PTEN和VEGF的表达与膀胱癌血管生成关系的研究

目的研究膀胱癌组织中抑癌基因PTEN和血管内皮生长因子（VEGF）的表达与膀胱癌血管生成的关系。方法应用免疫组织化学S-P法检测62例膀胱癌组织和18例慢性膀胱炎组织（对照组）中PTEN和VEGF的表达，同时分析不同PTEN和VEGF表达状态下，膀胱癌组织微血管密度（MVD）的变化。结果膀胱癌组和对照组PTEN阳性率分别为53．2％（33／62）和100．0％（18／18），2组比较差异有统计学意义（P＜0．01）；膀胱癌组和对照组VEGF阳性率分别为62．9％（39／62）和27．8％（5／18），2组比较差异有统计学意义（P＜0．01）；PTEN和VEGF的表达呈负相关（r=-0．832，P＜0．01）。将膀胱癌分为4组，组A为PTEN阴性VEGF阳性（n=19），组B为PTEN阴性VEGF阴性（n=10），组C为PTEN阳性VEGF阳性（n=20），组D为PTEN阳性VEGF阴性（n=13）。4组平均MVD分别为41．53、31．40、26．55、25．15，组A显著高于其他3组（P＜0．05）。结论膀胱癌PTEN基因失活可能通过增加VEGF的表达来促进血管生成，导致肿瘤恶性进展。

Relationship between expression of PTEN and VEGF and angiogenesis in bladder cancer

Objective To study the relationship of expr ession of PTEN and vascular endothelial growth factor (VEGF) with angiogenesis i n bladder cancers. Methods Using immunohistochemical S- P method,the expression of PTEN and VEGF was examined in 62 bladder cancer sampl es and 18 chronic cystitis samples (control group);and the microvessel density ( MVD) was compared among different expression states of PTEN and VEGF in bladder cancer tissues. Results The positive rates of PTEN in bl adder cancer and control groups were 53.2% (33/62) and 100.0% (18/18),respective ly.The difference between the 2 groups was significant ( P< 0.01).The posi tive rates of VEGF in bladder cancer and control groups were 62.9%(39/62)and 2 7.8% (5/18),respectively.There was significant difference between the 2 groups ( P< 0.01).There was a negative correlation between PTEN and VEGF expressio n (r=-0.832, P< 0.01 ).The bladder cancer group was subdivided into 4 groups:PTEN-negative and VEGF-positive cases as group A (n=19),PTEN-negat ive and VEGF-negative cases as group B (n=10),PTEN-positive and VEGF-posi tive cases as group C (n=20),PTEN-positive and VEGF-negative cases as grou p D (n=13).The mean MVD of groups A,B,C and D was 41.53,31.40,26.55 and 25.1 5,respectively.The mean MVD of group A was significantly higher than those of ot her 3 groups (P<0.05). Conclusions Inactivation of P TEN gene in bladder cancer may promote angiogenesis through pathway of increase in VEGF expression, and thus induce tumor progression.