These results indicate that transfection of cervical cancer cells with the wild-type p53 gene via Ad5CMV-p53 is a potential novel approach to the therapy of cervical cancer.
These data suggest that transfection of HPV-positive cervical cancer cells with a wild-type p53 gene in a form such as Ad5CMV-p53 is a potential novel therapy for cervical cancer.
Moreover, the odds of being diagnosed with an invasive stage of cervical cancer were 3.7 times higher (95% CI, 1.6-8.8) for women positive for the E6 protein and 17 times higher (95% CI, 5.5-58.3) for women positive for the bcl-2 protein compared with women negative for E6 and bcl-2.
To examine the role of cigarette smoking in the progression of cervical cancer initiated by HPV 18, we adapted these cells to growth in serum and high calcium and treated the cells with cigarette smoke condensate until tumorigenic cells (HEC-18-1C) were produced.
The PID-1 locus was further found in Southern analysis to be rearranged and amplified in another cervical cancer biopsy and a cervical carcinoma cell line (CaSki).
To evaluate both the incidence of c-myc gene mutation and the relationship of this finding to the clinico-pathologic characteristics of patients with cervical cancer, a polymerase chain reaction (PCR)-based heteroduplex gel electrophoresis method was used to screen DNA extracted from 102 cervical invasive carcinomas referred to the Department of Obstetrics and Gynaecology, The Chinese University of Hong Kong.
It seems that expression of CD44 splice variants is not a continuous process in the natural history of cervical cancer, and the pattern of CD44 splice variant expression is changed during carcinogenesis.
Recently we have demonstrated that tumor-specific cytotoxic T lymphocytes (CTLs) can be activated by cervical carcinoma cells expressing the costimulatory molecule CD80, which may be used as a therapeutic vaccine for patients with cervical cancer.
No evidence of correlation between polymorphism at codon 72 of p53 and risk of cervical cancer in Japanese patients with human papillomavirus 16/18 infection.
Deletions or point mutations in the p15INK4B or p16INK4A gene may not be required for the development of HPV-positive cervical cancer or for establishment of cervical cancer cell lines.