{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T10:42:41Z","timestamp":1790678561055,"version":"4.1.0"},"reference-count":22,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2011,12,23]],"date-time":"2011-12-23T00:00:00Z","timestamp":1324598400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2012,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Serous tubal intraepithelial carcinomas (STICs) have been proposed to be the most likely precursor of ovarian, tubal and \u2018primary peritoneal\u2019 (pelvic) high\u2010grade serous carcinoma (HGSC). As somatic mutation of\n                    <jats:italic>TP53<\/jats:italic>\n                    is the most common molecular genetic change of ovarian HGSC, occurring in more than 95% of cases, we undertook a mutational analysis of 29 pelvic HGSCs that had concurrent STICs to demonstrate the clonal relationship of STICs and HGSCs. In addition, we correlated the mutational data with p53 immunostaining to determine the role of p53 immunoreactivity as a surrogate for\n                    <jats:italic>TP53<\/jats:italic>\n                    mutations in histological diagnosis. Somatic\n                    <jats:italic>TP53<\/jats:italic>\n                    mutations were detected in all 29 HGSCs analysed and the identical mutations were detected in 27 of 29 pairs of STICs and concurrent HGSCs. Missense mutations were observed in 61% of STICs and frameshift\/splicing junction\/nonsense mutations in 39%. Interestingly, there were two HGSCs with two distinctly different\n                    <jats:italic>TP53<\/jats:italic>\n                    mutations each, but only one of the mutations was detected in the concurrent STICs. Missense mutations were associated with intense and diffuse (\u2265 60%) p53 nuclear immunoreactivity, while most of the null mutations were associated with complete loss of p53 staining (\n                    <jats:italic>p<\/jats:italic>\n                    &lt; 0.0001). Overall, this p53 staining pattern yielded a sensitivity of 87% and a specificity of 100% in detecting\n                    <jats:italic>TP53<\/jats:italic>\n                    missense mutations. In conclusion, the above findings support the clonal relationship of STIC and pelvic HGSC and demonstrate the utility of p53 immunostaining as a surrogate for\n                    <jats:italic>TP53<\/jats:italic>\n                    mutation in the histological diagnosis of STIC. In this regard, it is important to appreciate the significance of different staining patterns. Specifically, strong diffuse staining correlates with a missense mutation, whereas complete absence of staining correlates with null mutations. Copyright \u00a9 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.\n                  <\/jats:p>","DOI":"10.1002\/path.3023","type":"journal-article","created":{"date-parts":[[2011,10,12]],"date-time":"2011-10-12T07:48:50Z","timestamp":1318405730000},"page":"421-426","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":371,"title":["<i>TP53<\/i>\n                    mutations in serous tubal intraepithelial carcinoma and concurrent pelvic high\u2010grade serous carcinoma\u2014evidence supporting the clonal relationship of the two lesions"],"prefix":"10.1002","volume":"226","author":[{"given":"Elisabetta","family":"Kuhn","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert 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