{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,5]],"date-time":"2026-03-05T23:20:44Z","timestamp":1772752844944,"version":"3.50.1"},"reference-count":49,"publisher":"S. Karger AG","issue":"2-4","license":[{"start":{"date-parts":[[2007,1,1]],"date-time":"2007-01-01T00:00:00Z","timestamp":1167609600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2007,1,1]],"date-time":"2007-01-01T00:00:00Z","timestamp":1167609600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cytogenet Genome Res"],"published-print":{"date-parts":[[2007]]},"abstract":"<jats:p>Bladder carcinomas frequently show extensive deletions of chromosomes 9p and\/or 9q, potentially including the loci of the Fanconi anemia (FA) genes &lt;i&gt;FANCC&lt;\/i&gt; and &lt;i&gt;FANCG&lt;\/i&gt;. FA is a rare recessive disease due to defects in anyone of 13 FANC genes manifesting with genetic instability and increased risk of neoplasia. FA cells are hypersensitive towards DNA crosslinking agents such as mitomycin C and cisplatin that are commonly employed in the chemotherapy of bladder cancers. These observations suggest the possibility of disruption of the FA\/BRCA DNA repair pathway in bladder tumors. However, mutations in &lt;i&gt;FANCC&lt;\/i&gt; or &lt;i&gt;FANCG&lt;\/i&gt; could not be detected in any of 23 bladder carcinoma cell lines and ten surgical tumor specimens by LOH analysis or by FANCD2 immunoblotting assessing proficiency of the pathway. Only a single cell line, BFTC909, proved defective for FANCD2 monoubiquitination and was highly sensitive towards mitomycin C. This increased sensitivity was restored specifically by transfer of the &lt;i&gt;FANCF&lt;\/i&gt; gene. Sequencing of &lt;i&gt;FANCF&lt;\/i&gt; in BFTC909 failed to identify mutations, but methylation of cytosine residues in the &lt;i&gt;FANCF&lt;\/i&gt; promoter region was demonstrated by methylation-specific PCR, &lt;i&gt;Hpa&lt;\/i&gt;II restriction and bisulfite DNA sequencing. Methylation-specific PCR uncovered only a single instance of &lt;i&gt;FANCF&lt;\/i&gt; promoter hypermethylation in surgical specimens of further 41 bladder carcinomas. These low proportions suggest that in contrast to other types of tumors silencing of &lt;i&gt;FANCF &lt;\/i&gt;is a rare event in bladder cancer and that an intact FA\/BRCA pathway might be advantageous for tumor progression.<\/jats:p>","DOI":"10.1159\/000108297","type":"journal-article","created":{"date-parts":[[2007,11,14]],"date-time":"2007-11-14T10:29:10Z","timestamp":1195036150000},"page":"166-176","source":"Crossref","is-referenced-by-count":30,"title":["Disruption of the FA\/BRCA pathway in bladder 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