辽宁医学院学报
遼寧醫學院學報
료녕의학원학보
JOURNAL OF LIAONING MEDICAL UNIVERSITY
2014年
4期
3-6
,共4页
胃癌%HP%TGF-β1%NF-κB
胃癌%HP%TGF-β1%NF-κB
위암%HP%TGF-β1%NF-κB
gastric cancer%HP%TGF-β1%NF-κB
目的:结合HP ( Helicobacter pylori)感染状态与临床病理资料进行统计学分析,研究TGF ( transforming grow factor,转化生长因子)-β1及NF-κB蛋白在胃癌标本中的表达情况,探讨HP感染状态对胃癌的发生发展的意义。方法应用组织学改良Giemsa染色检测113例胃癌组织和57例慢性胃炎组织HP感染,采用免疫组织化学的方法检测88例HP (+)和25例HP (-)的胃癌组织标本中TGF-β1及NF-κB蛋白的表达情况。结果在胃癌组中 HP阳性率为77.9%(88/113),在慢性胃炎组中HP阳性率为50.9%(29/57)。胃癌组织中的HP感染率明显高于慢性胃炎组(χ2=12.87, P<0.01)。胃癌组HP感染的临床病理学参数显示,胃癌患者的肿瘤部位、大小、远处转移、分化程度、有无淋巴结转移与HP感染无相关性(P>0.05),而与胃癌组织浸润深度有关。免疫组织化学结果显示, TGF-β1蛋白在HP (+)胃癌组织中的表达率(76.1%)明显高于HP (-)胃癌组织中的表达率(52.0%)。 NF-κB蛋白在HP (+)胃癌组织中的表达率(62.5%)明显高于HP (-)胃癌组织中的表达率(40.0%)。结论胃组织在HP感染后可能通过TGF-β1及NF-κB两条起重要作用的通路调节细胞基因转录及信号传导导致胃癌的发生、发展和浸润转移过程。
目的:結閤HP ( Helicobacter pylori)感染狀態與臨床病理資料進行統計學分析,研究TGF ( transforming grow factor,轉化生長因子)-β1及NF-κB蛋白在胃癌標本中的錶達情況,探討HP感染狀態對胃癌的髮生髮展的意義。方法應用組織學改良Giemsa染色檢測113例胃癌組織和57例慢性胃炎組織HP感染,採用免疫組織化學的方法檢測88例HP (+)和25例HP (-)的胃癌組織標本中TGF-β1及NF-κB蛋白的錶達情況。結果在胃癌組中 HP暘性率為77.9%(88/113),在慢性胃炎組中HP暘性率為50.9%(29/57)。胃癌組織中的HP感染率明顯高于慢性胃炎組(χ2=12.87, P<0.01)。胃癌組HP感染的臨床病理學參數顯示,胃癌患者的腫瘤部位、大小、遠處轉移、分化程度、有無淋巴結轉移與HP感染無相關性(P>0.05),而與胃癌組織浸潤深度有關。免疫組織化學結果顯示, TGF-β1蛋白在HP (+)胃癌組織中的錶達率(76.1%)明顯高于HP (-)胃癌組織中的錶達率(52.0%)。 NF-κB蛋白在HP (+)胃癌組織中的錶達率(62.5%)明顯高于HP (-)胃癌組織中的錶達率(40.0%)。結論胃組織在HP感染後可能通過TGF-β1及NF-κB兩條起重要作用的通路調節細胞基因轉錄及信號傳導導緻胃癌的髮生、髮展和浸潤轉移過程。
목적:결합HP ( Helicobacter pylori)감염상태여림상병리자료진행통계학분석,연구TGF ( transforming grow factor,전화생장인자)-β1급NF-κB단백재위암표본중적표체정황,탐토HP감염상태대위암적발생발전적의의。방법응용조직학개량Giemsa염색검측113례위암조직화57례만성위염조직HP감염,채용면역조직화학적방법검측88례HP (+)화25례HP (-)적위암조직표본중TGF-β1급NF-κB단백적표체정황。결과재위암조중 HP양성솔위77.9%(88/113),재만성위염조중HP양성솔위50.9%(29/57)。위암조직중적HP감염솔명현고우만성위염조(χ2=12.87, P<0.01)。위암조HP감염적림상병이학삼수현시,위암환자적종류부위、대소、원처전이、분화정도、유무림파결전이여HP감염무상관성(P>0.05),이여위암조직침윤심도유관。면역조직화학결과현시, TGF-β1단백재HP (+)위암조직중적표체솔(76.1%)명현고우HP (-)위암조직중적표체솔(52.0%)。 NF-κB단백재HP (+)위암조직중적표체솔(62.5%)명현고우HP (-)위암조직중적표체솔(40.0%)。결론위조직재HP감염후가능통과TGF-β1급NF-κB량조기중요작용적통로조절세포기인전록급신호전도도치위암적발생、발전화침윤전이과정。
Objective To explore the expression of TGF-β1 and NF-κB protein in gastric cancer tissues with HP infection and to find out the effect of HP on gastric cancer according to statistical analyses involving HP infection status and clinical pathology. Meth-ods Giemsa staining was used to detect HP infection of gastric cancer group (113 cases) and of chronic gastritis (57cases). Immu-nohistochemistry is used to detect expression of TGF-β1 and NF-κB protein in HP (+) group (88 cases) and HP (-) group (25 cases) . Results HP infection rate in chronic gastritis group was 50.9% ( 29/57 ) . HP infection rate in gastric cancer group was 77.9% (88/113), which is higher than that of the former (χ2=12.87, P<0.01) . The clinicopathological parameters showed that HP infection was not related with gender, age, tumor location, size, degree of differentiation, distant metastasis, lymph node metasta-sis (P>0.05) but related with the depth of invasion of gastric cancer tissues. Immunohistochemistry showed that TGF-β1 protein ex-pression rate in the HP (+) gastric cancer tissues ( 76.1%) was significantly higher than that in the HP (-) gastric tissues (52.0%). NF-κB protein expression in the HP (+) gastric cancer tissues (62.5%) was significantly higher than the HP (-) gas-tric tissues (40.0%). Conclusion Once the gastric tissues are infected by HP, there is the possibility that TGF-β1 and NF-κB be-come the pathway for regulating genetic transcription and signals transmission in cells, leading to the occurrence, development and me-tastasis of gastric cancer.