摘要
目的:分析希佩尔-林道病(VHL)蛋白和血管内皮生长因子(VEGF)在家族性腺瘤性息肉病中的表达,并探讨其在腺瘤形成以及癌变过程中的可能作用机制。方法:收集我科2003年3月到2007年8月10例家族性腺瘤性息肉患者手术切除标本,分别取正常肠黏膜组织、≥1cm的腺瘤性息肉以及癌变腺瘤组织,采用SP法免疫组化方法检测VHL和VEGF在这些标本组织中的表达。结果:VHL阳性信号呈棕黄色主要表达于胞质内,VEGF阳性表达为棕黄色,主要表达于肿瘤细胞胞质。VHL在正常肠黏膜组织和≥1cm的腺瘤性息肉中的表达均较强,两者相差并不显著(χ2=2.4,P>0.05),但明显高于VHL基因在癌变腺瘤中的表达,差异具有统计学意义(χ2=7.2,P<0.05;χ2=14.4,P<0.05);VEGF在正常肠黏膜细胞、≥1cm的腺瘤性息肉到癌变腺瘤组织中阳性表达率不断升高,差异具有统计学意义(χ2=5.051,-P<0.05;χ2=11.52,P<0.05)。结论:VHL可能作为肿瘤抑制基因参与了家族性腺瘤性息肉的发展,VHL和VEGF血管内皮生长因子的异常表达与腺瘤到癌变的过程密切相关。
Objective: To analyze the expression of Von Hippel-Lindau (VHL) protein and vascular endothelial growth factor (VEGF) in patients with familial adenomatous polyposis (FAP) and discuss the possible mechanism of VHL protein and VEGF in adenoma formation and cancerization. Methods: The surgical resection specimens were obtained from 10 FAP patients from March 2003 to August 2007, the normal intestinal mucosa, ≥1 cm adenomas and cancerous adenomas were subjected to SP immunohistochemistry for analysis of the expression of VHI. protein and VEGF in these tissue samples. Results: VHL protein and VEGF was mainly detected in the cytoplasm of tumor cells. The expression of VHL protein in the normal intestinal mucosa was not different from that in ≥1 cm adenoma (P〉0. 05), but the VHL expression both in normal and in ≥1 cm adenoma tissue were higher than that in the cancerous adenoma cells (both P〈0.05). The positive expression rate of VEGF in the normal intestinal mucosa, ≥1 cm adenoma tissue and cancerous adenoma increased from low to high (P〈0.05). Conclusion: VHL may conduct as a tumor suppressor gene involved in the development of FAP, the abnormal expression of VHL protein and VEGF has closely related to the process of adenomatous cancerization.
出处
《武汉大学学报(医学版)》
CAS
北大核心
2009年第2期232-235,F0003,共5页
Medical Journal of Wuhan University