Abstract
Cervical carcinoma is a preventable disease based on its etiopathogenesis. This relies highly on its prompt diagnosis and treatment based on effective screening and treatment methods. Knowledge of its molecular pathways will drive the use of targeted therapies in the treatment of the disease. The objectives of this review are: to explore the biology and immunology of HPV; the various molecular pathways through which oncogenic HPV destroys normal cervical cells; and targeted therapies. Several molecular pathways have been identified but the use of drugs to act on specified molecular targets are at different stages of clinical trials.
Highlights
Carcinoma of the uterine cervix causes severe morbidity and death in the developing countries where screening services and treatments are deficient [1].Persistent infection with the high risk Human Papillomavirus (HPV) is a prerequisite for cervical cancer development [2].HPV is spread by skin-to-skin contact and sexual intercourse [3]
Carcinoma of the uterine cervix is a major cause of cancer related deaths in women especially in developing countries [5]
It is expected that when the clinical trials of targeted therapies are concluded, medical options may supersede surgical options especially following early disease diagnosis
Summary
Carcinoma of the uterine cervix causes severe morbidity and death in the developing countries where screening services and treatments are deficient [1].Persistent infection with the high risk Human Papillomavirus (HPV) is a prerequisite for cervical cancer development [2].HPV is spread by skin-to-skin contact and sexual intercourse [3]. Carcinoma of the uterine cervix causes severe morbidity and death in the developing countries where screening services and treatments are deficient [1]. Persistent infection with the high risk Human Papillomavirus (HPV) is a prerequisite for cervical cancer development [2]. The persistent infections progress over a latent period of 10 – 15 years to varying abnormal proliferation of cells and spread of hypervascularized necrotic tissues that characterize cancer of the uterine cervix. The overexpression of E6 and E7 oncoproteins by HPV is the main oncogenic stimulus for the cellular transformation in cervical cancer [4]. Carcinoma of the uterine cervix is a major cause of cancer related deaths in women especially in developing countries [5]. Understanding the molecular pathways and the development of safe and effective targeted therapies will improve overall outcomes in this disease
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