Role ofVascular Endothelial Growth Factor-C and -D mRNA in Breast Cancer

アクセス数 : 1267
ダウンロード数 : 130

今月のアクセス数 : 1
今月のダウンロード数 : 2
File
HiroshimaJMedSci_57_73.pdf 1.3 MB 種類 : fulltext
Title ( eng )
Role ofVascular Endothelial Growth Factor-C and -D mRNA in Breast Cancer
Creator
Teramoto Seiichi
Koseki Masato
Source Title
Hiroshima Journal of Medical Sciences
Volume 57
Issue 2
Start Page 73
End Page 78
Journal Identifire
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
Abstract
Vascular endothelial growth factor (VEGF)-C and VEGF-D belong to the VEGF family, and are thought to be involved in lymphangiogenesis and angiogenesis. At present, this is the only known system that can induce lymphatic vessel growth in the body. However, the roles of VEGF-C and VEGF-D in breast cancer tissue have not been clarified. In the present study, we measured the mRNA expression of VEGF-C and VEGF-D in the breast cancer tissue of 109 patients by real-time polymerase chain reaction (RT-PCR). Between non-infiltrating breast cancer (n=6) and infiltrating breast cancer (n=l03), there were no significant differences in the mRNA expression of VEGF-C and VEGF-D. In infiltrating cancer, the expression of HER2 exhibited a positive correlation to VEGF-C and VEGF-D mRNA expression (p=0.027, p=0.048). However, mRNA expression ofVEGF-C and VEGF-D did not exhibit any significant correlation to lymphatic vessel invasion or lymph node metastasis. Among patients without lymph node metastasis, the mRNA expression of VEGF-C and VEGF-D for patients with lymphatic vessel invasion was significantly higher than that for patients without lymphatic vessel invasion (p=0.001, p=0.050). The results suggest that, in breast cancer, VEGF-C and VEGF-D are involved in lymphatic vessel invasion prior to lymph node metastasis, and their expression decreases after lymph node metastasis occurs.
Keywords
Breast Cancer
VEGF-C
VEGF-D
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type departmental bulletin paper
Publisher
Hiroshima University Medical Press
Date of Issued 2008-06
Rights
(c) Hiroshima University Medical Press.
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0018-2052
[NCID] AA00664312