et al. 2007). In the case of having a tissue sample to be tested, early stage cervical cancer can be differentiated from healthy cervical tissue by gene expression profile due to comparisons done with healthy and lymph node metastatic tissues which found certain genes upregulated and down regulated (Biewenga, P. et al. 2008). Early stage cervical cancers can be cured by radical surgery or radiotherapy with similar effectiveness (Biewenga, P. et al. 2008). Overall the treatment options for cervical cancer are based on whatever the outcome of clinical staging is and include surgery, radiotherapy, chemotherapy, and/or chemoradiotherapy (Ellenson, L.H. & Wu, T.C. 2004). More sophisticated methods such as the use of MR imaging before, during and after radiation therapy is providing accuracy in the main evaluation of prognostic factors and staging (Engin, G. 2006).

Currently there is an HPV vaccine for women that have been shown to be 100% effective against HPV types 16 and 18, preventing subsequent development of CIN (Steller, M.A. 2003). This vaccine is the direct result of over two decades of research and ongoing trials to find a male equivalent vaccine are underway utilizing a number of species. Papillomavirus infections, however, are species restricted and do not infect of induce changes in the morphology of animal tissues, thus requiring the use of species specific HPV which is hard to equate to humans due to no cervico-vaginal challenge or natural sexual transmission (Schiller, J.T., & Lowy, D.R. 2006). Because of these issues it is difficult to evaluate potential benefits or efficacy.

Ultimately, cervical cancer requires HPV infection but once infection occurs the virus requires other factors such as its host's genetics, immunity, as well as environmental factors such as nutrition, hormonal supplementation like birth control, or cigarette smoking which causes vasoconstriction and overall inflammation. If given the right external factors to its own viral integration into the host's DNA than continuous HPV infection may lead to precancerous lesions and cervical cancer itself. With a number of genetic, molecular, and protein markers being elucidated, tailoring both the treatment and screening processes can bring down overall cervical cancer mortality worldwide.

References

Biewenga, P., et al. (2008). Gene Expression in Early Stage Cervical Cancer. Gynecologic Oncology, 108, 520-526.

Boulet, G.A.V., et al. (2008). Human Papillomavirus in Cervical Cancer Screening: Important

Role as Biomarker. Cancer Epidemiology, Biomarkers, and Prevention, 17(4), 810-817.

Ellenson, L.H., & Wu, T.C., (2004). Focus on Endometrial and Cervical Cancer....

Cancer Cell, 5,
533-538.

Engin, G. (2006). Cervical Cancer: MR imaging findings before, during, and after radiation therapy. Urogenital, 16. 313-324.

Gius, D. et al. (2007). Profiling microdissected epithelium and stroma to model genomic signatures for cervical carcinogenesis accommodating for covariates. Cancer Research

67, 7113-7123.

GlaxoSmithKline. (2007). Cervical Cancer Fact Sheet. www.glaxosmithkline.com

Hu, X., et al. (2010). TP53, MDM2, NQO1, and susceptibility to cervical cancer. Cancer Epidemiology, Biomarkers, and Prevention, 19(3), 755-761.

Ivansson, E.L., et al. (2008). MHC loci affecting cervical cancer risk: distinguishing the effects of HLA-DQB1 and non-HLA genes TNF, LTA, TAP1, and TAP2. Genes and Immunity 9, 613-623.

Janeway, C.A. et al. (2005). Manipulation of the Immune Response. Immunobiology: 6th Edition.

636-637.

Lazcano-Ponce, E. et al. (2008). Decreasing Cervical Cancer Mortality in Mexico: Effect of Papanicolaou Coverage, Birthrate, and the Importance of Diagnostic Validity of Cytology. Cancer Epidemiology, Biomarkers, and Prevention, 17(10), 2808-2817.

National Cancer Institute (2010). Cancer Advances in Focus: Cervical Cancer, www.cancer.gov

Schiller, J.T., & Lowy, D.R. (2006). Prospects for Cervical Cancer Prevention by Human

Papillomavirus Vaccination. Cancer Research, 66(21), 10229-10232.

Sreekantaiah, C., De Braekeleer, M., & Haas, O., (1991). Cytogenic Findings in Cervical

Carcinoma: A Statistical Approach. Cancer Genetics and Cytogenetics, 53, 75-81.

Steben, M., & Duarte-Franco, E. (2007). Human papillomavirus infection: Epidemiology and pathophysiology. Gynecologic Oncology, 107(2), S2-S5.

Steller, M.A. (2003). Human Papillomavirus, it's genes…and cancer vaccines. Cancer Cell,

January, 7-8.

Therman, E., Buchler, D.A., Nieminen, U., & Timonen, S. (1983). Mitotic Modifications and Aberrations in Human Cervical Cancer. Cancer Research 30(4), 185-197.

Walboomers, J.M.M. et al. (1999). Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. The Journal of Pathology, 189(1), 12-19.

Xiaoxia, H. et al. (2010). TP53, MDM2, NQO1, and Susceptibility to Cervical Cancer. Cancer Epidemiology, Biomarkers, and Prevention, 19(3), 755-761.

Yu, T., et al. (2005). The Role of Viral Integration in the Development of Cervical Cancer.

Cancer Genetics and Cytogenetics, 158, 27-34.

Zhu, X., et al. (2009). Proteomic Identification of differentially-expressed proteins in…