中华消化外科杂志
中華消化外科雜誌
중화소화외과잡지
CHINESE JOURNAL OF DIGESTIVE SURGERY
2009年
6期
453-456
,共4页
张沁宏%向德兵%李梦侠%廖培雷%李增鹏%王东
張沁宏%嚮德兵%李夢俠%廖培雷%李增鵬%王東
장심굉%향덕병%리몽협%료배뢰%리증붕%왕동
肝肿瘤%脱嘌呤/脱嘧啶核酸内切酶%突变型p53
肝腫瘤%脫嘌呤/脫嘧啶覈痠內切酶%突變型p53
간종류%탈표령/탈밀정핵산내절매%돌변형p53
Liver neoplasms%Apurinic/apyrimidinic endonuclease 1%Mutant p53
目的 探讨肝细胞癌(HCC)中脱嘌呤/脱嘧啶核酸内切酶(APE1)的表达特点及APE1与突变型p53表达的关系.方法 收集1991年至2004年第三军医大学大坪医院野战外科研究所病理科10例正常肝组织、40例结节性肝硬化组织和103例HCC组织标本,应用免疫组织化学SP二步法分别检测APE1和p53的表达情况.采用X~2检验、相关分析及K Independent-Samples Tests检验分析所得结果.结果 APE1在正常肝组织、肝硬化和HCC组织中均有不同程度的表达,阳性率分别为40.0%、82.5%、100.0%,三者比较差异有统计学意义(χ~2=47.852,P<0.01).正常肝组织APE1仅表达于细胞核;肝硬化和HCC组织中APE1出现异位表达,异位表达率分别为20.0%和53.4%(χ~2=20.757,P<0.01).不同APE1/p53表达模式的HCC临床分期及病理学分级比较差异有统计学意义(χ~2=12.910,14.481,P<0.01),APE1异位表达/p53阳性的HCC恶性程度高.结论 APE1过表达及异位表达与HCC的发生、发展密切相关;APE1异位表达和053突变可能在肿瘤的发生、发展过程中具有协同促进作用.
目的 探討肝細胞癌(HCC)中脫嘌呤/脫嘧啶覈痠內切酶(APE1)的錶達特點及APE1與突變型p53錶達的關繫.方法 收集1991年至2004年第三軍醫大學大坪醫院野戰外科研究所病理科10例正常肝組織、40例結節性肝硬化組織和103例HCC組織標本,應用免疫組織化學SP二步法分彆檢測APE1和p53的錶達情況.採用X~2檢驗、相關分析及K Independent-Samples Tests檢驗分析所得結果.結果 APE1在正常肝組織、肝硬化和HCC組織中均有不同程度的錶達,暘性率分彆為40.0%、82.5%、100.0%,三者比較差異有統計學意義(χ~2=47.852,P<0.01).正常肝組織APE1僅錶達于細胞覈;肝硬化和HCC組織中APE1齣現異位錶達,異位錶達率分彆為20.0%和53.4%(χ~2=20.757,P<0.01).不同APE1/p53錶達模式的HCC臨床分期及病理學分級比較差異有統計學意義(χ~2=12.910,14.481,P<0.01),APE1異位錶達/p53暘性的HCC噁性程度高.結論 APE1過錶達及異位錶達與HCC的髮生、髮展密切相關;APE1異位錶達和053突變可能在腫瘤的髮生、髮展過程中具有協同促進作用.
목적 탐토간세포암(HCC)중탈표령/탈밀정핵산내절매(APE1)적표체특점급APE1여돌변형p53표체적관계.방법 수집1991년지2004년제삼군의대학대평의원야전외과연구소병이과10례정상간조직、40례결절성간경화조직화103례HCC조직표본,응용면역조직화학SP이보법분별검측APE1화p53적표체정황.채용X~2검험、상관분석급K Independent-Samples Tests검험분석소득결과.결과 APE1재정상간조직、간경화화HCC조직중균유불동정도적표체,양성솔분별위40.0%、82.5%、100.0%,삼자비교차이유통계학의의(χ~2=47.852,P<0.01).정상간조직APE1부표체우세포핵;간경화화HCC조직중APE1출현이위표체,이위표체솔분별위20.0%화53.4%(χ~2=20.757,P<0.01).불동APE1/p53표체모식적HCC림상분기급병이학분급비교차이유통계학의의(χ~2=12.910,14.481,P<0.01),APE1이위표체/p53양성적HCC악성정도고.결론 APE1과표체급이위표체여HCC적발생、발전밀절상관;APE1이위표체화053돌변가능재종류적발생、발전과정중구유협동촉진작용.
Objective To detect the expression of apurinic/apyrimidinic endonuclease 1 (APEI) and explore its correlation with the expression of mutant p53 in hepatocellular carcinoma (HCC). Methods The expression of APE1 and mutant p53 was detected by SP immunohistochemical method in 10 specimens of normal liver tissue, 40 specimens of liver cirrhosis tissue and 103 specimens of HCC tissue which were collected at the Department of Pathology of Daping Hospital from 1991 to 2004. All data were analyzed by chi-square test, correla-tion analysis and K Independent-Samples Tests. Results The expression rate of APE1 in HCC was 100.0%, which was significantly higher than that in normal liver tissue (40.0%) and liver cirrhosis tissue (82.5%) (χ~2= 47.852, P < 0.01). The expression of APE1 was only detected in the nucleus in normal liver tissue. Ectopic expression of APE1 in cytoplasm was detected in liver cirrhosis tissue and HCC tissue, with the rate of 20.0% and 53.4%, respectively (χ~2=20.757, P <0.01). There was statistical difference in clinical staging and pathological grading of HCC with different combinations of APE1 expression (intranuclear or ectopic expression) and mutant p53 expression (positive or negative expression) (χ~2=12.910, 14.481, P < 0.01), and HCC with ectopic expression of APE1 and positive expression of p53 had high malignant degree. Conclusion Overexpression and ectopic expression of APE1 in cytoplasm may play important roles in the genesis and progression of HCC, and the ectopic expression of APE1 and p53 mutation may have synergistic effect.