{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T12:13:42Z","timestamp":1792412022445,"version":"4.4.0"},"reference-count":42,"publisher":"American Association for Cancer Research (AACR)","issue":"10","content-domain":{"domain":["aacrjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Cisplatin-based chemotherapy is the standard of care for patients with muscle-invasive urothelial carcinoma. Pathologic downstaging to pT0\/pTis after neoadjuvant cisplatin-based chemotherapy is associated with improved survival, although molecular determinants of cisplatin response are incompletely understood. We performed whole-exome sequencing on pretreatment tumor and germline DNA from 50 patients with muscle-invasive urothelial carcinoma who received neoadjuvant cisplatin-based chemotherapy followed by cystectomy (25 pT0\/pTis \u201cresponders,\u201d 25 pT2+ \u201cnonresponders\u201d) to identify somatic mutations that occurred preferentially in responders. ERCC2, a nucleotide excision repair gene, was the only significantly mutated gene enriched in the cisplatin responders compared with nonresponders (q &amp;lt; 0.01). Expression of representative ERCC2 mutants in an ERCC2-deficient cell line failed to rescue cisplatin and UV sensitivity compared with wild-type ERCC2. The lack of normal ERCC2 function may contribute to cisplatin sensitivity in urothelial cancer, and somatic ERCC2 mutation status may inform cisplatin-containing regimen usage in muscle-invasive urothelial carcinoma.<\/jats:p>\n                  <jats:p>Significance: Somatic ERCC2 mutations correlate with complete response to cisplatin-based chemosensitivity in muscle-invasive urothelial carcinoma, and clinically identified mutations lead to cisplatin sensitivity in vitro. Nucleotide excision repair pathway defects may drive exceptional response to conventional chemotherapy. Cancer Discov; 4(10); 1140\u201353. \u00a92014 AACR.<\/jats:p>\n                  <jats:p>See related commentary by Turchi et al., p. 1118<\/jats:p>\n                  <jats:p>This article is highlighted in the In This Issue feature, p. 1103<\/jats:p>","DOI":"10.1158\/2159-8290.cd-14-0623","type":"journal-article","created":{"date-parts":[[2014,8,5]],"date-time":"2014-08-05T20:24:46Z","timestamp":1407270286000},"page":"1140-1153","update-policy":"https:\/\/doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":586,"title":["Somatic\n                    <i>ERCC2<\/i>\n                    Mutations Correlate with Cisplatin Sensitivity in Muscle-Invasive Urothelial Carcinoma"],"prefix":"10.1158","volume":"4","author":[{"given":"Eliezer M.","family":"Van Allen","sequence":"first","affiliation":[{"name":"1Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts."},{"name":"2Broad Institute of MIT and Harvard, 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