{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T16:40:36Z","timestamp":1784133636817,"version":"3.55.0"},"reference-count":46,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2016,10,19]],"date-time":"2016-10-19T00:00:00Z","timestamp":1476835200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"National Cancer Institute of the National Institutes of Health","award":["P30CA046592"],"award-info":[{"award-number":["P30CA046592"]}]},{"name":"National Cancer Institute of the National Institutes of Health","award":["R01CA196619"],"award-info":[{"award-number":["R01CA196619"]}]}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2016,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Endometrioid carcinoma (<jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content>) is a relatively indolent ovarian carcinoma subtype that is nonetheless deadly if detected late. Existing genetically engineered mouse models (<jats:styled-content style=\"fixed-case\">GEMMs<\/jats:styled-content>) of the disease, based on transformation of the ovarian surface epithelium (<jats:styled-content style=\"fixed-case\">OSE<\/jats:styled-content>), take advantage of known ovarian <jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content> driver gene lesions, but do not fully recapitulate the disease features seen in patients. An <jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content> model in which the <jats:italic>Apc<\/jats:italic> and <jats:italic>Pten<\/jats:italic> tumour suppressor genes are conditionally deleted in murine <jats:styled-content style=\"fixed-case\">OSE<\/jats:styled-content> yields tumours that are biologically more aggressive and significantly less differentiated than human <jats:styled-content style=\"fixed-case\">ECs<\/jats:styled-content>. Importantly, <jats:styled-content style=\"fixed-case\">OSE<\/jats:styled-content> is not currently thought to be the tissue of origin of most ovarian cancers, including <jats:styled-content style=\"fixed-case\">ECs<\/jats:styled-content>, suggesting that tumour initiation in M\u00fcllerian epithelium may produce tumours that more closely resemble their human tumour counterparts. We have developed <jats:italic>Ovgp1\u2010<jats:styled-content style=\"fixed-case\">iCreER<jats:sup>T2<\/jats:sup><\/jats:styled-content><\/jats:italic> mice in which the <jats:italic>Ovgp1<\/jats:italic> promoter controls expression of tamoxifen (<jats:styled-content style=\"fixed-case\">TAM<\/jats:styled-content>)\u2010regulated Cre recombinase in oviductal epithelium \u2013 the murine equivalent of human Fallopian tube epithelium. <jats:italic>Ovgp1\u2010<jats:styled-content style=\"fixed-case\">iCreER<jats:sup>T2<\/jats:sup><\/jats:styled-content>;Apc<jats:sup>fl\/fl<\/jats:sup>;Pten<jats:sup>fl\/fl<\/jats:sup><\/jats:italic> mice treated with <jats:styled-content style=\"fixed-case\">TAM<\/jats:styled-content> or injected with adenovirus expressing Cre into the ovarian bursa uniformly develop oviductal or ovarian <jats:styled-content style=\"fixed-case\">ECs<\/jats:styled-content>, respectively. On the basis of their morphology and global gene expression profiles, the oviduct\u2010derived tumours more closely resemble human ovarian <jats:styled-content style=\"fixed-case\">ECs<\/jats:styled-content> than do <jats:styled-content style=\"fixed-case\">OSE<\/jats:styled-content>\u2010derived tumours. Furthermore, mice with oviductal tumours survive much longer than their counterparts with ovarian tumours. The slow progression and late metastasis of oviductal tumours resembles the relatively indolent behaviour characteristic of so\u2010called Type I ovarian carcinomas in humans, for which <jats:styled-content style=\"fixed-case\">EC<\/jats:styled-content> is a prototype. Our studies demonstrate the utility of <jats:italic>Ovgp1\u2010<jats:styled-content style=\"fixed-case\">iCreER<jats:sup>T2<\/jats:sup><\/jats:styled-content><\/jats:italic> mice for manipulating genes of interest specifically in the oviductal epithelium, and establish that the cell of origin is an important consideration in mouse ovarian cancer <jats:styled-content style=\"fixed-case\">GEMMs<\/jats:styled-content>. Copyright \u00a9 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/path.4783","type":"journal-article","created":{"date-parts":[[2016,8,19]],"date-time":"2016-08-19T05:32:41Z","timestamp":1471584761000},"page":"341-351","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":73,"title":["Impact of oviductal versus ovarian epithelial cell of origin on ovarian endometrioid carcinoma phenotype in the mouse"],"prefix":"10.1002","volume":"240","author":[{"given":"Rong","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Pathology University of Michigan Medical School  Ann Arbor MI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yali","family":"Zhai","sequence":"additional","affiliation":[{"name":"Department of Pathology University of Michigan Medical School  Ann Arbor MI 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