The inactivation of the wild-type p53 function resulting from a missense mutation, or the lack of detectable wild-type p53 protein due to the translational/post-translational deregulation of p53 protein levels may be the contributing factor in the tumorigenicity of these five cases of cervical cancer.
Properties of p53 mutations detected in primary and secondary cervical cancers suggest mechanisms of metastasis and involvement of environmental carcinogens.
Although a high incidence of HPV DNA integration and a low incidence of p53 mutation were confirmed in cancer of the uterine cervix, there was no inverse association between integration of HPV types 16 and/or 18 DNA and p53 mutation.
In conclusion, our data suggest that the MDR1 gene plays a role in drug resistance of certain cervical cancers, but also that other mechanisms may be involved.
In conclusion, our data suggest that the MDR1 gene plays a role in drug resistance of certain cervical cancers, but also that other mechanisms may be involved.
Structural alterations of the p53 gene were investigated in tissue specimens of gastric and cervical cancers and in cell lines of gastric, esophageal, and cervical cancers, by polymerase chain reaction-single-strand conformation polymorphism analysis.
To examine the correlations between ras oncogene expression and the development of cervical cancer, the authors studied the reactivity of cervical intraepithelial neoplasia (CIN) and microinvasive lesions of the human uterine cervix by using anti-ras p21 mouse monoclonal antibody rp35.
The addition of activated Ha-ras, an oncogene found in some cervical cancers expressing HPV16 or 18, to HPV16-immortalized human cervical cells results in malignancy as proven by the formation of cystic squamous cell carcinomas by HPV16-Ha-ras cells in nude mice.
The production of early and term placental alkaline phosphatase (ALP), human chorionic gonadotropin beta-subunit (beta-hCG) and pregnancy-specific beta 1-glycoprotein (SP1) was confirmed in the newly established uterine cervical cancer call line SKG-IIIa.
Sodium butyrate produces concordant expression of "early placental" alkaline phosphatase, pregnancy-specific beta 1-glycoprotein and human chronic gonadotropin beta-subunit in a newly established uterine cervical cancer cell line (SKG-IIIa).
Sodium butyrate produces concordant expression of "early placental" alkaline phosphatase, pregnancy-specific beta 1-glycoprotein and human chronic gonadotropin beta-subunit in a newly established uterine cervical cancer cell line (SKG-IIIa).
Sodium butyrate produces concordant expression of "early placental" alkaline phosphatase, pregnancy-specific beta 1-glycoprotein and human chronic gonadotropin beta-subunit in a newly established uterine cervical cancer cell line (SKG-IIIa).
Several human ovarian and cervical cancer cell lines spontaneously express the icIL-1Ra. icIL-1Ra-expressing cells did not have altered growth characteristics or altered short term responses to IL-1 compared with icIL-1Ra-nonexpressing cells.
Several human ovarian and cervical cancer cell lines spontaneously express the icIL-1Ra. icIL-1Ra-expressing cells did not have altered growth characteristics or altered short term responses to IL-1 compared with icIL-1Ra-nonexpressing cells.