Linked Life Data

20455851

Source:http://linkedlifedata.com/resource/pubmed/id/20455851

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-5-18
pubmed:abstractText
Melanoma causes a considerable public health burden because of its dramatic rise in incidence worldwide since the mid-1960s and because the metastatic disease remains incurable, has a short median survival and is characterized by resistance to almost all classes of cytotoxic agents. DNA repair pathways are multiple and are able to repair, usually in an error-free manner, all kinds of DNA damage induced by exogenous and endogenous genotoxic agents. This review describes the role of DNA repair process in protecting us from cancer and particularly nucleotide excision deficiencies that are associated with melanoma development. Resistance of tumoral cells to antitumoral regimen can be caused by overexpression of DNA repair processes. We showed that melanoma metastasis was associated with higher expression of some DNA repair pathways leading to a better surveillance of replication fork fidelity. We showed a partially coordinated regulation of these repair genes. P53 and several transcription factors may regulate numerous of these repair genes. The repair pathways that are overexpressed in metastatic melanoma are those particularly efficient in repairing the major DNA damage produced by cytotoxic treatments. This implies that better analysis of DNA repair regulation is necessary to identify novel therapeutic targets and to allow clinicians to propose tailored therapies.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1875-5666
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
413-8
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
DNA repair pathways and human metastatic malignant melanoma.
pubmed:affiliation
Laboratory Genomes and Cancers, Centre National de la Recherche Scientifique FRE2939, Institut Gustave Roussy, University Paris-Sud, France. sarasin@igr.fr
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't