{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:17:30Z","timestamp":1784557050110,"version":"3.55.0"},"reference-count":54,"publisher":"Bioscientifica","issue":"1","content-domain":{"domain":["erc.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2012,2]]},"abstract":"<jats:p>\n                    <jats:italic>BRCA1\/2<\/jats:italic>\n                    germ line mutation carriers have a high risk of developing fallopian tube carcinoma (FTC), thought to occur through different early (p53 signatures) and later (dysplasia, intra-epithelial carcinoma) premalignant stages. Promoter hypermethylation of tumour suppressor genes is known to play a key role in (early) carcinogenesis. However, little is known about methylation in normal and (pre)malignant fallopian tube tissue. We identified 14 areas of p53 accumulation in the fallopian tubes of\n                    <jats:italic>BRCA<\/jats:italic>\n                    mutation carriers. Cells from these areas were harvested together with cells from adjacent benign appearing areas. An age-matched non-\n                    <jats:italic>BRCA<\/jats:italic>\n                    sporadic control group (\n                    <jats:italic>n<\/jats:italic>\n                    =13) and eight sporadic FTCs were included as negative and positive controls respectively. Methylation-specific multiplex ligation-dependent probe amplification was used to assess promoter methylation of 70 tumour suppressor genes in all samples. We observed a gradual increase in methylation from sporadic control tissue (median cumulative methylation index (CMI) 568.19) through normal tissue and from areas of p53 accumulation in\n                    <jats:italic>BRCA<\/jats:italic>\n                    carriers (median CMI 687.54 and 676.72) to FTC (median CMI 780.97). Furthermore, the methylation percentage of many individual tumour suppressor genes differed significantly between these groups, gradually increasing as for CMI. Between areas with and without p53 accumulation in\n                    <jats:italic>BRCA<\/jats:italic>\n                    mutation carriers no significant differences were found. In this paper, we have shown that\n                    <jats:italic>BRCA<\/jats:italic>\n                    mutation carriers display increased methylation of tumour suppressor genes in their non-malignant fallopian tube epithelium, closer to methylation levels in FTC than to normal sporadic tissue. Methylation could, therefore, play an important role in the increased risk of gynaecological malignancies in\n                    <jats:italic>BRCA<\/jats:italic>\n                    mutation carriers.\n                  <\/jats:p>","DOI":"10.1530\/erc-11-0338","type":"journal-article","created":{"date-parts":[[2011,12,5]],"date-time":"2011-12-05T20:39:37Z","timestamp":1323117577000},"page":"69-81","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":8,"title":["Promoter hypermethylation patterns in fallopian tube epithelium of BRCA1 and BRCA2 germ line mutation carriers"],"prefix":"10.1530","volume":"19","author":[{"given":"Jonathan G","family":"Bijron","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petra","family":"van der Groep","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eleonora B","family":"van Dorst","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura M S","family":"Seeber","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daisy M D S","family":"Sie-Go","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ren\u00e9 H M","family":"Verheijen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul J","family":"van Diest","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"issue":"23","key":"1_6259647","first-page":"5489","volume":"58","author":"Ahuja","year":"1998","journal-title":"Cancer Research","ISSN":"https:\/\/id.crossref.org\/issn\/0008-5472","issn-type":"print"},{"issue":"5","key":"2_17591912","doi-asserted-by":"publisher","first-page":"1117","DOI":"10.1086\/375033","volume":"72","author":"Antoniou","year":"2003","journal-title":"American journal of human genetics","ISSN":"https:\/\/id.crossref.org\/issn\/0002-9297","issn-type":"print"},{"issue":"18","key":"3_18447866","doi-asserted-by":"publisher","first-page":"5998","DOI":"10.1158\/1078-0432.CCR-04-0667","volume":"10","author":"Bae","year":"2004","journal-title":"Clinical Cancer Research","ISSN":"https:\/\/id.crossref.org\/issn\/1078-0432","issn-type":"print"},{"issue":"3","key":"4_38133190","doi-asserted-by":"publisher","first-page":"363","DOI":"10.1111\/j.1365-2559.2010.03642.x","volume":"57","author":"Bol","year":"2010","journal-title":"Histopathology","ISSN":"https:\/\/id.crossref.org\/issn\/0309-0167","issn-type":"print"},{"issue":"1","key":"5_38933792","doi-asserted-by":"publisher","first-page":"206","DOI":"10.1016\/j.ygyno.2010.11.037","volume":"121","author":"Brunner","year":"2011","journal-title":"Gynecologic oncology","ISSN":"https:\/\/id.crossref.org\/issn\/0090-8258","issn-type":"print"},{"issue":"25","key":"6_29283150","doi-asserted-by":"publisher","first-page":"3985","DOI":"10.1200\/JCO.2007.12.2622","volume":"25","author":"Callahan","year":"2007","journal-title":"Journal of Clinical Oncology","ISSN":"https:\/\/id.crossref.org\/issn\/0732-183X","issn-type":"print"},{"issue":"6","key":"7_19715916","doi-asserted-by":"crossref","first-page":"1327","DOI":"10.1097\/01.AOG.0000187892.78392.3f","volume":"106","author":"Cass","year":"2005","journal-title":"Obstetrics &amp; 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