الفهرس 
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Abstract
To study the molecular abnormalities involved in the multistage development of cervical carcinoma, the presence of oncogenic human papillomavirus (hpv) dna infection and fragile histidine triad (fhit) gene deletion located at chromosome locus, were investigated, using polymerase chain reaction (pcr) . Human papillomavirus (hpv) are associated with benign and malignant neoplasms of the cervix. Specific hpv types appear to be the most important etiologic factor for cervical carcinoma. One of the criteria for their etiologic role requires an assessment of whether virtually all or only a small of lesions contion viral genome. The e6 and e7 proteins of oncogenic hpv such as hpv types 16 and 18, which interact with p53 and rb, respectively, inhabit the tumor suppressor function of these cellular proteins. Although, the human papillomavirus (hpv) is the most significant causative agent in the development of cervical cancer, its presence by itself in almost all cervical cancer, is unable to transform a normal cell to cancerous one. Instead, additional cellular mutations are required to supplement the hpv oncoproteins e6 and e7. therefore, additional genetic alterations may be necessary for malignant development and progression in the uterine cervix.