癌症
癌癥
암증
CHINESE JOURNAL OF CANCER
2001年
5期
468-473
,共6页
贺修胜%苏琦%陈主初%贺修桃%车世友
賀脩勝%囌琦%陳主初%賀脩桃%車世友
하수성%소기%진주초%하수도%차세우
胃肿瘤%不典型增生%p16/MTS1/CDK4Ⅰ/CDKN2基因%突变%缺失%表达
胃腫瘤%不典型增生%p16/MTS1/CDK4Ⅰ/CDKN2基因%突變%缺失%錶達
위종류%불전형증생%p16/MTS1/CDK4Ⅰ/CDKN2기인%돌변%결실%표체
目的:研究 p16基因表达与胃癌发生发展、侵袭、转移的关系及 p16基因外显子 2缺失、突变在胃癌发生中的地位。方法:运用链霉菌抗生物素蛋白 -过氧化酶 (S-P)免疫组织化学方法检测胃癌及癌前病变组织中 p16蛋白的表达;采用聚合酶链反应 (PCR) 、聚合酶链反应 -单链构象多态性 (PCR-SSCP)分析方法检测胃癌中 p16基因外显子 2的缺失、突变。结果: (1)p16蛋白表达阳性率:①正常胃粘膜 96.25% (77/ 80),不典型增生 92.00% (45/ 50),胃癌 47.54% (58/ 122),胃癌组中 p16蛋白表达低于正常胃粘膜及不典型增生( P<0.05);②粘液腺癌 (10.00%, 1/ 10)低于低分化腺癌 (51.22%, 21/ 41)、未分化癌 (57.69%, 15/ 26)和印戒细胞癌 (62.50%, 10/ 16) ( P< 0.05);③ 30例原发癌和淋巴结转移癌配对标本中 p16蛋白表达阳性率:原发癌 46.67%( 14/30),淋巴结转移癌 16.67% (5/ 30),淋巴结转移癌低于原发癌 (P< 0.05); (2)p16基因缺失与突变分析: 25例胃癌中检测出缺失 5例 ,但未发现突变。结论:① p16蛋白表达缺失与胃癌的发生、组织学类型及淋巴结转移有关。② p16基因外显子 2缺失可能与胃癌发生有关 ;而 p16基因突变可能与胃癌发生无关。
目的:研究 p16基因錶達與胃癌髮生髮展、侵襲、轉移的關繫及 p16基因外顯子 2缺失、突變在胃癌髮生中的地位。方法:運用鏈黴菌抗生物素蛋白 -過氧化酶 (S-P)免疫組織化學方法檢測胃癌及癌前病變組織中 p16蛋白的錶達;採用聚閤酶鏈反應 (PCR) 、聚閤酶鏈反應 -單鏈構象多態性 (PCR-SSCP)分析方法檢測胃癌中 p16基因外顯子 2的缺失、突變。結果: (1)p16蛋白錶達暘性率:①正常胃粘膜 96.25% (77/ 80),不典型增生 92.00% (45/ 50),胃癌 47.54% (58/ 122),胃癌組中 p16蛋白錶達低于正常胃粘膜及不典型增生( P<0.05);②粘液腺癌 (10.00%, 1/ 10)低于低分化腺癌 (51.22%, 21/ 41)、未分化癌 (57.69%, 15/ 26)和印戒細胞癌 (62.50%, 10/ 16) ( P< 0.05);③ 30例原髮癌和淋巴結轉移癌配對標本中 p16蛋白錶達暘性率:原髮癌 46.67%( 14/30),淋巴結轉移癌 16.67% (5/ 30),淋巴結轉移癌低于原髮癌 (P< 0.05); (2)p16基因缺失與突變分析: 25例胃癌中檢測齣缺失 5例 ,但未髮現突變。結論:① p16蛋白錶達缺失與胃癌的髮生、組織學類型及淋巴結轉移有關。② p16基因外顯子 2缺失可能與胃癌髮生有關 ;而 p16基因突變可能與胃癌髮生無關。
목적:연구 p16기인표체여위암발생발전、침습、전이적관계급 p16기인외현자 2결실、돌변재위암발생중적지위。방법:운용련매균항생물소단백 -과양화매 (S-P)면역조직화학방법검측위암급암전병변조직중 p16단백적표체;채용취합매련반응 (PCR) 、취합매련반응 -단련구상다태성 (PCR-SSCP)분석방법검측위암중 p16기인외현자 2적결실、돌변。결과: (1)p16단백표체양성솔:①정상위점막 96.25% (77/ 80),불전형증생 92.00% (45/ 50),위암 47.54% (58/ 122),위암조중 p16단백표체저우정상위점막급불전형증생( P<0.05);②점액선암 (10.00%, 1/ 10)저우저분화선암 (51.22%, 21/ 41)、미분화암 (57.69%, 15/ 26)화인계세포암 (62.50%, 10/ 16) ( P< 0.05);③ 30례원발암화림파결전이암배대표본중 p16단백표체양성솔:원발암 46.67%( 14/30),림파결전이암 16.67% (5/ 30),림파결전이암저우원발암 (P< 0.05); (2)p16기인결실여돌변분석: 25례위암중검측출결실 5례 ,단미발현돌변。결론:① p16단백표체결실여위암적발생、조직학류형급림파결전이유관。② p16기인외현자 2결실가능여위암발생유관 ;이 p16기인돌변가능여위암발생무관。
Objective: This study was designed to investigate the relationship between p16 protein expression and gastric carcinogenesis,depth of invasion, lymph node metastasis, and evaluate the role of deletion and mutation of p16 gene in exon 2 in gastric carcinoma. Methods: p16 protein expression in gastric carcinoma and precancerous lesion was examined by streptavidin-peroxidase conjugated(S-P) method; The deletion and mutation of p16 gene were examined respectively by polymerase chain reaction(PCR) and polymerase chain reaction single-strand conformation polymorphism analysis(PCR-SSCP) in gastric carcinoma. Results: ① The positive rates of p16 protein expression were 96.25% (77/80) in normal gastric mucosa, 92.00% (45/50) in dysplastic gastric mucosa, and 47.54% (58/122) in gastric carcinoma. The positive rate of p16 protein expression in gastric carcinoma was significantly lower than that in normal gastric mucosa and in dysplastic gastric mucosa (P<0.05). ② The positive rate of p16 protein expression in mucoid carcinoma (10.00% ,1/10) was significantly lower than that of poorly differentiated carcinoma (51.22% ,21/41), undifferentiated carcinoma (57.69% ,15/26), and signet ring cell carcinoma (62.50% ,10/16) (P< 0.05). ③ The positive rates of p16 protein in 30 cases paired primary and lymph node metastatic gastric carcinoma were 46.67 % (14/30) in primary gastric carcinoma,16.67% (5/30) in lymph node metastatic gastric carcinoma. The positive rate of lymph node metastatic carcinoma was significantly lower than that of primary carcinoma(P<0.05). ④ Evaluation of mutation and deletion of p16 gene: There was no mutation of p16 gene in exon 2, but there were 5 cases displayed deletion of p16 gene in exon 2 in the 25 primary gastric carcinoma. Conclusions: ① The expression loss of p16 protein is related to carcinogenesis, histopathological subtypes,and lymph metastasis of gastric carcinoma. ② The mutation of p16 gene in exon 2 may not be involved in gastric carcinogenesis. But the deletion of p16 gene in exon 2 might be involved in gastric carcinogenesis.