The role of β-catenin signaling in the malignant potential of cystitis glandularis

被引:45
作者
Bryan, RT [1 ]
Nicholls, JH
Harrison, RF
Jankowski, JA
Wallace, DMA
机构
[1] Queen Elizabeth Hosp, Dept Urol, Birmingham B15 2TH, W Midlands, England
[2] Univ Birmingham, Dept Pathol, Birmingham, W Midlands, England
[3] Univ Birmingham, Epithelial Lab, Birmingham, W Midlands, England
[4] Univ Leicester, Leicester Royal Infirm, Dept Med, Leicester, Leics, England
[5] Univ Leicester, Leicester Royal Infirm, Dept Oncol, Leicester, Leics, England
关键词
bladder; cadherins; cystitis; inflammation; metaplasia;
D O I
10.1097/01.ju.0000092740.51330.39
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Purpose: Chronic inflammation is a risk factor for malignant transformation in the bladder. The pro-inflammatory cytokine tumor necrosis factor-alpha (TNFalpha) is a mediator of such inflammation that induces nuclear localization of the adherens junction component beta-catenin. This mechanism has a key role in the initiation and progression of the premalignant lesion Barrett's metaplasia of the esophagus. Cystitis glandularis is a metaplastic lesion of the bladder urothelium occurring in the presence of chronic inflammation and in up to 13% of asymptomatic bladders. Two subtypes are described (typical and intestinal/colonic) with uncertain malignant potential. Etiologically and histologically cystitis glandularis mimics Barrett's metaplasia. We investigated the roles of beta-catenin and TNFalpha in cystitis glandularis. Materials and Methods: Immunohistochemistry and immunofluorescence were used to demonstrate the expression and localization of E-cadherin, beta-catenin and TNFalpha in 9 sections of typical cystitis glandularis and 4 of intestinal/colonic cystitis glandularis. Appropriate controls were used for all experiments. Results: Immunohistochemistry demonstrated normal membranous expression of E-cadherin and beta-catenin in all cystitis glandularis sections with increased TNFalpha expression. Immunofluorescence showed nuclear localization of beta-catenin in the intestinal/colonic subtype only, which was not observed in typical cystitis glandularis. Conclusions: The presence of nuclear beta-catenin suggests that intestinal/colonic cystitis glandularis shares the same signaling pathway with the premalignant lesion Barrett's metaplasia of the esophagus and the intestinal/colonic subtype of cystitis glandularis may have the potential to progress to malignancy. This finding has important implications for the management of this lesion.
引用
收藏
页码:1892 / 1896
页数:5
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