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目的 探讨溃疡性结肠炎相关性大肠癌组织中P53、K-ras及hMSH2蛋白表达。方法 以溃疡性结肠炎伴不典型增生(UD)和溃疡性结肠炎相关性大肠癌 (UCACRC)组织为实验组,溃疡性结肠炎(UC)和散发性大肠癌 (SCRC)组织为对照组,应用免疫组化法检测组织中P53、K-ras、hMSH2蛋白的表达状况;聚合酶链式反应 单链构象多态性分析法 (PCR SSCP)检测组织中的微卫星不稳定性(MSI)状态(6个位点),并进行统计学分析。结果 P53蛋白过表达的阳性率在UC(1 /25例)与UD(3 /7例)组间,UC与UCACRC(4 /8例)组间差异均有统计学意义(P<0. 05,P<0. 01),UCACRC与SCRC(17 /30例)组间差异无统计学意义(P>0. 05);突变型K ras表达的阳性率在UC(4 /25例)与UD(4 /7例)组间,UC与UCACRC(7 /8例)组间差异均有统计学意义(P<0. 05,P<0. 01),UCACRC与SCRC(24 /30例)组间差异无统计学意义(P>0. 05);hMSH2蛋白缺失率在UC(2 /25例)与UD(0 /7例)组间、UD与UCACRC(4 /8例)组间、UCACRC与SCRC(13 /30例)组间差异均无统计学意义 (P>0. 05)。MSI阳性率在UC(0 /25例)与UD(3 /7例)组间差异有统计学意义(P<0. 01),在UD与UCACRC(2 /8例)组间、UCACRC与SCRC(7 /30例)组间差异无统计学意义(P>0. 05)。结论 P53、K ras基因突变、MSI在UCACRC的发生发展过程中可能是
Objective To investigate the expression of P53, K-ras and hMSH2 protein in colorectal carcinoma associated with ulcerative colitis. Methods The ulcerative colitis with atypical hyperplasia (UD) and ulcerative colitis-associated colorectal cancer (UCACRC) tissues were used as the experimental group, ulcerative colitis (UC) and sporadic colorectal cancer (SCRC) The expression of P53, K-ras and hMSH2 in tissues was detected by immunohistochemistry. Microsatellite instability (MSI) in tissues was detected by polymerase chain reaction single strand conformation polymorphism (PCR SSCP) (6 sites), and statistical analysis. Results The positive rate of P53 protein overexpression was between UC (1/25 cases) and UD (3/7 cases), and the difference between UC and UCACRC (4/8 cases) was statistically significant (P <0.05 , P <0.01). There was no significant difference between UCACRC and SCRC (17/30) patients (P> 0.05). The positive rate of K ras expression in UC (4/25 cases) There were significant differences between UC and UCACRC (7 of 8 cases) (P <0.05, P <0.01), UCACRC and SCRC (24/30 cases) There was no significant difference between the two groups (P> 0.05). The rate of deletion of hMSH2 protein was significantly higher in UC patients (2/25 cases) and UD (0/7 cases), between UD and UCACRC (4/8 cases) And SCRC (13/30 cases), there was no significant difference between the two groups (P> 0.05). The positive rates of MSI between UC (0/25 cases) and UD (3/7 cases) were statistically significant (P <0.01). Between UD and UCACRC (2/8 cases) (7/30 cases) between the two groups showed no significant difference (P> 0.05). Conclusion The mutation of P53 and K ras genes and MSI may be the occurrence and development of UCACRC