{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,8]],"date-time":"2026-01-08T05:01:05Z","timestamp":1767848465135,"version":"3.49.0"},"reference-count":0,"publisher":"S. Karger AG","issue":"Suppl. 1","license":[{"start":{"date-parts":[[2000,1,1]],"date-time":"2000-01-01T00:00:00Z","timestamp":946684800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2000,1,1]],"date-time":"2000-01-01T00:00:00Z","timestamp":946684800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gynecol Obstet Invest"],"published-print":{"date-parts":[[2000]]},"abstract":"<jats:p>In a series of studies, we have hypothesised that endometriotic proliferation is, in part, precipitated by mutations in oncogenes or deletions in tumor suppressor genes that have been shown to be important steps in the transformation from a benign to a malignant epithelium. We reported previously that we could find no mutations in the &lt;i&gt;TP53&lt;\/i&gt; and &lt;i&gt;RASK&lt;\/i&gt; genes in cases of endometriosis. However, having shown that endometriotic deposits were monoclonal, we showed loss of heterozygosity on chromosomes 9p (18%), 11q (18%), and 22q (15%) \u2013 in total 28% of endometriotic lesions showed loss of heterozygosity at one or more sites [1]. We could not demonstrate any loss of heterozygosity in normal endometrium. We examined adjacent endometriosis, atypical endometriosis, and endometrioid carcinoma of the ovary and showed common genetic alterations that are consistent with a common lineage. These common alterations were not seen in lesions that were distant from each other [2]. In endometrioid tumors, we reported an increased frequency of mutations in the &lt;i&gt;PTEN\/MMAC&lt;\/i&gt; tumor suppressor genes that was not seen in clear cell or serous carcinoma, suggesting distinct developmental pathways for these tumors [3].<\/jats:p>","DOI":"10.1159\/000052878","type":"journal-article","created":{"date-parts":[[2003,4,15]],"date-time":"2003-04-15T19:06:15Z","timestamp":1050433575000},"page":"44-50","source":"Crossref","is-referenced-by-count":70,"title":["Molecular Genetic Defects in Endometriosis"],"prefix":"10.1159","volume":"50","author":[{"given":"Eric J.","family":"Thomas","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"I.G.","family":"Campbell","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"127","published-online":{"date-parts":[[2000,11,17]]},"container-title":["Gynecologic and Obstetric Investigation"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/52878","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/52878","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,24]],"date-time":"2025-04-24T04:17:28Z","timestamp":1745468248000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000052878"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2000]]},"references-count":0,"journal-issue":{"issue":"Suppl. 1","published-online":{"date-parts":[[2000,10,1]]}},"URL":"https:\/\/doi.org\/10.1159\/000052878","archive":["Portico"],"relation":{},"ISSN":["0378-7346","1423-002X"],"issn-type":[{"value":"0378-7346","type":"print"},{"value":"1423-002X","type":"electronic"}],"subject":[],"published":{"date-parts":[[2000]]}}}