Vasohibin-1 in human breast carcinoma: A potential negative feedback regulator of angiogenesis

Vasohibin-1 in human breast carcinoma: A potential negative feedback regulator of angiogenesis
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DOI:
10.1111/j.1349-7006.2008.01015.x
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发表时间:
2009-01-01
期刊:
影响因子:
5.7
通讯作者:
Sasano, Hironobu
Sasano, Hironobu
中科院分区:
医学2区
文献类型:
--
作者:
Tamaki, Kentaro;Moriya, Takuya;Sasano, Hironobu

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Vasohibin-1是近年来发现的一种负反馈抑制因子,可抑制血管内皮生长因子-A诱导的血管生成。vasohibin-1在人乳腺癌中的状态尚未被检测。我们检查了151例乳腺标本,其中浸润性导管癌(IDC)98例,导管原位癌(DCIS)12例,纤维腺瘤(FA)16例,炎性病变6例,纤维囊性变9例,非病理性乳腺组织7例。我们免疫定位vasohibin-1,并比较其免疫反应VEGF-A,碱性成纤维细胞生长因子(bFGF),VEGF受体2(Flk-1),CD 31,CD 34和Ki-67/MIB-1。同时分析乳腺癌患者的总生存期(OS)和无病生存期(DFS)与血管抑素-1免疫反应性的关系。此外,我们评估了Ki-67和CD 31以及Ki-67和vasohibin-1双重免疫染色,以进一步表征新血管形成。Vasohibin-1在乳腺癌组织中表达,在IDC和炎性病变中表达强度明显高于其他类型(P < 0.001)。此外,Vasohibin-1与VEGF-A、bFGF、Flk-1之间均呈显著正相关(P < 0.001)。VAS-1与OS呈正相关(P = 0.004),与DFS呈正相关(P
Vasohibin-1 is a recently identified negative feedback inhibitor or suppressor of angiogenesis induced by vascular endothelial growth factor (VEGF)-A. The status of vasohibin-1 in human breast carcinoma has not been examined. We examined 151 breast specimens including 98 cases of invasive ductal carcinoma (IDC), 12 of ductal carcinoma in situ (DCIS), 16 of fibroadenoma (FA), six of inflammatory lesion, nine of fibrocystic change and seven of non-pathological breast tissue. We immunolocalized vasohibin-1 and compared its immunoreactivity to that of VEGF-A, basic fibroblastic growth factor (bFGF), VEGF receptor 2 (Flk-1), CD31, CD34 and Ki-67/MIB-1. The correlation of vasohibin-1 immunoreactivity with overall survival (OS), and disease-free survival (DFS) of the patients with breast carcinoma was also evaluated. In addition, we evaluated Ki-67 and CD31, and Ki-67 and vasohibin-1 double-immunostaining for further characterization of neovascularization. Vasohibin-1 was detected in endothelial cells of human breast and its immunodensity was significantly higher in IDC and inflammatory lesions than the other types (P < 0.001). In addition, a significant positive correlation was detected between vasohibin-1 and VEGF-A, bFGF or Flk-1 (P < 0.001). There was also positive associations between vasohibin-1 and OS (P = 0.004) and between vasohibin-1 and DFS (P