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机构地区:[1]中南大学湘雅医院妇产科,长沙410008 [2]中南大学湘雅医院病理科,长沙410008
出 处:《中南大学学报(医学版)》2005年第2期183-186,共4页Journal of Central South University :Medical Science
基 金:湖南省科委科研基金资助
摘 要:目的:研究凋亡调节蛋白bcl 2及bax在子宫肉瘤和子宫肌瘤中的表达及意义。方法:用免疫组织化学ABC法检测34份子宫平滑肌肉瘤标本(Ⅰ期18例,Ⅱ期1例,Ⅲ期8例,Ⅳ期7例)和34份子宫平滑肌瘤以及34份正常子宫肌层标本中的bcl 2及bax蛋白的表达。结果:子宫肌瘤中bcl 2表达强于子宫肉瘤和正常子宫肌层(P<0. 01),肉瘤中的表达强于正常子宫肌层(P<0. 05 )。正常子宫肌层中bax的表达强于子宫肌瘤和子宫肉瘤(P<0. 01),但bax在肌瘤和肉瘤之间的表达无显著性差异(P>0. 05)。Ⅰ,Ⅱ期子宫肉瘤中bcl 2和bax蛋白表达均高于Ⅲ,Ⅳ期者(P<0. 01)。bcl 2表达阳性的子宫肉瘤的预后好于bcl 2表达阴性者。结论:bcl 2和bax的表达失调在子宫肌瘤和子宫肉瘤的发病机制中起一定作用。bcl 2和bax主要在子宫肉瘤发生的早期起作用,bcl 2与肉瘤预后相关。Objective To determine the expression and significance of the apoptosis regulatory protein bcl-2 and bax in uterine leiomyosarcomas and uterine leiomyomas. Methods The expression of bcl-2 and bax were examined by immunohistochemical ABC staining with specific antibodies in 34 cases of uterine leiomyosarcomas (18 cases in stageⅠ, 1 in stageⅡ, 8 in stage Ⅲ, and 7 in stage Ⅳ), 34 uterine leiomyomas and 34 normal myometrium samples. Results Bcl-2 expression was higher in uterine leiomyomas than that in normal myometrium and in uterine leiomyosarcoma ( P < 0.01); bcl-2 expression in uterine leiomyosarcoma was higher than that in normal myometrium ( P < 0.05). Bax expression in normal myometrium was higher than that in leiomyomas and in uterine leiomyosarcoma ( P <0.01). There was no obvious difference in bax expression between leiomyomas and leiomyosarcoma ( P >0.05). Both the expressions of bcl-2 and bax proteins in stage Ⅰ~Ⅱ were higher than those of in stage Ⅲ~Ⅳ ( P <0.01). The bcl-2 positive leiomyosarcoma has a favorable clinical outcome than that of bcl-2 negative. Conclusion The imbalance between the expression of bcl-2 and bax may play a certain role in the genesis of the uterine leiomyomas and leiomyosarcomas. Bcl-2 and bax may be involved in the early stage of the tumor genesis of uterine leiomyosarcoma.Bcl-2 might correlate with the prognosis of the uterine leiomyosarcoma.
关 键 词:子宫肉瘤 子宫肌瘤 表达及 bcl-2表达 免疫组织化学ABC法 蛋白BCL-2 子宫平滑肌肉瘤 BAX蛋白表达 子宫肌层 子宫平滑肌瘤 显著性差异 凋亡调节 发病机制 表达失调 预后相关 标本 Ⅱ期 Ⅳ期
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