CAJ | 학술논문

目的通过分析子宫内膜上皮内瘤变(EIN)诊断、分类与子宫内膜增生WHO(2003)分类的关系,探讨β-catenin、Glut-1和PTEN蛋白在子宫内膜样腺癌发生过程中的表达及其意义.方法根据EIN诊断及分类标准,对83例子宫内膜增生病例进行再分类.采用免疫组织化学SP法,对10例增殖期子宫内膜、83例子宫内膜增生及24例子宫内膜样腺癌组织中β-catenin、Glut-1及PTEN蛋白的表达进行检测.结果 (1)83例子宫内膜增生病例中共检出24例EIN病例,总检出率为28.9%(24/83).24例EIN病例中,来自复杂型不典型性增生16例(66.7%,16/24),但EIN的检出率与不典型增生的分级无明显关系(P＞0.05).(2)β-catenin蛋白在增殖期子宫内膜中呈正常表达,良性子宫内膜增生的异常表达率为10.2%(6/59),而EIN和子宫内膜样腺癌的异常表达率(50%,12/24;66.7%,16/24)分别明显高于良性子宫内膜增生(P＜0.01),但二者间的异常表达率差异无统计学意义(P＞0.05).(3)Glut-1蛋白在增殖期子宫内膜、良性子宫内膜增生组织中均呈低表达,而在EIN和子宫内膜样腺癌中的高表达率分别为58.3%(14/24)和70.8%(17/24),均显著高于增殖期子宫内膜及良性子宫内膜增生(P＜0.01),但二者高表达率间差异无统计学意义(P＞0.05).(4)PTEN蛋白在EIN病例中的失表达率(37.5%,9/24)与子宫内膜样腺癌(62.5%,15/24)、增殖期子宫内膜(2/10)及良性子宫内膜增生(28.8%,17/59)比较差异均无统计学意义(P＞0.05),但子宫内膜样腺癌的失表达率则明显高于增殖期子宫内膜及良性子宫内膜增生病例,其差异均具有统计学意义(P＜0.05).结论 β-catenin蛋白的异常表达和Glut-1蛋白高表达是子宫内膜样腺癌发生过程中的早期事件,二者在区别良性子宫内膜增生、EIN和子宫内膜样腺癌中可能是有用的免疫标志物.PTEN蛋白失表达是子宫内膜样腺癌发生过程中的极早期事件,但将其作为EIN病变的诊断性标志物并不恰当. 目的通過分析子宮內膜上皮內瘤變(EIN)診斷、分類與子宮內膜增生WHO(2003)分類的關繫,探討β-catenin、Glut-1和PTEN蛋白在子宮內膜樣腺癌髮生過程中的錶達及其意義.方法根據EIN診斷及分類標準,對83例子宮內膜增生病例進行再分類.採用免疫組織化學SP法,對10例增殖期子宮內膜、83例子宮內膜增生及24例子宮內膜樣腺癌組織中β-catenin、Glut-1及PTEN蛋白的錶達進行檢測.結果 (1)83例子宮內膜增生病例中共檢齣24例EIN病例,總檢齣率為28.9%(24/83).24例EIN病例中,來自複雜型不典型性增生16例(66.7%,16/24),但EIN的檢齣率與不典型增生的分級無明顯關繫(P＞0.05).(2)β-catenin蛋白在增殖期子宮內膜中呈正常錶達,良性子宮內膜增生的異常錶達率為10.2%(6/59),而EIN和子宮內膜樣腺癌的異常錶達率(50%,12/24;66.7%,16/24)分彆明顯高于良性子宮內膜增生(P＜0.01),但二者間的異常錶達率差異無統計學意義(P＞0.05).(3)Glut-1蛋白在增殖期子宮內膜、良性子宮內膜增生組織中均呈低錶達,而在EIN和子宮內膜樣腺癌中的高錶達率分彆為58.3%(14/24)和70.8%(17/24),均顯著高于增殖期子宮內膜及良性子宮內膜增生(P＜0.01),但二者高錶達率間差異無統計學意義(P＞0.05).(4)PTEN蛋白在EIN病例中的失錶達率(37.5%,9/24)與子宮內膜樣腺癌(62.5%,15/24)、增殖期子宮內膜(2/10)及良性子宮內膜增生(28.8%,17/59)比較差異均無統計學意義(P＞0.05),但子宮內膜樣腺癌的失錶達率則明顯高于增殖期子宮內膜及良性子宮內膜增生病例,其差異均具有統計學意義(P＜0.05).結論 β-catenin蛋白的異常錶達和Glut-1蛋白高錶達是子宮內膜樣腺癌髮生過程中的早期事件,二者在區彆良性子宮內膜增生、EIN和子宮內膜樣腺癌中可能是有用的免疫標誌物.PTEN蛋白失錶達是子宮內膜樣腺癌髮生過程中的極早期事件,但將其作為EIN病變的診斷性標誌物併不恰噹.
목적 통과분석자궁내막상피내류변(EIN)진단、분류여자궁내막증생WHO(2003)분류적관계,탐토β-catenin、Glut-1화PTEN단백재자궁내막양선암발생과정중적표체급기의의.방법 근거EIN진단급분류표준,대83례자궁내막증생병례진행재분류.채용면역조직화학SP법,대10례증식기자궁내막、83례자궁내막증생급24례자궁내막양선암조직중β-catenin、Glut-1급PTEN단백적표체진행검측.결과 (1)83례자궁내막증생병례중공검출24례EIN병례,총검출솔위28.9%(24/83).24례EIN병례중,래자복잡형불전형성증생16례(66.7%,16/24),단EIN적검출솔여불전형증생적분급무명현관계(P＞0.05).(2)β-catenin단백재증식기자궁내막중정정상표체,량성자궁내막증생적이상표체솔위10.2%(6/59),이EIN화자궁내막양선암적이상표체솔(50%,12/24;66.7%,16/24)분별명현고우량성자궁내막증생(P＜0.01),단이자간적이상표체솔차이무통계학의의(P＞0.05).(3)Glut-1단백재증식기자궁내막、량성자궁내막증생조직중균정저표체,이재EIN화자궁내막양선암중적고표체솔분별위58.3%(14/24)화70.8%(17/24),균현저고우증식기자궁내막급량성자궁내막증생(P＜0.01),단이자고표체솔간차이무통계학의의(P＞0.05).(4)PTEN단백재EIN병례중적실표체솔(37.5%,9/24)여자궁내막양선암(62.5%,15/24)、증식기자궁내막(2/10)급량성자궁내막증생(28.8%,17/59)비교차이균무통계학의의(P＞0.05),단자궁내막양선암적실표체솔칙명현고우증식기자궁내막급량성자궁내막증생병례,기차이균구유통계학의의(P＜0.05).결론 β-catenin단백적이상표체화Glut-1단백고표체시자궁내막양선암발생과정중적조기사건,이자재구별량성자궁내막증생、EIN화자궁내막양선암중가능시유용적면역표지물.PTEN단백실표체시자궁내막양선암발생과정중적겁조기사건,단장기작위EIN병변적진단성표지물병불흡당.
Objective To explore the expression of p-catenin,Glut-1,PTEN in uterine endometrioid adenocarcinoma and their roles in tumorigenesis.Methods A total of 83 cases of endometrial hyperplasia were selected and reclassified according to EIN diagnostic criteria.Expressions of p-catenin,Glut-1 and PTEN proteins were investigated by immunohistochemistry in 10 proliferative endometrium,83 endometrial hyperplasia and 24 endometrioid adenocarcinoma.Results(1)24 EIN(28.9%)lesions were reclassified among 83 previously diagnosed endometrial hyperplasia,of which,16 of 24 EIN cases(66.7%)had a prior diagnosis of complex atypical hyperplasia The relation between EIN diagnosis and grade of atypical hyperplasia was not obvious(P＞0.05).(2)Normal(membranous)expression of p-catenin was present in 10 cases of proliferative endometrium.Abnormal(marked membranous/cytoplasmic,cytoplasmic and/or nuclear or negative)expression rates of p-catenin in EIN lesions(50%,12/24)and endometrioid adenocarcinoma(66.1%,16/24)were significantly higher than that of benign hyperplasia(10.2%,6/59)respectively(P＜0.01).However,the difference was not significant between EIN lesions and endometrioid adenocarcinomas(P＞0.05).(3)Low level expressions of Glut-1 was present in proliferative endometrium and benign hyperplasia.Overexpression of Glut-1 was present in 58.3%(14/24)of EIN and 70.8% (17/24)of endometrioid adenocarcinoma,respectively,and statistically not significant(P＞0.05).(4)Percentages of loss of PTEN expression showed no difference between EIN lesions(37.5%,9/24)and proliferative endometrium(2/10),benign hyperplasia(28.8%,17/59),endometrioid adenocarcinoma (62.5%,15/24;P＞0.05).However,loss of PTEN expression in endometrioid adenocarcinoma was significantly higher than those in proliferative endometrium and benign hyperplasia(P＜0.05).Conclusions Abnormal expression of p-catenin and overexpression of Glut-1 may be the early events in tumorigenesis of endometrioid adenocarcinoma.The expression of both markers may be useful in distinguishing a benign hyperplasia from EIN and endometrioid adenocarcinoma.Lack of PTEN expression may be the earliest event in endometrial carcinogenesis.However,it can not be used yet as a diagnostic marker for the EIN lesioa