中国组织化学与细胞化学杂志
中國組織化學與細胞化學雜誌
중국조직화학여세포화학잡지
CHINESE JOURNAL OF HISTOCHEMISY AND CYTOCHEMISY
2014年
4期
325-330
,共6页
胃肿瘤%FAK%幽门螺杆菌%L 型
胃腫瘤%FAK%幽門螺桿菌%L 型
위종류%FAK%유문라간균%L 형
Gastric neoplasm%FAK%Helicobacter Pylori%L-form
目的:探讨局部黏着斑激酶(focal adhesion kinase ,FAK )在胃癌组织中的表达意义及与幽门螺杆菌 L 型(Heli-cobacter pylori-L ,Hp-L)感染的关系。方法(1)应用免疫组织化学 Elivision 法检测120例胃癌组织及40例切缘正常胃粘膜组织(对照组)中 FAK 蛋白的表达情况,采用免疫组织化学和革兰染色法检测 Hp-L 型的感染情况;(2)采用逆转录多聚酶链反应(RT-PCR)技术检测40例新鲜胃癌组织及对应切缘正常胃黏膜组织(对照组)中 FAK 的 mRNA 表达。结果胃癌组FAK 蛋白的表达阳性率高于对照组(P<0.05),且 FAK 的高表达与分化程度、浸润深度、淋巴结转移和 TNM 分期有关(P<0.05),与年龄、性别、肿瘤大小无关(P>0.05);RT-PCR 显示,肿瘤组织、远端正常对照组织的 FAK 表达量差异明显(P<0.01)。胃癌组 Hp-L 型检出率72.5%(87/120)与对照组37.5%(15/40)有显著性差异(P<0.05),与免疫组化 Hp-L 型抗原表达率65.0%(78/120)无显著性差异(P>0.05),Hp-L 检出阳性率为69.2%(83/120);胃癌组中 Hp-L 型感染阳性组的 FAK表达阳性率高于 Hp-L 型阴性组(P<0.05),且 Hp-L 型阳性率和 FAK 蛋白的表达呈正相关(r =0.291,P <0.05)。结论FAK 蛋白和 mRNA 在胃癌中的表达增加,且与胃癌的浸润、转移相关,其机制可能与幽门螺杆菌 L 型(Hp-L 型)感染有关。
目的:探討跼部黏著斑激酶(focal adhesion kinase ,FAK )在胃癌組織中的錶達意義及與幽門螺桿菌 L 型(Heli-cobacter pylori-L ,Hp-L)感染的關繫。方法(1)應用免疫組織化學 Elivision 法檢測120例胃癌組織及40例切緣正常胃粘膜組織(對照組)中 FAK 蛋白的錶達情況,採用免疫組織化學和革蘭染色法檢測 Hp-L 型的感染情況;(2)採用逆轉錄多聚酶鏈反應(RT-PCR)技術檢測40例新鮮胃癌組織及對應切緣正常胃黏膜組織(對照組)中 FAK 的 mRNA 錶達。結果胃癌組FAK 蛋白的錶達暘性率高于對照組(P<0.05),且 FAK 的高錶達與分化程度、浸潤深度、淋巴結轉移和 TNM 分期有關(P<0.05),與年齡、性彆、腫瘤大小無關(P>0.05);RT-PCR 顯示,腫瘤組織、遠耑正常對照組織的 FAK 錶達量差異明顯(P<0.01)。胃癌組 Hp-L 型檢齣率72.5%(87/120)與對照組37.5%(15/40)有顯著性差異(P<0.05),與免疫組化 Hp-L 型抗原錶達率65.0%(78/120)無顯著性差異(P>0.05),Hp-L 檢齣暘性率為69.2%(83/120);胃癌組中 Hp-L 型感染暘性組的 FAK錶達暘性率高于 Hp-L 型陰性組(P<0.05),且 Hp-L 型暘性率和 FAK 蛋白的錶達呈正相關(r =0.291,P <0.05)。結論FAK 蛋白和 mRNA 在胃癌中的錶達增加,且與胃癌的浸潤、轉移相關,其機製可能與幽門螺桿菌 L 型(Hp-L 型)感染有關。
목적:탐토국부점착반격매(focal adhesion kinase ,FAK )재위암조직중적표체의의급여유문라간균 L 형(Heli-cobacter pylori-L ,Hp-L)감염적관계。방법(1)응용면역조직화학 Elivision 법검측120례위암조직급40례절연정상위점막조직(대조조)중 FAK 단백적표체정황,채용면역조직화학화혁란염색법검측 Hp-L 형적감염정황;(2)채용역전록다취매련반응(RT-PCR)기술검측40례신선위암조직급대응절연정상위점막조직(대조조)중 FAK 적 mRNA 표체。결과위암조FAK 단백적표체양성솔고우대조조(P<0.05),차 FAK 적고표체여분화정도、침윤심도、림파결전이화 TNM 분기유관(P<0.05),여년령、성별、종류대소무관(P>0.05);RT-PCR 현시,종류조직、원단정상대조조직적 FAK 표체량차이명현(P<0.01)。위암조 Hp-L 형검출솔72.5%(87/120)여대조조37.5%(15/40)유현저성차이(P<0.05),여면역조화 Hp-L 형항원표체솔65.0%(78/120)무현저성차이(P>0.05),Hp-L 검출양성솔위69.2%(83/120);위암조중 Hp-L 형감염양성조적 FAK표체양성솔고우 Hp-L 형음성조(P<0.05),차 Hp-L 형양성솔화 FAK 단백적표체정정상관(r =0.291,P <0.05)。결론FAK 단백화 mRNA 재위암중적표체증가,차여위암적침윤、전이상관,기궤제가능여유문라간균 L 형(Hp-L 형)감염유관。
Objective To investigate the signifcance of focal adhesion kinase(FAK)expression in gas-tric carcinoma(GC)and its relationship with the Helicobacter pylori L-form (Hp-L) infection .Methods (1) Immunohistochemical staining was used to detect the expression of FAK protein in 120 samples of gastric cancer tissue and 40 normal gastric mucosa margin (control group) .Gram's and immunohistochemical stai-ning were used to detect the Hp-L infection .(2) The expression of FAK mRNA in 40 cases of fresh gas-tric cancer tissue and the normal gastric mucosa margin (control group) was detected by semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) .Results :The positive rate of FAK protein ex-pression in gastric carcinoma group was significantly higher than in the control group ( P < 0 .05) ,and FAK protein expression increased with differentiation , depth of invasion , lymph node metastasis and TNM stage (P < 0 .05) ,but not correlated with patients'sex ,age and tumor size (P > 0 .05) .RT-PCR showed significant differences in the FAK expression between tumor and the distal normal control tissues (P< 0 .01) .The positive rate of the Hp-L form infection (72 .5% ) in gastric cancer was significantly high-er than that in the control group (37 .5% ) with Gram stain (P< 0 .05) .The antigen of Hp-L in 65 .0% ca-ses was detected by immunohistochemical techniques .There was no difference in the results between the two staining methods ( P> 0 .05) .The positive rate of the infection of Hp-L was 69 .2% (83/120) .In the gastric cancer group ,the expression of FAK was significantly higher in Hp-L infection positive cases than that in negative ones (r = 0 .291 ,P< 0 .05) .Conclusion The expression of FAK protein and mRNA in gas-tric cancer is increased and correlated with tumor's invasion and metastasis ,and the mechanism may be re-lated to Helicobacter pylori L-form infection .