血管内皮生长因子及其受体KDR在疣状胃炎及胃癌组织中的表达及意义

Expression of vascular endothelial growth factor and its receptor KDR in verrucose gastritis and gastric cancer

目的:研究血管内皮生长因子(vascularendothelial growth factor,VEGF)及其受体2(kinase insert domain-containing receptor,KDR)在疣状胃炎(verrucose gastritis,VG)与胃癌中的表达的关系.方法:用免疫组织化学方法检测30例慢性浅表性胃炎、80例VG和30例胃癌组织中VEGF和KDR的表达;通过13C呼气试验判断所有入组患者有无幽门螺旋杆菌(Helicobacter pylori,H.pylori)感染.结果:VG、胃癌患者的H.pylori感染率显著高于慢性浅表性胃炎患者(2=26.4,29.697;P<0.01),而两者之间比较差异无统计学意义(2=2.229,P>0.05).VG和胃癌组织中VEGF和KDR的表达与慢性浅表性胃炎组比较差异有统计学意义(2=20.008,29.697;15.428,24.300,P<0.01);VEGF和KDR在疣状胃炎及胃癌组织中的表达差异无统计学(2=3.461,3.793;P>0.05);成熟型的疣状胃炎组织中VEGF和KDR的表达与非成熟型的疣状胃炎比较差异有统计学意义(2=6.084,10.026;P<0.05),而与胃癌组织比较差异无统计学意义(2=0.728,0.080;P>0.05);H.pylori+的疣状胃炎组织中VEGF和KDR的表达与H.pylori-的疣状胃炎组比较差异有统计学意义(2=5.637,5.398;P<0.05),而与胃癌组织比较差异无统计学意义(2=0.839,1.006;P>0.05).结论:H.pylori参与了VG的形成过程.VEGF和KDR在疣状胃炎中的表达与在胃癌中的表达相似,提示VG与胃癌之间可能存在相关性,VEGF和KDR可能参与了疣状胃炎癌变的过程.VEGF和KDR在成熟型和H.pylori+的疣状胃炎中的高表达提示成熟型的VG和H.pylori感染可能存在增加VG癌变的风险.

AIM： To investigate the relationship between verrucose gastritis and gastric cancer. METHODS： The expression of vascular endo- thelial growth factor （VEGF） and kinase insert domain-containing receptor （KDR） in chronic superficial gastritis, verrucose gastritis and gas- tric cancer was detected by immunohistochem- istry. Helicobacter pylori （H. pylori） infection was detected by the 13C breath test. RESULTS： The rates of H. pylori infection in patients with verrucose gastritis and gastric can- cer were both higher than that in patients with chronic superficial gastritis （X2 = 26.4, 29.697, both P 〈 0.01）, but there was no significant dif-ference in the rate of H. pylori infection between patients with verrucose gastritis and those with gastric cancer （X2 =2.229, P 〉 0.05）. The positive rates of VEGF and KDR expression in verrucose gastritis and gastric cancer were significantly higher than those in chronic superficial gastritis （X2 = 20.008, 29.697; 15.428, 24.300, all P 〈 0.01）, but there were no significant differences in the positive rates of VEGF and KDR expression be- tween verrucose gastritis and gastric cancer （X2 = 3.461, 3.793, both P 〉 0.05）. The positive rates of VEGF and KDR expression in mature verrucose gastritis were significantly higher than those in non-mature verrucose gastritis （X2=6.084, 10.026, both P 〈 0.05）, but there were no signifi- cant differences between matured verrucose gas- tritis and gastric cancer （X2 = 0.728, 0.080, both P 〉 0.05）. The positive rates of VEGF and KDR ex- pression were significantly higher in verrucose gastritis patients with H. pylori infection than in those without H. pylori infection （X2 = 5.637, 5.398, both P 〈 0.05）, but there were no significant dif- ferences between verrucose gastritis patients with H. pylori infection and patients with gastric cancer （X2 = 0.839, 1.006, both P 〉 0.05）. CONCLUSION： H. pylori infection is involved in the formation of verrucous gastritis. Expression of VEGF and KDR in verrucose gastritis is simi- lar to that in gastric cancer, suggesting that both VEGF and KDR may be involved in the evolu- tion of verrucose gastritis to gastric cancer. The observation that expression of VEGF and KDR in mature verrucose gastritis and patients with H. pylori infection was higher may imply that mature verrucose gastritis and H. pylori infection increase the risk of malignant transformation of verrucose gastritis.