Zhao Min, Qiu Xiao-ping, Dai Tian-li, Tan Yun, Wu Xin-xing

Background: The role of human papillomavirus (HPV) in the development of cervical carcinoma has been clearly established but other factors could be involved in cervical tumorigenesis such as loss of heterozygosity (LOH) and microsatellite instability (MI). The aim of the present study was to investigate the relationship between HPV infection, genetic instability and cervical carcinoma and to determine the location of suppressor-like genes, the loss of function of which might be important in the incidence or progression of cervical carcinomas. Methods: 50 primary cervical carcinoma samples from patients from high-incidence area of China, i.e. 16 in situ cancer samples, 10 samples of stage I, 16 samples of stage II and 8 samples of stage III were analyzed. DNA was extracted from cervical biopsy samples and peripheral blood samples and analyzed by PCR using 8 highly polymorphic microsatellite primers: D3S1478, D3S1766, D6S260, D11S925, D18S35, D18S474, D18S64, and D18S68. Also, HPV status of tumors was determined by PCR. Results: HPV16 was detected in 88% of cases, and LOH with < 3 different loci per case — in 66% of cases. The highest frequency of the allelic loss was found in D18S474 (18q21, 40.5%) and MI was found in 4 cases (8%). Conclusion: different percentages LOH on specific chromosomal regions were found and MI was very unfrequent in cervical carcinoma. The putative suppressor gene(s) likely to be located on specific chromosome region such as 18q21, and genetic charge play a key role in cervical tumorigenesis.

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