IL1RN and KRT13 Expression in Bladder Cancer: Association with Pathologic Characteristics and Smoking Status.
IL1RN and KRT13 Expression in Bladder Cancer: Association with Pathologic Characteristics and Smoking Status.
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DOI：
10.1155/2014/184602
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发表时间：
2014
影响因子：
1.4
通讯作者：
Bolenz C
中科院分区：
文献类型：
--
作者：
Worst TS;Reiner V;Gabriel U;Weiß C;Erben P;Martini T;Bolenz C
目的.验证微阵列数据的细胞角蛋白13（KRT 13）和白细胞介素-1受体拮抗剂（IL-1 RN）的表达在膀胱尿路上皮癌（UCB），并与我们的研究结果与病理特征和吸烟。 方法. UCB组织样本（n = 109）和对照样本（n = 14）来自经尿道切除术和根治性膀胱癌标本。进行KRT 13和IL 1 RN的免疫组织化学染色，并评估半定量表达评分。使用标准化问卷评估吸烟状况。表达评分与病理特征（肿瘤分期和分级）和吸烟状况相关。结果与KRT 13和IL 1 RN表达高的对照相比，在UCB组织样品中观察到KRT 13和IL 1 RN表达的缺失（P = 0.007，P = 0.008）。肌肉浸润性肿瘤中IL 1 RN表达显着降低（P = 0.003）。在当前吸烟者的组织样本中，与从不吸烟者相比，发现IL 1 RN显著下调（P = 0.013）。结论KRT 13和IL 1 RN的表达减少是UCB的共同特征，并与侵袭性疾病相关。吸烟可能会增加IL 1 RN的丢失，表明参与UCB进展的促炎介质过多。进一步验证吸烟对IL 1 RN表达的影响是必要的。
Purpose. To validate microarray data on cytokeratin 13 (KRT13) and interleukin-1 receptor antagonist (IL1RN) expression in urothelial carcinoma of the urinary bladder (UCB) and to correlate our findings with pathologic characteristics and tobacco smoking. Methods. UCB tissue samples (n = 109) and control samples (n = 14) were obtained from transurethral resection and radical cystectomy specimens. Immunohistochemical staining of KRT13 and IL1RN was performed and semiquantitative expression scores were assessed. Smoking status was evaluated using a standardized questionnaire. Expression scores were correlated with pathologic characteristics (tumor stage and grade) and with smoking status. Results. Loss of KRT13 and IL1RN expression was observed in UCB tissue samples when compared to controls (P = 0.007, P = 0.008) in which KRT13 and IL1RN expression were high. IL1RN expression was significantly reduced in muscle-invasive tumors (P = 0.003). In tissue samples of current smokers, a significant downregulation of IL1RN was found when compared to never smokers (P = 0.013). Conclusion. Decreased expressions of KRT13 and IL1RN are common features of UCB and are associated with aggressive disease. Tobacco smoking may enhance the loss of IL1RN, indicating an overweight of proinflammatory mediators involved in UCB progression. Further validation of the influence of smoking on IL1RN expression is warranted.