中华小儿外科杂志
中華小兒外科雜誌
중화소인외과잡지
CHINESE JOURNAL OF PEDIATRIC SURGERY
2010年
12期
885-887
,共3页
吕欣%俞松%王凯%曹江%魏珩%李堂江%万硕
呂訢%俞鬆%王凱%曹江%魏珩%李堂江%萬碩
려흔%유송%왕개%조강%위형%리당강%만석
血管瘤%内皮细胞%雷帕霉素结合蛋白质类
血管瘤%內皮細胞%雷帕黴素結閤蛋白質類
혈관류%내피세포%뢰파매소결합단백질류
Hemangioma%Endothelial cells%Rapamycin binding proteins
目的 探讨mTOR/p70S6K信号通路在小儿血管瘤的发生、发展及消退过程中的作用.方法 收集未经其他治疗、单纯手术切除并经病理诊断为血管瘤的标本31例,结合Mulliken分类法与增殖细胞核抗原(PCNA)表达对血管瘤进行分类和分期,免疫组织化学检测并比较增生期血管瘤和消退期血管瘤组织中雷帕霉素靶蛋白(mTOR)和p70S6K-a的表达水平.结果 18例增殖期血管瘤mTOR、p70S6K-a的积分光密度分别为6336.47±1655.89,588.72±223.87;13例消退期血管瘤mTOR、p70S6K-a的积分光密度分别为846.22±297.09,3235.64±947.86;血管瘤增殖期p70S6K-a的积分光密度明显低于消退期,差异有统计学意义(P<0.01).血管瘤增殖期mTOR的积分光密度明显高于消退期,差异有统计学意义(P<0.01).结论 小儿血管瘤组织中有mTOR、p70S6K-α表达,mTOR/p70S6K信号通路可能在小儿血管瘤的病理演变中发挥作用.
目的 探討mTOR/p70S6K信號通路在小兒血管瘤的髮生、髮展及消退過程中的作用.方法 收集未經其他治療、單純手術切除併經病理診斷為血管瘤的標本31例,結閤Mulliken分類法與增殖細胞覈抗原(PCNA)錶達對血管瘤進行分類和分期,免疫組織化學檢測併比較增生期血管瘤和消退期血管瘤組織中雷帕黴素靶蛋白(mTOR)和p70S6K-a的錶達水平.結果 18例增殖期血管瘤mTOR、p70S6K-a的積分光密度分彆為6336.47±1655.89,588.72±223.87;13例消退期血管瘤mTOR、p70S6K-a的積分光密度分彆為846.22±297.09,3235.64±947.86;血管瘤增殖期p70S6K-a的積分光密度明顯低于消退期,差異有統計學意義(P<0.01).血管瘤增殖期mTOR的積分光密度明顯高于消退期,差異有統計學意義(P<0.01).結論 小兒血管瘤組織中有mTOR、p70S6K-α錶達,mTOR/p70S6K信號通路可能在小兒血管瘤的病理縯變中髮揮作用.
목적 탐토mTOR/p70S6K신호통로재소인혈관류적발생、발전급소퇴과정중적작용.방법 수집미경기타치료、단순수술절제병경병리진단위혈관류적표본31례,결합Mulliken분류법여증식세포핵항원(PCNA)표체대혈관류진행분류화분기,면역조직화학검측병비교증생기혈관류화소퇴기혈관류조직중뢰파매소파단백(mTOR)화p70S6K-a적표체수평.결과 18례증식기혈관류mTOR、p70S6K-a적적분광밀도분별위6336.47±1655.89,588.72±223.87;13례소퇴기혈관류mTOR、p70S6K-a적적분광밀도분별위846.22±297.09,3235.64±947.86;혈관류증식기p70S6K-a적적분광밀도명현저우소퇴기,차이유통계학의의(P<0.01).혈관류증식기mTOR적적분광밀도명현고우소퇴기,차이유통계학의의(P<0.01).결론 소인혈관류조직중유mTOR、p70S6K-α표체,mTOR/p70S6K신호통로가능재소인혈관류적병리연변중발휘작용.
Objective To investigate the role of mTOR/p70S6K signaling pathway in the development of hemangioma in children. Methods Hemangioma specimens from 31 patients without any other treatment except surgery were classified by Mulliken's classification. The expression of proliferating cell nuclear antigen (PCNA), mammalian target of rapamycin (mTOR) and p70 ribosomal S6-kinase (p70S6K-α) were detected with immunohistochemistry. Results Eighteen cases of hemagioma specimens were classified as in proliferating phase, 13 as in involuting phase. For hemangiomas in proliferating phase, the IOD of mTOR and p70S6K-α were 6336. 47 ± 1655. 89 and 588. 72 ± 223. 87 respectively, while for hemagiomas in the involuting phase, the IOD of mTOR and p70S6K-α were 846. 22± 297. 09 and 3235. 64 ± 947. 86 respectively. IOD of p70S6K-α in hemangiomas in the involving phase was significantly higher than that in the proliferating phase (P<0. 01 ). IOD of mTOR in the hemagiomas in proliferating phase was significantly higher than that in the involuting phase (P<0. 01 ). Conclusions The mTOR/p70S6K signaling pathways may play an important role in growth and development of pediatric hemangioma.