Linked Life Data

12559770

Source:http://linkedlifedata.com/resource/pubmed/id/12559770

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-1-31
pubmed:abstractText
Chronic obstructive pulmonary disease (COPD) is caused mostly by cigarette smoking but its specific molecular mechanisms are obscure. Current theories suggest that the inflammation and oxidative stress induced by smoking lead to proteolytic imbalance and progressive lung structural derangement, with disease susceptibility being controlled by inherited variations in protective or inflammatory genes. However, cigarette smoke is directly mutagenic. Acquired somatic mutations, rather than inherited polymorphisms, might therefore be major determinants of COPD. Somatic mutations in oncogenes such as p53, Ras, EGFR and PTEN abound in the epithelium of smokers. These mutations are persistent, explaining the paradox that smoking cessation does not resolve inflammation. Moreover, the recognition that these somatic mutations converge on key inflammation, host defense and steroid response pathways might help to explain the clinical defects in these processes in COPD and guide discovery of future therapies.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0165-6147
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
71-6
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Acquired somatic mutations in the molecular pathogenesis of COPD.
pubmed:affiliation
Department of Pharmacology, Cooperative Research Center for Chronic Inflammatory Diseases, The University of Melbourne, Parkville, Australia. gpa@unimelb.edu.au
pubmed:publicationType
Journal Article, Review