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Losses of FHIT and p16 in oral carcinogenesis – a FISH based study

Losses of FHIT and p16 in oral carcinogenesis – a FISH based study. Johannes Bier. background – „leukoplakia“ 1/2 . oral leukoplakia main epithelial lesion of the mucosa of the mouth (prevalence: 2.3%) heterogeneous group with varying risk

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Losses of FHIT and p16 in oral carcinogenesis – a FISH based study

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  1. Losses of FHIT and p16 in oral carcinogenesis – a FISH based study Johannes Bier

  2. background – „leukoplakia“ 1/2 • oral leukoplakia main epithelial lesion of the mucosa of the mouth (prevalence: 2.3%) • heterogeneous group with varying risk • premalignant epithelial precursor lesion of OSCC (3-8% transform into cancer) • whitish patches • several grades: hyperplasia, low/high grade dysplasia, CIS, invasive cancer • mainly due to carcinogens, i.e. nicotine, alcohol, but also idiopathic

  3. background – „leukoplakia“ 2/2 • no standardized regime for treatment • follow-up with biopsy and histopathology currently gold standard • molecular biological techniques to be future proposals ? • no specific markers to predict malignant transformation yet • LOH and polyploidy ?

  4. so what?

  5. there are hints... • molecular progression model for oral carcinogenesis: accumulation of genetic changes (Califano et al.,1996) (adopted from Fearon & Vogelstein 1990: colon cancer) • studies on LOH proposed 3p and 9p to be important for progression (Rosin et al., 2000; Mao et al.,1996) • greater probability of progression into OSCC

  6. 3p and 9p... • 3p14 alias FHIT (fragile histidine triade), 9p21 alias p16 • both tumor suppressor genes • considered to indicate transition from hyperplasia to dysplasia

  7. FISH what?! leukoplakia with hyperplasia – probes for FHIT centromere gene

  8. FISH what?! invasive carcinoma – probes for FHIT centromer gene

  9. results - deletion FHIT / p16

  10. results - polysomy FHIT / p16

  11. discussion • already >90% of hyperplasia deletion for FHIT Califano et al. = 20% • our threshold: 25% / 13%  LOH studies 50% • FHITearlier event than p16; results underline role of FHIT regarding cell cycle regulation • possibility to distinguish deletion – amplification • hyperplasia does not show polysomy 3p or 9p • polysomy 3 indicator of increasing oral carcinogenesis

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