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Download Human Cancer Viruses: Principles of Transformation and by John Nicholas, Kuan-Teh Jeang, T. C. Wu PDF

By John Nicholas, Kuan-Teh Jeang, T. C. Wu

The 1st identity of a tumor-causing virus, Rous sarcoma virus, happened nearly a hundred years in the past, however it used to be now not till the Nineteen Seventies that the genetic foundation for oncogenesis by way of this and different acutely reworking retroviruses used to be preferred. considering the fact that then, a variety of viral oncogenes and their corresponding mobile proto-oncogene opposite numbers were pointed out, and those experiences have contributed a lot to our figuring out of crucially very important features of cellphone biology and transformation. This booklet offers an updated evaluation of the 6 significant viruses that reason human cancers - HPV, HBV, HCV, EBV, KSHV and HTLV-1 - with admire to their molecular biology and epidemiology and to scientific facets of disorder, treatment and prevention.Contributed via over a dozen across the world popular scientists, the chapters are comprehensively written and illustrated. This ebook is acceptable for complicated scholars, postdoctoral researchers, scientists and clinicians who desire to comprehend the mechanisms resulting in mobile transformation and oncogenesis by means of those viruses as a foundation for the advance of particular healing and antiviral remedies.

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Additional resources for Human Cancer Viruses: Principles of Transformation and Pathogenesis (Translational Research in Biomedicine)

Sample text

By contrast, primary invasion of the more differentiated, surface cells of the epithelium is less favorable for viral maintenance and CIN progression because as these cells further differentiate, they are eventually shed from the host, leading to loss of viral DNA [11]. Therefore, in summary the transition from initial HPV entrance into the epithelium to the development of CIN is an improbable event that is potentially influenced by the host immune response to the virus as well as the differentiation status of the primary infected cells.

The loss of these oncoproteins triggers apoptosis or senescence of cervical cancer cells. Importantly, E6 associates with and promotes the degradation of the tumor suppressor protein p53 [9], while E7 inhibits the activity of the retinoblastoma protein (Rb) [10]. The decrease in levels of p53 renders cells incapable of undergoing growth arrest or apoptosis in response to DNA damage, and the loss of Rb abolishes the cell cycle checkpoint at G1. Thus, in combination these events create a cellular environment that promotes the development of a cancerous phenotype.

HPVs are commonly classified into genera based on their evolutionary origin, with the ␣- and ␤-papillomaviruses comprising the vast majority (about 90%) of currently identified HPV types. These viruses cause lesions at different epithelial sites. ␤-Papillomaviruses are both less common and not as likely to cause human disease compared to the ␣-genera. ␤-Papillomaviruses cause cutaneous infections which are typically clinically inapparent except in immunocompromised patients [2, 3]. g. HPV-2) are also cutaneous viruses and as such do not represent a great health threat to the patient [4].

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