Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1998-1-16
pubmed:abstractText
It has been reported that genes regulating apoptosis may play a role in tumoral angiogenesis. This study examined the relationship between tumour vascularization, a measure of tumour angiogenesis, and bcl-2 and p53 expression in operable non-small-cell lung cancer (NSCLC). The relationship between bcl-2, p53 and tumour vascularization and epidermal-growth-factor-receptor(EGFR) and c-erbB-2 expression was also studied. Tissue sections from resected tumour specimens of 107 NSCLC patients were evaluated immunohistochemically for vascular grade and bcl-2, p53, EGFR and c-erbB-2 expression. bcl-2 expression was found in 20/107 (19%) cases and was associated with squamous-cell histology (p = 0.03). A strong inverse relationship was found between bcl-2 expression and vascular grade (p = 0.005). All c-erbB-2-positive cases were negative for bcl-2 expression (p = 0.01). Overall no association was found between c-erbB-2 expression and vascular grade. However, in bcl-2-negative cases positive c-erbB-2 expression correlated with low angiogenesis (p = 0.05). No relationship was found between p53 and EGFR expression and bcl-2, c-erbB-2 or vascular grade. The improved prognosis reported in bcl-2-positive NSCLC may be related to low tumour vascularization. The results suggest that the anti-apoptotic gene bcl-2 plays a role in regulating tumour angiogenesis. Since normal lung epithelium expresses bcl-2, a sequence of tumour progression involving loss of bcl-2, then activation of c-erbB-2 or increase in tumour vascularization is proposed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0020-7136
pubmed:author
pubmed:issnType
Print
pubmed:day
19
pubmed:volume
74
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
565-70
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9421349-Aged, pubmed-meshheading:9421349-Analysis of Variance, pubmed-meshheading:9421349-Carcinoma, Non-Small-Cell Lung, pubmed-meshheading:9421349-Female, pubmed-meshheading:9421349-Gene Expression, pubmed-meshheading:9421349-Genes, Tumor Suppressor, pubmed-meshheading:9421349-Genes, bcl-2, pubmed-meshheading:9421349-Genes, p53, pubmed-meshheading:9421349-Humans, pubmed-meshheading:9421349-Lung Neoplasms, pubmed-meshheading:9421349-Male, pubmed-meshheading:9421349-Middle Aged, pubmed-meshheading:9421349-Neovascularization, Pathologic, pubmed-meshheading:9421349-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:9421349-Receptor, Epidermal Growth Factor, pubmed-meshheading:9421349-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:9421349-Retrospective Studies, pubmed-meshheading:9421349-Survival Analysis, pubmed-meshheading:9421349-Tumor Suppressor Protein p53
pubmed:year
1997
pubmed:articleTitle
Potential role of bcl-2 as a suppressor of tumour angiogenesis in non-small-cell lung cancer.
pubmed:affiliation
ICRF Medical Oncology Unit, Radcliffe Hospital, Oxford, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't