{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T19:17:17Z","timestamp":1787944637243,"version":"build-2784847793"},"reference-count":27,"publisher":"Oxford University Press (OUP)","license":[{"start":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T00:00:00Z","timestamp":1784246400000},"content-version":"am","delay-in-days":1,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100014599","name":"Mark Foundation for Cancer Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100014599","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"NIH","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"National Cancer Institute"},{"name":"MSK SPORE in Bladder Cancer","award":["P50 CA221745"],"award-info":[{"award-number":["P50 CA221745"]}]},{"name":"MSK Cancer Center Support Grant","award":["P30 CA008748"],"award-info":[{"award-number":["P30 CA008748"]}]},{"name":"American Society of Clinical Oncology Young"},{"DOI":"10.13039\/100000002","name":"NIH","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Ruth L. Kirschstein National Research Service","award":["T32 CA082088"],"award-info":[{"award-number":["T32 CA082088"]}]},{"name":"Bochner Fleischer Scholarship and an NCI Mentored Clinical Scientist Research Career Development","award":["K08 CA272960"],"award-info":[{"award-number":["K08 CA272960"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Urothelial cancer typically affects older adults, yet early-onset urothelial cancer (age 45\u2009years and younger) cases are rising and remain poorly characterized. We hypothesized that early-onset urothelial cancer exhibits distinct clinical and genomic features that reflect a different biological etiology from standard-onset urothelial cancer.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We compared clinical, pathologic, and genomic characteristics of patients with early-onset urothelial cancer vs standard-onset urothelial cancer evaluated at Memorial Sloan Kettering Cancer Center from 2000 through 2024. Clinical data included 9221 patients, with tumor and germline genomic profiling by Memorial Sloan Kettering-Integrated Mutation Profiling of Actionable Cancer Targets (MSK-IMPACT) assay in 2753 patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Early-onset urothelial cancer accounted for 335 of 9221 (3.6%) patients. Early-onset urothelial cancer patients were more likely never-smokers (43% vs 26%, P\u2009&amp;lt;\u2009.001), female (30% vs 25%, P\u2009=\u2009.034), and of Asian race (7.4% vs 3.1%, P\u2009&amp;lt;\u2009.001). Early-onset urothelial cancer tumors were more often low-grade (41% vs 23%, P\u2009&amp;lt;\u2009.001) and of pure nonurothelial histology (4.0% vs 1.7%, P\u2009=\u2009.003). Early-onset urothelial cancer showed marked enrichment for HRAS mutations, independent of histologic subtype, and HRAS-mutated tumors had reduced APOBEC-associated mutation signatures. Germline pathogenic variants were detected in 21.0% of early-onset vs 17.2% of standard-onset urothelial cancer patients (P\u2009=\u2009.43), driven mostly by mismatch repair and MUTYH gene alterations. Rare cases of somatic mosaicism in HRAS and ERCC2 were observed in patients with very early-onset disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Early-onset urothelial cancer represents a biologically distinct subset characterized by HRAS-driven oncogenesis, reduced APOBEC mutagenesis, frequent germline variants, and, rarely, somatic mosaicism. These findings suggest developmental or genetic mechanisms underlying early-onset urothelial cancer and supporting age- and biology-informed approaches to risk assessment, genetic counseling, and targeted therapy development.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/jnci\/djag229","type":"journal-article","created":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T11:50:12Z","timestamp":1784202612000},"source":"Crossref","is-referenced-by-count":0,"title":["Comprehensive clinical and genomic analysis of early-onset cancer of the bladder and upper urinary tract"],"prefix":"10.1093","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0225-0148","authenticated-orcid":false,"given":"Hong","family":"Truong","sequence":"first","affiliation":[{"name":"Urology Service, Department of Surgery, Memorial Sloan Kettering Cancer Center , New York, NY,","place":["United 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