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Pramod Singh Khatri* and Pratik Gautam


The carcinoma of the cervix is the second most common cancer amongst women around the world, with its higher occurrence in developing nations. Solid clinical and experimental evidence showed that the high-risk (HR) types of human papilloma virus (HPV) assume a focal part in bringing about cervical cancer. It is generally acknowledged that the development of intrusive cervical cancer from intraepithelial neoplasia (cervical intraepithelial neoplasia [CIN] 1-2/3) includes molecular changes and in this manner is a preventable if identified and treated early. In the pathogenesis of cervical carcinoma there are three noteworthy segments, two of them identified with the role of human papillomaviruses (HPV). First, the impact of viral E6 and E7 proteins. Second, the reconciliation of viral DNA in chromosomal region. Some of these viral incorporations occur intermittently at particular chromosomal regions, for example, 8q24 and, both harboring HPV18 and HPV16. Also, thirdly, there are other intermittent genetic modifications which are not connected to HPV. Recurrent losses of heterogeneity (LOH) have been distinguished in chromosome regions 3p14–22, 4p16, 5p15, 6p21–22, 11q23, 17p13.3 without impact on p53,18q12–22 and 19q13, every one of them proposing the genetic alteration of tumor suppressor genes not yet recognized. Intermittent amplification has been mapped to 3q+ arm, with the common region in 3q24–28 in 90% of invasive carcinomas. The development of cervical carcinoma requires the successive recurrence and selection of a few genetic alterations. The distinguishing proof of the particular genes involved, and their connection with particular cancer properties and stages could enhance the comprehension and perhaps the management of cervical carcinoma.In this way, a top to bottom comprehension of the apoptotic genes that control molecular mechanism in cervical cancer are of critical significance. Valuable targets for therapeutic treatment would be those that adjust apoptotic pathways in a way where the departure of HPV from reconnaissance by the host immune system is avoided. Such a methodology coordinated at the apoptotic genes may be helpful in the treatment of cervical carcinoma.

Keywords: cervical carcinoma; genetic damage; papillomavirus; viral integration; LOH.

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