中国肿瘤临床
中國腫瘤臨床
중국종류림상
CHINESE JOURNAL OF CLINICAL ONCOLOGY
2014年
2期
102-104
,共3页
秦海明%金庆%程琳%宋福林%崔彤
秦海明%金慶%程琳%宋福林%崔彤
진해명%금경%정림%송복림%최동
浸润性尿路膀胱上皮癌%人类表皮生长因子受体-2%免疫组织化学%荧光原位杂交
浸潤性尿路膀胱上皮癌%人類錶皮生長因子受體-2%免疫組織化學%熒光原位雜交
침윤성뇨로방광상피암%인류표피생장인자수체-2%면역조직화학%형광원위잡교
invasive urothelial bladder carcinoma%human epidermal growth factor receptor-2%immunohistochemistry%fluores-cence in situ hybridization
目的:探讨不同分期(T2~T4)的尿路膀胱上皮癌(urothelial bladder carcinoma,UBC)中人类表皮生长因子受体-2(HER2)蛋白表达和基因扩增状态。方法:将49例不同分期的膀胱癌患者的肿瘤组织进行HER2免疫组织化学染色,以及HER2基因的双色荧光原位杂交(FISH)检测。结果:膀胱癌患者男性居多。而且分期越高,HER2染色阳性率越高。但所有患者均未出现基因扩增,有12例患者出现17号染色体多倍体。分期越高,多倍体发生越多。结论:膀胱癌患者HER2蛋白增高不是由于基因扩增所致,其它的转录和后转录机制参与并调节了蛋白的表达。
目的:探討不同分期(T2~T4)的尿路膀胱上皮癌(urothelial bladder carcinoma,UBC)中人類錶皮生長因子受體-2(HER2)蛋白錶達和基因擴增狀態。方法:將49例不同分期的膀胱癌患者的腫瘤組織進行HER2免疫組織化學染色,以及HER2基因的雙色熒光原位雜交(FISH)檢測。結果:膀胱癌患者男性居多。而且分期越高,HER2染色暘性率越高。但所有患者均未齣現基因擴增,有12例患者齣現17號染色體多倍體。分期越高,多倍體髮生越多。結論:膀胱癌患者HER2蛋白增高不是由于基因擴增所緻,其它的轉錄和後轉錄機製參與併調節瞭蛋白的錶達。
목적:탐토불동분기(T2~T4)적뇨로방광상피암(urothelial bladder carcinoma,UBC)중인류표피생장인자수체-2(HER2)단백표체화기인확증상태。방법:장49례불동분기적방광암환자적종류조직진행HER2면역조직화학염색,이급HER2기인적쌍색형광원위잡교(FISH)검측。결과:방광암환자남성거다。이차분기월고,HER2염색양성솔월고。단소유환자균미출현기인확증,유12례환자출현17호염색체다배체。분기월고,다배체발생월다。결론:방광암환자HER2단백증고불시유우기인확증소치,기타적전록화후전록궤제삼여병조절료단백적표체。
Objective: To explore the expression and gene amplification status of human epidermal growth factor receptor-2 (HER2) in the different stages of invasive urothelial bladder carcinoma. Methods:Tumor tissues from 49 patients with different stages of invasive urothelial bladder carcinoma were tested by immunohistochemical staining for HER2 and HER2 gene fluorescence in situ hybridization. Results:The number of male patients was higher than that of females. The positive rate of HER2 protein expression was higher in the patients with the higher stage of invasive urothelial bladder carcinoma. However, no gene amplification was observed in all patients. Twelve patients had ployploid chromosome 17. More ployploids were observed in the patients with the higher stage of inva-sive urothelial bladder carcinoma. Conclusion:The increase in the protein expression of HER2 in the invasive urothelial bladder carci-noma patients was not caused by gene amplification. Other transcriptional and post-transcriptional mechanisms were probably involved in the regulation of the HER2 protein.