The Relationship between Microvessel Count and the Expression of Vascular Endothelial Growth Factor, p53, and K-ras in Non-Small Cell Lung Cancer.
10.3346/jkms.2001.16.4.417
- Author:
Yu Ho KANG
1
;
Kyu Sik KIM
;
Young Kwon YU
;
Sung Chul LIM
;
Young Chul KIM
;
Kyung Ok PARK
Author Information
1. Department of Internal Medicine, Chonnam National University Medical School, Research Institute of Medical Science, Kwangju, Korea. kyc0923@chonnam.ac.kr
- Publication Type:Original Article
- Keywords:
Vascular Endothelial Growth Factor;
K-ras;
Protein p53;
Carcinoma, Non-Small-Cell Lung
- MeSH:
Adult;
Aged;
Carcinoma, Non-Small-Cell Lung/*blood supply/chemistry/mortality;
Endothelial Growth Factors/*analysis;
Female;
Human;
Lung Neoplasms/*blood supply/chemistry/mortality;
Lymphokines/*analysis;
Male;
Middle Age;
Neovascularization, Pathologic/*metabolism;
Protein p53/*analysis;
Survival Rate;
ras Proteins/*analysis
- From:Journal of Korean Medical Science
2001;16(4):417-423
- CountryRepublic of Korea
- Language:English
-
Abstract:
Using immunohistochemical staining, we studied the relationship between the microvessel count (MC) and the expression of K-ras, mutant p53 protein, and vascular endothelial growth factor (VEGF) in 61 surgically resected non-small cell lung cancers (NSCLC) (42 squamous cell carcinoma, 14 adenocarcinoma, 2 large cell carcinoma, 2 adenosquamous carcinoma, and 1 mucoepidermoid carcinoma). MC of the tumors with lymph node (LN) metastasis was significantly higher than that of tumors without LN metastasis (66.1+/-23.1 vs. 33.8+/-13.1, p<0.05). VEGF was positive in 54 patients (88.5%). MC was 58.1+/-25.2 (mean+/-S.D.) in a x200 field, and it was significantly higher in VEGF(+) tumors than in VEGF(-) tumors (61.4+/-23.7 vs. 32.9+/-23.8, p<0.05). VEGF expression was higher in K-ras-positive or mutant p53-positive tumors than in negative tumors (p<0.05). MC was significantly higher in K-ras(+) tumors than in K-ras(-) tumors, although it did not differ according to the level of mutant p53 protein expression. Survival did not differ with VEGF, mutant p53, or K-ras expression, or the level of MC. In conclusion, there is a flow of molecular alterations from K-ras and p53, to VEGF expression, leading to angiogenesis and ultimately lymph node metastasis. Correlations between variables in close approximation and the lack of prognostic significance of individual molecular alterations suggest that tumorigenesis and metastasis are multifactorial processes.