Copy number loss or silencing of apoptosis-effector genes in cancer

Cancer cells undergo a variety of DNA copy number gains and losses (CNV), raising two important questions related to cancer development: (i) Which genes are affected? (ii) And how do CNVs, that do not represent complete deletions but do represent gene-dosage alterations, impact cancer cell functions...

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Bibliographic Details
Published in:Gene 2015-01, Vol.554 (1), p.50-57
Main Authors: Mauro, James A., Butler, Shanitra N., Ramsamooj, Michael, Blanck, George
Format: Article
Language:English
Subjects:
Apoptosis
Apoptosis-effector genes
Cell Proliferation
Chromatin - metabolism
Computational Biology
Copy number variation
COSMIC
Data Mining
DNA Copy Number Variations
ENCODE
Gene Dosage
Gene Expression Regulation, Neoplastic
Gene Silencing
Genome, Human
Humans
Mutation
Neoplasms - genetics
TCGA
Transcription Factors - metabolism
Tumor Suppressor Protein p53 - metabolism
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Summary:Cancer cells undergo a variety of DNA copy number gains and losses (CNV), raising two important questions related to cancer development: (i) Which genes are affected? (ii) And how do CNVs, that do not represent complete deletions but do represent gene-dosage alterations, impact cancer cell functions? Recent studies have indicated that CNVs in cancer can impact genes for regulatory proteins long known to be associated with cancer development, but less is understood about CNVs affecting effector genes. Also, we have recently indicated the likely importance of transcription factor binding site (TFBS) copies in effector genes, in regulating the transition from a proliferative to an apoptotic state. Here we report data-mining analyses that indicate that copies of apoptosis-effector genes are commonly lost in cancer development, in comparison to proliferation-effector genes, and when not, apoptosis effector genes have silenced chromatin structures.
ISSN:0378-1119
1879-0038
DOI:10.1016/j.gene.2014.10.021