Viral hit and run-oncogenesis: Genetic and epigenetic scenarios

Niller, Hans Helmut and Wolf, Hans and Minarovits, Janos (2011) Viral hit and run-oncogenesis: Genetic and epigenetic scenarios. CANCER LETTERS, 305 (2). pp. 200-217. ISSN 0304-3835, 1872-7980

Full text not available from this repository. (Request a copy)

Abstract

It is well documented that viral genomes either inserted into the cellular DNA or coreplicating with it in episomal form can be lost from neoplastic cells. Therefore, "hit and run"-mechanisms have been a topic of longstanding interest in tumor virology. The basic idea is that the transient acquisition of a complete or incomplete viral genome may be sufficient to induce malignant conversion of host cells in vivo, resulting in neoplastic development. After eliciting a heritable change in the gene expression pattern of the host cell (initiation), the genomes of tumor viruses may be completely lost, i.e. in a hit and run-scenario they are not necessary for the maintenance of the malignant state. The expression of viral oncoproteins and RNAs may interfere not only with regulators of cell proliferation, but also with DNA repair mechanisms. DNA recombinogenic activities induced by tumor viruses or activated by other mechanisms may contribute to the secondary loss of viral genomes from neoplastic cells. Viral oncoproteins can also cause epigenetic dysregulation, thereby reprogramming cellular gene expression in a heritable manner. Thus, we expect that epigenetic scenarios of viral hit and run-tumorigenesis may facilitate new, innovative experiments and clinical studies in spite of the fact that the regular presence of a suspected human tumor virus in an early phase of neoplastic development and its subsequent regular loss have not been demonstrated yet. We propose that virus-specific "epigenetic signatures", i.e. alterations of the host cell epigenome, especially altered DNA methylation patterns, may help to identify viral hit and run-oncogenic events, even after the complete loss of tumor viruses from neoplastic cells. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

Item Type: Article
Uncontrolled Keywords: EPSTEIN-BARR-VIRUS; MERKEL CELL POLYOMAVIRUS; RECOMBINATION-ACTIVATING GENES; BURKITTS-LYMPHOMA CELLS; HERPES-SIMPLEX-VIRUS; ENCODED LATENT MEMBRANE-PROTEIN-1; NASOPHARYNGEAL CARCINOMA-CELLS; CLASSICAL HODGKINS-DISEASE; INDUCED CYTIDINE DEAMINASE; HUMAN TUMOR-CELLS; Epstein-Barr virus; Tumor virus; Recombination; Chromatin; DNA-methylation; Transformation; Tumor suppressor gene
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Medizinische Mikrobiologie und Hygiene
Depositing User: Petra Gürster
Date Deposited: 30 Apr 2020 09:08
Last Modified: 30 Apr 2020 09:08
URI: https://pred.uni-regensburg.de/id/eprint/20646

Actions (login required)

View Item View Item