On the absence of mutations in nucleotide excision repair genes in sporadic solid tumors
Genet. mol. res. (Online)
;
7(1): 152-160, Jan. 2008. ilus, tab, graf
Article
in English
| LILACS
| ID: lil-553782
ABSTRACT
In general, stochastic tumors show genomic instability associated with the proliferation of DNA point mutations, that is, a mutator phenotype. This feature cannot be explained by a dysfunctional mismatch repair alone, and indicates that nucleotide excision repair (NER) and/or base excision repair should be suppressed. However, mutations in NER genes are not causally implicated in the oncogenesis of sporadic solid tumors, according to the Cancer Gene Census at http//www.sanger.ac.uk/genetics/CGP/Census/. This brings up an apparent paradox how to explain the recurrent non-existence in NER genes of somatic mutations causally related to cancer? In a recent study, we have shown that the origin of point mutations in cancer cell genomes can be explained by a structurally conserved NER with a functional disorder generated from its entanglement with a disabled apoptosis gene network. In the present study, we further characterize NER gene network properties and show that it has a highly connected architecture. This feature suggests that the absence of mutations in NER genes in sporadic solid tumors is a result of their participation in many essential cellular functions.
Full text:
Available
Index:
LILACS (Americas)
Main subject:
Point Mutation
/
DNA Repair
/
Gene Regulatory Networks
/
Neoplasms
Limits:
Humans
Language:
English
Journal:
Genet. mol. res. (Online)
Journal subject:
Molecular Biology
/
Genetics
Year:
2008
Type:
Article
Affiliation country:
Brazil
Institution/Affiliation country:
UNIPAMPA/BR
/
Universidade Federal do Rio Grande do Sul/BR
/
Universidade Luterana do Brasil/BR
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