Since immortalization by HPV E6/E7 is an important early event in cervical carcinogenesis, the EGFR is a potential target for chemoprevention or therapy in women who have a high risk for cervical cancer.
The aim of this study was to systematically analyze the molecular mechanism leading to epidermal growth factor receptor overexpression in cervical cancer.
For cervical cancer, our results suggested that potential drugs are likely to involve the EGFR pathway; and with the breast cancer dataset, we identified candidates that are involved in prostaglandin inhibition.
Membranous expression of ectodomain isoforms of the epidermal growth factor receptor predicts outcome after chemoradiotherapy of lymph node-negative cervical cancer.
For the purpose of identifying prognostic factors for pretreated uterine cancer, DNA ploidy, proliferative index (P.I.) and epidermal growth factor receptor (EGFR) expression were analyzed in a large prospective series of 76 cervical cancer and 64 endometrial cancer patients observed for 5 years or more (median 76 months).
The coexpression of ErbB1 and ErbB4 in cervical carcinoma suggests that they may be involved in receptor heterodimerization leading to the activation of signaling pathway in the cervical carcinoma.