Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/37316
Title: Mechanisms of aneuploidy induction by RAS and RAF oncogenes
Authors: Pritchard, Catrin Ann
Kamata, Tamihiro
First Published: 30-Aug-2011
Publisher: e-Century Publishing
Citation: American Journal of Cancer Research, 2011, 1(7): pp. 955-971
Abstract: Most cancers progress with the accumulation of genetic mutations with time and this is frequently associated with the acquisition of genomic instability in the form of whole chromosome changes, chromosomal rearrangements, gene amplifications or smaller changes at the nucleotide level. Whole chromosome instability (W-CIN), characterised by aneuploidy, is a major form of genomic instability observed in human cancers and several lines of evidence now support the argument that W-CIN is a promoter of tumourigenesis rather than being a passenger event. The primary mechanism proposed for evolution of CIN is abnormalities in mitosis/cytokinesis. However, mutations in genes directly involved in controlling mitosis/cytokinesis are rare in human cancers and so the mechanisms underpinning the evolution of CIN in cancers are not currently clear. On the other hand, mutations in RAS or BRAF are frequently found in human cancers, many of which demonstrate CIN, suggesting a possible link between deregulated signaling through the RAS/RAF/MEK/ERK pathway and CIN. In this review, we focus on a potential relationship between deregulated RAS/RAF signaling and CIN, and discuss possible mechanisms connecting the two. (AJCR0000083).
ISSN: 2156-6976
Links: http://www.ajcr.us/ajcr0000083A.html
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3196290/
http://hdl.handle.net/2381/37316
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © 2011, e-Century Publishing. The file associated with this record is distributed under the Creative Commons “Attribution Non-Commercial No Derivatives” licence, further details of which can be found via the following link: http://creativecommons.org/licenses/by-nc-nd/4.0/
Appears in Collections:Published Articles, Dept. of Cancer Studies and Molecular Medicine

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