Linked Life Data

12807736

Source:http://linkedlifedata.com/resource/pubmed/id/12807736

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2003-8-6
pubmed:abstractText
Both chronic ulcerative colitis and smoking are associated with colorectal cancer in humans. In the present study, we investigated the effects of cigarette smoke (CS) exposure on inflammation-associated tumorigenesis in the mouse colon. Male balb/c mice were allocated into six groups: control, CS (2%), CS (4%), colitis, colitis + CS (2%) and colitis + CS (4%). They were given water or 3% dextran sulfate sodium (DSS) in drinking water for 7 days to induce colitis, with or without 1 h daily exposure to 2 or 4% CS. They were then allowed to drink water for 14 days. The cycle of 7 day DSS +/- CS/14 day H2O treatments were repeated twice. Mice were killed immediately or 1 month after the three cycles of treatments. Results indicated colonic adenoma was only found in the colitis group (one out of 11), Colitis + CS (2%) group (seven out of 12) and colitis + CS (4%) group (four out of five) 1 month after three cycles of DSS and/or CS treatment. CS exposure dose-dependently increased adenoma formation in mice with inflamed mucosa. CS exposure plus colitis was strongly associated with a high incidence of dysplasia (P < 0.01) and adenocarcinoma formation (P < 0.01) compared with induction of colitis alone. Colitis induced cell proliferation and apoptosis in colonic tissues. Cigarette smoking significantly attenuated the apoptotic effect by DSS probably via the induction of anti-apoptotic protein bcl-2. The ratio of apoptosis over proliferation was also significantly lower in the colitis + CS groups. Vascular endothelial growth factor and angiogenesis in the colon were also increased by cigarette smoking in animals with colitis. In conclusion, CS promotes inflammation-associated adenoma/adenocarcinoma formation in the mouse colon in a dose-dependent manner. This tumor development is associated with the inhibition of cellular apoptosis and supported by increased angiogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0143-3334
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1407-13
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12807736-Adenoma, pubmed-meshheading:12807736-Animals, pubmed-meshheading:12807736-Apoptosis, pubmed-meshheading:12807736-Blotting, Western, pubmed-meshheading:12807736-Cell Division, pubmed-meshheading:12807736-Cell Transformation, Neoplastic, pubmed-meshheading:12807736-Chronic Disease, pubmed-meshheading:12807736-Colitis, Ulcerative, pubmed-meshheading:12807736-Colonic Neoplasms, pubmed-meshheading:12807736-Dextran Sulfate, pubmed-meshheading:12807736-Endothelial Growth Factors, pubmed-meshheading:12807736-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:12807736-Lymphokines, pubmed-meshheading:12807736-Male, pubmed-meshheading:12807736-Mice, pubmed-meshheading:12807736-Mice, Inbred BALB C, pubmed-meshheading:12807736-Neovascularization, Pathologic, pubmed-meshheading:12807736-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:12807736-Smoking, pubmed-meshheading:12807736-Vascular Endothelial Growth Factor A, pubmed-meshheading:12807736-Vascular Endothelial Growth Factors
pubmed:year
2003
pubmed:articleTitle
Cigarette smoke exposure increases ulcerative colitis-associated colonic adenoma formation in mice.
pubmed:affiliation
Department of Pharmacology, Faculty of Medicine, The University of Hong Kong, Hong Kong, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't