{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,15]],"date-time":"2026-04-15T00:40:47Z","timestamp":1776213647538,"version":"3.50.1"},"reference-count":61,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2006,11,10]],"date-time":"2006-11-10T00:00:00Z","timestamp":1163116800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Chromosomes &amp;amp; Cancer"],"published-print":{"date-parts":[[2007,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Common fragile sites (CFS) are nonstaining gaps or breaks in chromosomes that are expressed under conditions inducing replicative stress. CFS have been suggested to play a role in epithelial cancers by their association with loss of heterozygosity, loss of gene expression, and\/or gene amplification in the form of homogeneously staining regions (hsrs). In oral squamous\u2010cell carcinomas (OSCC), amplification of chromosomal band 11q13 occurs in the form of an hsr. We suggested previously that CFS flanking 11q13 may be susceptible to breakage induced by tobacco or other carcinogens and\/or human papillomavirus, promoting formation of the 11q13 amplicon. Examination of OSCC cell lines with 11q13 amplification using fluorescence in situ hybridization showed loss of <jats:italic>FRA11F<\/jats:italic> sequences, whereas cell lines without 11q13 amplification displayed an intact <jats:italic>FRA11F<\/jats:italic> site. Cell lines with more complex 11q rearrangements expressed <jats:italic>FRA11F<\/jats:italic> in the form of an inverted duplication, characteristic of breakage\u2010fusion\u2010bridge cycles. Our findings suggest that gene amplification involving chromosomal band 11q13 in OSCC may be initiated by breakage at <jats:italic>FRA11F<\/jats:italic>. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/gcc.20394","type":"journal-article","created":{"date-parts":[[2006,11,10]],"date-time":"2006-11-10T16:46:42Z","timestamp":1163177202000},"page":"143-154","source":"Crossref","is-referenced-by-count":41,"title":["Relationship between <i>FRA11F<\/i> and 11q13 gene amplification in oral cancer"],"prefix":"10.1002","volume":"46","author":[{"given":"Shalini C.","family":"Reshmi","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xin","family":"Huang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"David W.","family":"Schoppy","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert 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