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- W2166472125 endingPage "1162" @default.
- W2166472125 startingPage "1162" @default.
- W2166472125 abstract "Oncogenic transformation occurs via many different mechanisms. Alterations in the expression of certain key genes (oncogenes and/or tumor suppressor genes) contribute to the development of the tumorigenic state of uncontrolled cell proliferation. Tumor viruses' studies have contributed over the last 2 decades significantly in cancer etiology, first by providing valuable information on the mechanisms and dissection of cell signaling and growth control pathways and second by being causative agents of human neoplasia. Viruses contribute to the development of the neoplastic state through many mechanisms: inactivation of tumor suppressor genes, hyperstimulation of cellular proto-oncogene transcription, or by viral protein interference with the cellular transcription, signal transduction, DNA repair and apoptosis pathways and induction of chronic oxidative stress. On the other hand, only recently research has provided evidence of the epigenetic pathway involvement and especially the DNA methylation machinery. To this end, both hypomethylation-induced oncogenic activation and/or hypermethylation-induced tumor suppressor gene silencing are linked with viral-induced carcinogenesis. In this review, we discuss the current status of knowledge on viral-associated carcinogenesis with emphasis on the mechanisms of oxidative stress and DNA damage induction in humans by viruses as well as implications in cancer treatment." @default.
- W2166472125 created "2016-06-24" @default.
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- W2166472125 creator A5037398633 @default.
- W2166472125 creator A5044126331 @default.
- W2166472125 creator A5053902049 @default.
- W2166472125 date "2010-01-01" @default.
- W2166472125 modified "2023-10-18" @default.
- W2166472125 title "Viral-induced human carcinogenesis: an oxidative stress perspective" @default.
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