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

アクセス数 : 1265
ダウンロード数 : 128

今月のアクセス数 : 4
今月のダウンロード数 : 2
ファイル情報(添付)
HiroshimaJMedSci_57_73.pdf 1.3 MB 種類 : 全文
タイトル ( eng )
Role ofVascular Endothelial Growth Factor-C and -D mRNA in Breast Cancer
作成者
Teramoto Seiichi
Koseki Masato
収録物名
Hiroshima Journal of Medical Sciences
57
2
開始ページ 73
終了ページ 78
収録物識別子
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
抄録
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.
著者キーワード
Breast Cancer
VEGF-C
VEGF-D
NDC分類
医学 [ 490 ]
言語
英語
資源タイプ 紀要論文
出版者
Hiroshima University Medical Press
発行日 2008-06
権利情報
(c) Hiroshima University Medical Press.
出版タイプ Version of Record(出版社版。早期公開を含む)
アクセス権 オープンアクセス
収録物識別子
[ISSN] 0018-2052
[NCID] AA00664312