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目的定性和定量分析脆性组氨酸三联体基因蛋白(Fhit蛋白)在食管癌及癌前病变(不典型增生)组织中的表达,探讨Fhit蛋白与食管癌发生发展的关系。方法收集色素内镜初筛并经组织病理学证实标本94例,应用免疫组化及流式细胞术(FCM),定性及定量检测Fhit蛋白在食管癌变过程中的表达情况。结果①从食管鳞状上皮→不典型增生(癌前病变)→原位癌→浸润癌,随着食管病变的加重,定性及定量检测Fhit蛋白表达均呈逐渐降低趋势;②免疫组化结果显示:正常组、不典型增生Ⅰ级组、不典型增生Ⅱ级组、不典型增生Ⅲ级组、原位癌组、浸润癌组中Fhit蛋白表达分别为82.35%、75.00%、43.75%、35.29%、30.00%、33.33%;正常组与食管不典型增生Ⅰ级组Fhit蛋白表达差异无统计学意义(P>0.05),与其余各组相比差异有统计学意义(P<0.05);浸润癌组与正常组、不典型增生Ⅰ级组差异均有统计学意义(P<0.05),浸润癌组与不典型增生Ⅱ级、Ⅲ级组、原位癌组差异无统计学意义(P>0.05);③FCM结果显示:不典型增生Ⅰ级、Ⅱ级组间Fhit蛋白表达量差异有统计学意义(P<0.001),不典型增生Ⅱ级、Ⅲ级组间差异有统计学意义(P<0.05),不典型增生Ⅱ级与正常组间差异有统计学意义(P<0.001),不典型增生Ⅲ级与食管癌组间差异无统计学意义(P>0.05)。结论Fhit蛋白表达缺失是食管癌变过程的早期事件,随病理组织学分级的增高Fhit蛋白表达阳性率逐渐降低,其蛋白表达的缺失在食管癌发生、发展过程中可能起着重要作用。
Objective To qualitatively and quantitatively analyze the expression of Fhit protein in esophageal cancer and precancerous lesions (atypical hyperplasia) and to investigate the relationship between Fhit protein and the occurrence and development of esophageal cancer. Methods Collected 94 cases of primary endometrial pigment epithelial cells and confirmed by histopathology, the expression of Fhit protein in esophageal carcinogenesis was detected by immunohistochemistry and flow cytometry (FCM). Results ① The esophageal squamous epithelium → atypical hyperplasia (precancerous lesions) → carcinoma in situ → invasive carcinoma showed that the expression of Fhit protein decreased gradually with the increase of esophageal lesions. ② The results of immunohistochemistry The expression of Fhit protein in normal group, atypical hyperplasia grade Ⅰ group, atypical hyperplasia grade Ⅱ group, atypical hyperplasia grade Ⅲ group, in situ carcinoma group and invasive carcinoma group were 82.35%, 75.00%, 43.75%, 35.29% , 30.00% and 33.33%, respectively. There was no significant difference in Fhit protein expression between normal group and esophageal atypical hyperplasia grade Ⅰ group (P> 0.05), but there was significant difference compared with other groups (P <0.05) (P <0.05). There was no significant difference between invasive cancer group and atypical hyperplasia grade Ⅱ, Ⅲ group and carcinoma in situ (P> 0.05) ); ③FCM results showed that there was significant difference in Fhit protein expression between atypical hyperplasia level Ⅰ and Ⅱ (P <0.001), and between atypical hyperplasia level Ⅱ and Ⅲ (P <0.05) ), Atypical hyperplasia grade Ⅱ and normal group, the difference was statistically significant (P <0.001), dysplasia Ⅲ With esophageal cancer between groups was not statistically significant (P> 0.05) differences. Conclusions The loss of Fhit protein expression is an early event in the process of esophageal carcinogenesis. The positive expression rate of Fhit protein gradually decreases with the increasing of histological grade. The loss of protein expression may play an important role in the occurrence and development of esophageal carcinoma.