ERBB2\/HER2-amplified tumors exhibited left-sided predominance, with microsatellite stable (MSS)-restricted analyses revealing selective mutual exclusivity with KRAS (Log2 OR\u2009=\u2009\u22121.58; q\u2009=\u20090.019) and TP53 co-occurrence (Log2 OR = 2.04; q\u2009=\u20090.019). Hierarchical clustering confirmed that mutated and amplified tumors consistently occupy separate clusters across anatomical sites.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>ERBB2\/HER2 mutations and amplifications represent molecularly and clinically distinct subgroups. ERBB2\/HER2-mutated tumors are characterized by an MSI-enriched, hypermutated background with frequent concurrent KRAS alterations, whereas amplified tumors exhibit selective KRAS mutual exclusivity and TP53 co-occurrence. These exploratory findings support alteration-specific therapeutic strategies in CRC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/oncolo\/oyag302","type":"journal-article","created":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T11:56:54Z","timestamp":1785412614000},"source":"Crossref","is-referenced-by-count":0,"title":["Genomic landscape and clinical characteristics of\n                    <i>ERBB2\/HER2<\/i>\n                    -mutated colorectal cancers"],"prefix":"10.1093","volume":"31","author":[{"given":"Muhammed Dogukan","family":"Aksu","sequence":"first","affiliation":[{"name":"Division of Medical Oncology, Department of Oncology, Mayo Clinic , Rochester, MN, 55905,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paola Zinser","family":"Peniche","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Hematology and Oncology, University of Pittsburgh School of Medicine , Pittsburgh, PA, 15213,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Doga Kahramangil","family":"Baytar","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Hematology and Oncology, University of Pittsburgh School of Medicine , Pittsburgh, PA, 15213,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bhaghyasree","family":"Jambunathan","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Hematology and Oncology, University of Pittsburgh School of Medicine , Pittsburgh, PA, 15213,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu Jen Alexander","family":"Jan","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Hematology and Oncology, University of Pittsburgh School of Medicine , Pittsburgh, PA, 15213,","place":["United 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