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2 Viral Oncogene Hypothesis ; ..

Cancer cells escape normal growth control mechanisms as a consequence of activating mutations, or increased expression of one or more cellular protooncogenes, and/or inactivating mutations, or decreased expression of one or more tumor suppressor genes.

When a proto-oncogene is altered to become an oncogene, we speak of its beingACTIVATED.

Human adenoviruses are a group of small DNA viruses that commonly cause respiratory infections. Human adenoviruses have not been linked to any human cancer, but some serotypes, such as adenovirus types 2, 5, 12, 18, and 31, are capable of transforming rodent cells in culture and inducing tumors in hamsters or rats. Two viral oncogenes, E1A and E1B, have been identified as responsible for the adenovirus tumorigenicity and thus have served as useful tools for studying many important cellular processes in tumor biology [].

What are Proto-Oncogenes? - News Medical

76: 792, 1992), a gene with many relatives, including proto-oncogenes flg (FGF1) and bck (FGF2).

MICRO-RNA GENES ("gene silencers" -- no "household names" yet, but Fire and Melloreceived the 2006 Nobel Prize for discovering the phenomenon) do not code for proteins, but produceRNA's that bind to messenger RNA sequences of proto-oncogenes (Am.

RET is a proto-oncogene tyrosine kinase (Nature 363: 458, 1993; NEJM 335: 943, 1996), and was the first activatedoncogene that was discovered being passed from parent to child (Science 267: 381, 1995).

An oncovirus is a virus that can cause cancer

As we have noted, a proto-oncogene that has acquired the ability to cause cancer (i.e., has become an oncogene) is said to be ACTIVATED.

ESCs (Embryonic Stem Cells) are derived from the ICM (Inner Cell Mass) of the developing Blastocysts, multicellular structures originating from four (Human) to...

RNA splicing plays an important role in regulating viral oncogene expression and is highly conserved among tumor viruses. Through alternative RNA splicing, several species of mRNAs can be derived from a primary transcript of a single viral oncogene to encode different truncated proteins or different oncoproteins. Although various studies over the years have shown that the levels and status of individual cellular splicing factors in virus-infected cells modulate alternative splicing of viral oncogene transcripts, a clear picture of how this modulation might take place during viral oncogene expression has not yet emerged. Because viral RNA transcripts are not naked in the cells and the movement of different sets of RNA-binding proteins on and off a particular RNA molecule is dynamic, it will be very interesting to know how the selection of alternative splice sites in an RNA is precisely defined and triggered. In the case of an HPV16 or HPV18 E6E7 bicistronic transcript, retention of the first intron is needed to express E6, but splicing of this intron promotes E7 translation initiation to produce E7[]. What is required for the decision to splice this intron or not, resulting in the expression of two different oncoproteins from the same transcript, and when this decision occurs are intriguing questions. A recent finding of EGF pathway that might be involved in this regulation is fascinating []. Thus, investigation into these questions will not only help to resolve this puzzle in tumor virology, but will also shed some light on complex biology as a whole.

(Contrast the proto-oncogenes, which exert their effect when asingle copy is activated to an oncogene.)
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04/05/2000 · Original Article

148. Pichler K, Schneider G, Grassmann R. MicroRNA miR-146a and further oncogenesis-related cellular microRNAs are dysregulated in HTLV-1-transformed T lymphocytes. 2008;5:100

HIV-Associated Kaposi's Sarcoma with a High CD4 Count …

143. Hall AP, Irvine J, Blyth K. . Tumours derived from HTLV-I tax transgenic mice are characterized by enhanced levels of apoptosis and oncogene expression. 1998;186:209-214

Project DRIVE: A Compendium of Cancer Dependencies ..

Viral strategies for manipulating the expression of cellular genes to enhance viral persistence, viral latency, and survival of infected cells have provided numerous clues to the mechanisms of gene expression and their dysregulation during tumor development. These functions are mainly undertaken by virus-encoded oncogenes, which are present in virtually all well-characterized tumor viruses except the hepatitis C virus. The fact that all characterized viral oncoproteins are “sticky” and interact with cellular proteins in infected cells makes each of them multifunctional and essential for cell immortalization and transformation. By interacting with several dozens or even hundreds of cellular factors, viral oncoproteins from different tumor viruses eventually end up in apparently similar scenarios of viral carcinogenesis by targeting cellular tumor suppressors, deregulating signal transduction pathways, redirecting gene transcription, and/or stimulating anti-apoptotic programs in the host. In the past two decades, the study of cancer biology has been driven by the dynamic networking capacity of individual viral oncoproteins.

Diseases » NF-kB Transcription Factors | Boston University

Sometimes there are so manycopies that "double minute" chromosomes are formed from them Oncogenes were originally discovered in TRANSFORMING RETROVIRUSES ("the RNA tumor viruses").

Risk Factors for Lymphoma - Brandi Williamson Photography

Although much has been learned about the aberrant expression of cellular microRNAs in various tumor virus-induced cancers, the mechanism of this aberrant expression remains largely unknown. However, several exciting reports suggest that viral oncoproteins may play an important role in this aberrant regulation of cellular microRNA expression, including those oncogenic or tumor suppressive microRNAs.

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