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Objective: To explore the loss of heterozygosity(LOH) on chromosome 6q in ovarian cancer, and localize a minimum area in deletion region. Methods: 93 ovarian tumors were analyzed for LOH studies with 10 microsatellite markers spanning chromosome 6q. To further localize a minimum area in deletion region. Nineteen microsatellite markers were used to refined a minimum area. Results: Forty three tumors(46%) were demonstrated allelic losses, which spanned less than two megabase areas, franked by a distal marker D6S311 and a proximal marker D6S1649, and likely harbored ovarian tumor suppressor gene(s). With analysis of density of LOH, increased DNA copy number at loci of 6q was demonstrated between D6S1649 and D6S311. Conclusion: It is possible that duplication after the allelic loss might be a main mechanism that leads to carcinogenesis in ovarian tumor. The refinement of these candidate tumor suppressor genes loci might facilitate future loss of heterozygosity studies and enable the isolation of candidate genes from this region.
Objective: To explore the loss of heterozygosity (LOH) on chromosome 6q in ovarian cancer, and localize a minimum area in deletion region. Methods: 93 ovarian tumors were analyzed for LOH studies with 10 microsatellite markers spanning chromosome 6q. Nineteen microsatellite markers were used to refine a minimum area. Results: Forty three tumors (46%) were rendered allelic losses, which spanned less than two megabase areas, franked by an distal marker D6S311 and a proximal marker D6S1649, and likely harbored ovarian tumor suppressor gene (s). With analysis of density of LOH, increased DNA copy number at loci of 6q was illustrated between D6S1649 and D6S311. Conclusion: It is possible that duplication after the allelic loss might be a main mechanism that leads to carcinogenesis in ovarian tumor. The refinement of these candidate tumor suppressor genes loci might facilitate future loss of heterozygosity studies and enable the isolat ion of candidate genes from this region.