{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T09:54:46Z","timestamp":1785578086163,"version":"3.56.0"},"reference-count":24,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2020,4,21]],"date-time":"2020-04-21T00:00:00Z","timestamp":1587427200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["acsjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer"],"published-print":{"date-parts":[[2020,7]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Emerging evidence has suggested that DNA repair gene alterations may be important in prostate cancer pathogenesis. In the current study, the authors sought to characterize alterations in DNA repair pathway genes in both primary and metastatic prostate tumors with attention to tissue distribution as well as specific genomic alterations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The authors studied the distribution and type of alterations in 24 genes that are considered important for DNA repair in 944 prostate cancers harvested from localized and metastatic tumors. Tumor DNA underwent hybrid capture for all coding exons of 287 or 395 cancer\u2010related genes plus select introns from 19 or 31 genes frequently rearranged in cancer. Captured libraries were sequenced to a median exon coverage depth of &gt;\u00d7500. Specific genomic alterations were characterized and the frequencies of mutations by tissue site (prostate vs metastases) were compared using logistic regression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      A total of 152 patients from the cohort of 944 men (16%) harbored a germline or somatic mutation in \u22651 DNA repair genes. The most frequently mutated genes were\n                      <jats:italic>BRCA2<\/jats:italic>\n                      (11.4%) and\n                      <jats:italic>ATM<\/jats:italic>\n                      (5.8%), followed by\n                      <jats:italic>MSH6<\/jats:italic>\n                      (2.5%) and\n                      <jats:italic>MSH2<\/jats:italic>\n                      (2.1%). Mutations were identified in approximately 20.1% of primary prostate tumors compared with 18.8% of bone metastases. When stratified by tissue site, the highest rates of DNA repair mutations were found in solid organ metastases, including brain and visceral metastases, compared with prostate.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>DNA repair gene mutations are more common in metastatic than localized prostate tumors. Visceral and other solid organ metastases appear enriched for these mutations compared with localized tumors or bone and lymph node metastases.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cncr.32908","type":"journal-article","created":{"date-parts":[[2020,4,21]],"date-time":"2020-04-21T16:34:15Z","timestamp":1587486855000},"page":"2980-2985","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Germline and somatic DNA repair gene alterations in prostate cancer"],"prefix":"10.1002","volume":"126","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2301-2683","authenticated-orcid":false,"given":"Marc A.","family":"Dall\u2019Era","sequence":"first","affiliation":[{"name":"Department of Urology University of California at Davis Sacramento California"},{"name":"University of California at Davis Comprehensive Cancer Center Sacramento California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John D.","family":"McPherson","sequence":"additional","affiliation":[{"name":"University of California at Davis Comprehensive Cancer Center Sacramento California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Allen C.","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Urology University of California at Davis Sacramento California"},{"name":"University of California at Davis Comprehensive Cancer Center Sacramento California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ralph W.","family":"DeVere White","sequence":"additional","affiliation":[{"name":"Department of Urology University of California at Davis Sacramento California"},{"name":"University of California at Davis Comprehensive Cancer Center Sacramento California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey P.","family":"Gregg","sequence":"additional","affiliation":[{"name":"University of California at Davis Comprehensive Cancer Center Sacramento California"},{"name":"Foundation Medicine Cambridge Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr","given":"Primo N.","family":"Lara","sequence":"additional","affiliation":[{"name":"Department of Urology University of California at Davis Sacramento California"},{"name":"University of California at Davis Comprehensive Cancer Center Sacramento 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