临床与实验病理学杂志
臨床與實驗病理學雜誌
림상여실험병이학잡지
Chinese Journal of Clinical and Experimental Pathology
2015年
10期
1089-1094
,共6页
胃肿瘤%幽门螺杆菌L型%XPF蛋白%p53蛋白%免疫组织化学
胃腫瘤%幽門螺桿菌L型%XPF蛋白%p53蛋白%免疫組織化學
위종류%유문라간균L형%XPF단백%p53단백%면역조직화학
gastric neoplasms%Helicobacter pylori L-form%XPF%p53%immunohistochemistry
目的:探讨XPF和p53蛋白在胃癌组织中的表达及与幽门螺杆菌L型( Helicobacter pylori L-form, Hp-L型)感染的关系。方法应用免疫组化ABC法和Giemsa染色法检测239例胃癌和癌旁正常胃黏膜组织(对照组)中XPF、p53、Hp-L型蛋白的表达及Hp-L型感染情况。结果(1) XPF和p53蛋白在胃癌组及对照组中的表达差异均有统计学意义( P均<0.01)。XPF和p53的表达呈正相关(r=0.196,P<0.01)。 XPF表达仅与Laurén分类有关(P<0.05)。 p53表达仅与浸润深度有关(P<0.05)。(2)胃癌组织中Giemsa染色Hp-L型检出和Hp-L型抗原表达同时阳性的阳性率为73.22%(175/239),与对照组相比差异有统计学意义(P<0.01)。(3)胃癌组织中Hp-L型阳性组XPF和p53蛋白的阳性率高于Hp-L型阴性组(P均<0.01)。胃癌组织中Hp-L型阳性与XPF和p53的阳性表达均呈正相关(r=0.32和0.296,P均<0.01)。(4)单因素分析发现肿瘤浸润深度、远处转移、TNM分期、XPF和p53表达均与胃癌患者预后有关( P<0.05)。 Cox风险模型多因素分析发现XPF是影响胃癌预后的独立因素(P<0.05),XPF阳性者具有更短的生存期。当与浸润深度及远处转移结合评估时,校正危险度增加3.791倍。结论 XPF与p53、Hp-L型在胃癌发生、发展过程中起重要作用,且XPF高表达预示预后不良。 Hp-L型感染可能上调XPF和p53的表达。
目的:探討XPF和p53蛋白在胃癌組織中的錶達及與幽門螺桿菌L型( Helicobacter pylori L-form, Hp-L型)感染的關繫。方法應用免疫組化ABC法和Giemsa染色法檢測239例胃癌和癌徬正常胃黏膜組織(對照組)中XPF、p53、Hp-L型蛋白的錶達及Hp-L型感染情況。結果(1) XPF和p53蛋白在胃癌組及對照組中的錶達差異均有統計學意義( P均<0.01)。XPF和p53的錶達呈正相關(r=0.196,P<0.01)。 XPF錶達僅與Laurén分類有關(P<0.05)。 p53錶達僅與浸潤深度有關(P<0.05)。(2)胃癌組織中Giemsa染色Hp-L型檢齣和Hp-L型抗原錶達同時暘性的暘性率為73.22%(175/239),與對照組相比差異有統計學意義(P<0.01)。(3)胃癌組織中Hp-L型暘性組XPF和p53蛋白的暘性率高于Hp-L型陰性組(P均<0.01)。胃癌組織中Hp-L型暘性與XPF和p53的暘性錶達均呈正相關(r=0.32和0.296,P均<0.01)。(4)單因素分析髮現腫瘤浸潤深度、遠處轉移、TNM分期、XPF和p53錶達均與胃癌患者預後有關( P<0.05)。 Cox風險模型多因素分析髮現XPF是影響胃癌預後的獨立因素(P<0.05),XPF暘性者具有更短的生存期。噹與浸潤深度及遠處轉移結閤評估時,校正危險度增加3.791倍。結論 XPF與p53、Hp-L型在胃癌髮生、髮展過程中起重要作用,且XPF高錶達預示預後不良。 Hp-L型感染可能上調XPF和p53的錶達。
목적:탐토XPF화p53단백재위암조직중적표체급여유문라간균L형( Helicobacter pylori L-form, Hp-L형)감염적관계。방법응용면역조화ABC법화Giemsa염색법검측239례위암화암방정상위점막조직(대조조)중XPF、p53、Hp-L형단백적표체급Hp-L형감염정황。결과(1) XPF화p53단백재위암조급대조조중적표체차이균유통계학의의( P균<0.01)。XPF화p53적표체정정상관(r=0.196,P<0.01)。 XPF표체부여Laurén분류유관(P<0.05)。 p53표체부여침윤심도유관(P<0.05)。(2)위암조직중Giemsa염색Hp-L형검출화Hp-L형항원표체동시양성적양성솔위73.22%(175/239),여대조조상비차이유통계학의의(P<0.01)。(3)위암조직중Hp-L형양성조XPF화p53단백적양성솔고우Hp-L형음성조(P균<0.01)。위암조직중Hp-L형양성여XPF화p53적양성표체균정정상관(r=0.32화0.296,P균<0.01)。(4)단인소분석발현종류침윤심도、원처전이、TNM분기、XPF화p53표체균여위암환자예후유관( P<0.05)。 Cox풍험모형다인소분석발현XPF시영향위암예후적독립인소(P<0.05),XPF양성자구유경단적생존기。당여침윤심도급원처전이결합평고시,교정위험도증가3.791배。결론 XPF여p53、Hp-L형재위암발생、발전과정중기중요작용,차XPF고표체예시예후불량。 Hp-L형감염가능상조XPF화p53적표체。
Purpose To investigate the relationship between Helicobacter pylori L-form ( Hp-L) infection and expression of XPF and p53 in gastric carcinoma. Methods XPF, p53 and Hp-L were examined in 239 cases of gastric carcinoma and healthy individuals by means of Giemsa stain and immunohistochemical staining with ABC method. Results XPF and p53 expression in gastric carcinoma was significantly higher than that of the surrounding tissue (P<0. 01). There were positive correlation between the expression of XPF and p53 (r=0. 196, P<0. 01). The expression of XPF was related to the Laurén classification (P<0. 05). The expression of p53 was associated to the depth of invasion (P<0. 05). (2) 175 (73. 22%) cases were Hp-L positive by both Giemsa and immunohisto-chemical staining. Hp-L expression in gastric carcinoma were significantly higher than that of the surrounding tissue (P<0. 01). (3) In the Hp-L positive group, XPF and p53 were significantly higher than in that of the Hp-L negative group (P<0. 01). Positive corre-lation existed between positive Hp-L staining and the expression of XPF and p53 (r=0. 32, r=0. 296, P<0. 01). (4) Univariate a-nalysis showed that depth of invasion, distant metastasis, TNM stage, XPF and p53 were related to the prognosis of gastric carcinoma ( P<0. 05). Multivariate Cox model analysis showed that XPF was an independent prognostic factor for the patients (P<0. 05). The pa-tients with positive expression of XPF had a shorter survival time. When combined with the depth of invasion and distant metastasis, the correction risk increased by 3. 791 times. Conclusion XPF, p53 and Hp-L may play very important roles in the development of gastric carcinoma. The high expression of XPF implies poorer prognosis. Hp-L infection may be related to the up-regulated expression of XPF and p53.