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HMGA2和E-cadherin在膀胱移行细胞癌组织中的表达及其意义 被引量:1

Expressions and clinical significances of HMGA2 and E-cadherin in bladder transitional cell carcinoma tissue
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摘要 目的:探讨HMGA2和E-cadherin在膀胱移行细胞癌组织中的表达及其与临床分期、病理分级及预后的关系。方法:选取健康人正常膀胱组织5例、膀胱移行细胞癌组织49例。49例膀胱移行细胞癌组织分为非肌层浸润组(41例)、肌层浸润组(8例);低级别组(24例)、高级别组(25例)。应用免疫组织化学方法检测正常膀胱组织和膀胱移行细胞癌组织中HMGA2和E-cadherin蛋白的表达情况,并结合临床资料进行分析。结果:5例正常膀胱组织中HMGA2呈阴性表达、E-cadherin呈阳性表达;在49例膀胱癌组织中HMGA2阳性表达率为41%、E-cadherin的阴性表达率为43%;其中在非肌层浸润组(Tis~T1)、肌层浸润组(T2)膀胱癌组织中HMGA2的阳性表达率分别为34%和75%,HMGA2在肌层浸润组阳性表达率显著高于非肌层浸润组(P<0.05);E-cadherin阴性表达率分别为37%和75%,E-cadherin在肌层浸润组阴性表达率显著高于非肌层浸润组(P<0.05);在低级别、高级别肿瘤中HMGA2的阳性表达率分别为25%和56%,HMGA2在高级别组阳性表达率显著高于低级别组(P<0.05),E-cadherin阴性表达率分别为25%和60%,E-cadherin在高级别组阴性表达率显著高于低级别组(P<0.05);术后随访18~40个月,随访42例膀胱癌患者中复发18例。在复发组与未复发组中HMGA2的阳性表达率分别为56%和25%,HMGA2在复发组阳性表达率显著高于非复发组(P<0.05);E-cadherin阴性表达率分别为67%和33%,E-cadherin在复发组阴性表达率显著高于非复发组(P<0.05)。结论:HMGA2、E-cadherin的异常表达与膀胱移行细胞癌的恶性程度有关联,可以作为检测膀胱移行细胞癌临床分期、病理分级及预后的重要指标。 Objective To investigate the expressions of HMGA2 and E-cadherin in bladder transitional cell carcinoma(BTCC)tissue and their relationship with clinical stage,pathological grade and prognosis.Methods The expressions of HMGA2and E-cadherin in 49cases of BTCC(including 41cases of non-muscle invasive bladder cancer,8cases of muscle invasive bladder cancer;24cases of low grade bladder cancer,25cases of high grade bladder cancer)and 5specimens of normal bladder tissues were detected by immunohistochemtry,and their correlations to the clinicopathologic features were analyzed.Results The HMGA2expression was negative,but the E-cadherin expression was positive in 5cases of normal bladder tissue.The positive expression rate of HMGA2 and negative expression rate of E-cadherin in bladder cancer tissue was 41% and 43%,respectively;the positive expression rate of HMGA2and negative expression rate of E-cadherin in non-muscle invasive bladder cancer and muscle invasive bladder cancer were 34%,75% and 37%,75%,respectively;the positive expression rate of HMGA2in muscle invasive bladder cancer was apparently higher than that in non-muscle invasive bladder cancer(P0.05);the negative expression rate of E-cadherin in muscle invasive bladder cancer was apparently higher than that in non-muscle invasive bladder cancer(P0.05).The positive expression rate of HMGA2and negative expression rate of E-cadherin in low grade and high grade of BTCC were 25%,56%and 25%,60%,respectively;the positive expression rate of HMGA2in high grade of BTCC was apparently higher than that in low grade(P 0.05);the negative expression rate of E-cadherin in high grade of BTCC was apparently higher than that in low grade of BTCC(P0.05).The correlation between HMGA2and E-cadherin was statistically significant(P 0.05).42patients were followed up for 18-40months,among which,18reccured.The positive expression rate of HMGA2and negative expression rate of E-cadherin in recurrence and non-recurrence groups were 56%,25% and 67%,33%,respectively;the positive expression rate of HMGA2in recurrence group was apparently higher than that in non-recurrence group(P0.05);the negative expression rate of E-cadherin in recurrence group was apparently higher than that in non-recurrence group(P0.05).Conclusion The abnormal expressions of HMGA2 and E-cadherin are related to the malignant tendency of BTCC,and they may be used as markers to predict clinical stage,pathological grade and prognosis of BTCC.
出处 《吉林大学学报(医学版)》 CAS CSCD 北大核心 2013年第5期944-947,I0004,共5页 Journal of Jilin University:Medicine Edition
基金 吉林省科技厅科研基金资助课题(201115047)
关键词 膀胱肿瘤 高迁移率族蛋白A2 上皮钙依赖黏附蛋白E 免疫组织化学 uring bladder neoplasms high mobility group protein A2 E-cadherin immunohistochemistry
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  • 1Wisniewski JR, Schwanbeck R. High mobility group Ⅰ/Y: multifunctiona/ chromosomal proteins causally involved in tumor pro-gression and malignant transformation (review) [J]. Int J Mol Med, 2000, 6 (4): 409-419.
  • 2Bustin M, Reeves R. High-mobility-group chromosomal proteins: architectural components that facilitate chromatin function[J]. Prog Nucleic Acid Res Mol Biol, 1996,54 (1): 35-100.
  • 3Hirning-Folz U, Wilda M, Rippe V, et al. The expression pattern of Hmgie gene during development[J]. Genes Chromosomes Cancer, 1998, 23 (4): 350-357.
  • 4Zhou X, Benson KF, Ashar HR, et al. Mutation responsible for mouse pygmy phenotype in the developmentally regulate factor HMGI-C [J ]. Nature, 1995, 376 (6543):771-774.
  • 5Aliano S, Cirmena G, Garuti A, et al. HMGA2 overexpression in polycythemia vera with t (12; 21) (q14; q22) [J]. Cancer Genet Cytogenet, 2007, 177 (2): 115- 119.
  • 6Etienne A, Carbuceia N, Adelaide J, et al, Rearrangements involving 12q in myeloproliferative disorders, possible role of HMGA2 and SOCS2 genes [J]. Cancer Genet Cytogenet, 2007, 176 (1): 80-88.
  • 7Storlazzi CT, Albano F, Locunsolo C, et al. t (3; 12) ( q26:q14 ) in polycythemia vera is associated with upregulation of the HMGA2 gene [J]. Leukernia , 2006, 20 (12): 2190-2192.
  • 8Pierantoni GM, Fedele M, Pentimalli F, et al. High mobility group Ⅰ(Y) proteins bind HIPK2, a serine threonine kinase protein which inhibits ceil growth [J]. Oncogene, 2001, 20 ( 43 ): 6132-6141.
  • 9Borrmann L, Schwanbeek R, Heyduk T, et al. High mobility group A2 protein and its derivatives bind a ,specific region of the promoler of DNA repair gene ERCC1 and modulate its activity [ J ]. Nucleic Acids Res, 2003, 31 (23): 6841-6851.
  • 10Hess JL. Chromosomal translocation in benign tumors. The HMGIproteins[J]. Am J Clin Pathol, 1998, 109 (3); 251-261.

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