天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2010年
1期
20-22,后插1
,共4页
宫颈肿瘤%癌%宫颈上皮内瘤样病变%蛋白激酶类%真核细胞起始因子2%免疫组织化学
宮頸腫瘤%癌%宮頸上皮內瘤樣病變%蛋白激酶類%真覈細胞起始因子2%免疫組織化學
궁경종류%암%궁경상피내류양병변%단백격매류%진핵세포기시인자2%면역조직화학
uterine cervical neoplasms%carcinoma%cervical intraepithelial neoplasia%protein kinases%eukaryotic%initiation factor-2%immunohistochemistry
目的:探讨蛋白激酶R(PKR)→真核细胞翻译起始因子2α(EIF2α)信号传导通路中PKR、磷酸化型PKR、EIF2α(p-PKR、p-EIF2α)表达与宫颈病变的相关性、在宫颈肿瘤形成演进过程中的作用及对宫颈癌患者预后的影响.方法:采用免疫组化法检测PKR、p-PKR、p-EIF2α在63例宫颈癌、114例宫颈上皮内瘤样病变(CINⅠ~Ⅲ)、15例正常宫颈组织中的表达.结果:PKR在各组的阳性表达率随宫颈病变级别升高而升高,并与宫颈病变级别呈正相关(P < 0.05);p-PKR、p-EIF2α在各组的阳性表达率随宫颈病变级别升高而先升高、后下降;在宫颈癌组,PKR的阳性表达率明显高于p-PKR(P < 0.01);宫颈癌患者临床分期晚者病情进展快(P < 0.01),p-PKR、p-EIF2α阴性表达者病情进展快(P < 0.05).结论:PKR的表达与宫颈病变级别相关;在宫颈高级别病变中存在PKR、EIF2α磷酸化障碍或p-PKR、p-EIF2α去磷酸化机制,使宫颈病变进展,可能导致宫颈癌患者预后不良.
目的:探討蛋白激酶R(PKR)→真覈細胞翻譯起始因子2α(EIF2α)信號傳導通路中PKR、燐痠化型PKR、EIF2α(p-PKR、p-EIF2α)錶達與宮頸病變的相關性、在宮頸腫瘤形成縯進過程中的作用及對宮頸癌患者預後的影響.方法:採用免疫組化法檢測PKR、p-PKR、p-EIF2α在63例宮頸癌、114例宮頸上皮內瘤樣病變(CINⅠ~Ⅲ)、15例正常宮頸組織中的錶達.結果:PKR在各組的暘性錶達率隨宮頸病變級彆升高而升高,併與宮頸病變級彆呈正相關(P < 0.05);p-PKR、p-EIF2α在各組的暘性錶達率隨宮頸病變級彆升高而先升高、後下降;在宮頸癌組,PKR的暘性錶達率明顯高于p-PKR(P < 0.01);宮頸癌患者臨床分期晚者病情進展快(P < 0.01),p-PKR、p-EIF2α陰性錶達者病情進展快(P < 0.05).結論:PKR的錶達與宮頸病變級彆相關;在宮頸高級彆病變中存在PKR、EIF2α燐痠化障礙或p-PKR、p-EIF2α去燐痠化機製,使宮頸病變進展,可能導緻宮頸癌患者預後不良.
목적:탐토단백격매R(PKR)→진핵세포번역기시인자2α(EIF2α)신호전도통로중PKR、린산화형PKR、EIF2α(p-PKR、p-EIF2α)표체여궁경병변적상관성、재궁경종류형성연진과정중적작용급대궁경암환자예후적영향.방법:채용면역조화법검측PKR、p-PKR、p-EIF2α재63례궁경암、114례궁경상피내류양병변(CINⅠ~Ⅲ)、15례정상궁경조직중적표체.결과:PKR재각조적양성표체솔수궁경병변급별승고이승고,병여궁경병변급별정정상관(P < 0.05);p-PKR、p-EIF2α재각조적양성표체솔수궁경병변급별승고이선승고、후하강;재궁경암조,PKR적양성표체솔명현고우p-PKR(P < 0.01);궁경암환자림상분기만자병정진전쾌(P < 0.01),p-PKR、p-EIF2α음성표체자병정진전쾌(P < 0.05).결론:PKR적표체여궁경병변급별상관;재궁경고급별병변중존재PKR、EIF2α린산화장애혹p-PKR、p-EIF2α거린산화궤제,사궁경병변진전,가능도치궁경암환자예후불량.
Objective:To identify the relationship between expression of protein kinase R(PKR), phosphating PKR, EIF2α(p-PKR, p-EIF2α) in PKR→EIF2α signal transduction passage and the grades of cervical lesions, the role in generation and progression of cervical tumor and their effects to prognosis of cervical cancer patients. Methods:The expressions of PKR, p-PKR and p-EIF2α in human cervical cancer tissue of 63 cases, cervical intraepithelial neoplasia(CINⅠ-Ⅲ) of 114 cases and normal cervical epithelium of 15 cases were detected by immunohistochemical technique. Results:With the increase in grades of cervical lesions, the positive-expression rate of PKR increased and significantly correlated with the grades of cervical lesions(P < 0.05). With the increase in grades of cervical lesions, the positive-expression rates of p-PKR and p-EIF2α increased firstly, and then decreased. In cervical cancer group, the positive-expression rate of PKR was much higher than that of p-PKR(P < 0.01). The development and progression was quicker in later clinical stages of cervical cancer than that of earlier clinical stages of cervical cancer (P < 0.01). The development and progression of cervical cancer was quicker in patients with negative-expression of p-PKR and p-EIF2α than that in patients with positive-expression of p-PKR and p-EIF2α(P < 0.05). Conclusion:The positive-expression rate of PKR was correlated with the grades of cervical lesions. There are some factors which can impede PKR and EIF2α to be phosphorylated or make p-PKR and p-EIF2α dephosphorylate in high level cervical lesions, which promotes the development and progression of cervical lesions, worsens the prognosis of cervical cancer.