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CD163+ macrophages predict a poor prognosis in patients with primary T1 high-grade urothelial carcinoma of the bladder.
World Journal of Urology ( IF 2.8 ) Pub Date : 2019-03-15 , DOI: 10.1007/s00345-018-02618-1
Guoliang Yang 1 , Lianhua Zhang 1 , Mengyao Liu 2 , Qiang Liu 3 , Xuehui Duan 1 , Juanjie Bo 1
Affiliation  

PURPOSE Macrophages are a major cell type that can infiltrate solid tumors and exhibit distinct phenotypes in different tumor microenvironments. This study investigates the prognostic value of tumor-infiltrated CD163+ macrophages in patients with T1 high-grade (T1HG) bladder cancer. METHODS CD163+ macrophages were assessed by immunohistochemistry in 94 T1HG bladder cancer samples. Kaplan-Meier analyses and Cox proportional hazards' regression models were applied to evaluate recurrence-free survival, progression-free survival and disease-specific survival. RESULTS With a median follow-up of 60 months, 37 (39.4%) patients experienced disease recurrence, 14 (14.9%) progression, 11 (11.7%) disease-specific mortality. High CD163+ macrophages were associated with higher risk of disease recurrence and progression (P < 0.05, for both). In multivariate Cox proportional hazards regression analysis, high CD163+ macrophages were a significant negative predictor of recurrence-free survival, progression-free survival and disease-specific survival (P < 0.05 for all). CONCLUSION CD163+ macrophages are a poor prognostic factor in T1HG bladder cancer. This finding provide the ground for further testing it in predicting the outcome of this challenging disease.

中文翻译:

CD163 +巨噬细胞预示着原发性T1高度膀胱尿路上皮癌患者的预后不良。

目的巨噬细胞是一种主要的细胞类型,可以浸润实体瘤并在不同的肿瘤微环境中表现出不同的表型。这项研究调查了肿瘤浸润的CD163 +巨噬细胞在T1级(T1HG)膀胱癌患者中的预后价值。方法采用免疫组织化学方法对94例T1HG膀胱癌样本进行CD163 +巨噬细胞评估。Kaplan-Meier分析和Cox比例风险回归模型用于评估无复发生存,无进展生存和疾病特异性生存。结果中位随访60个月,有37例(39.4%)患者复发疾病,14例(14.9%)进展,11例(11.7%)疾病特异性死亡率。高CD163 +巨噬细胞与更高的疾病复发和进展风险相关(两者均P <0.05)。在多变量Cox比例风险回归分析中,高CD163 +巨噬细胞是无复发生存,无进展生存和疾病特异性生存的显着阴性预测指标(所有P均<0.05)。结论CD163 +巨噬细胞是T1HG膀胱癌的不良预后因素。这一发现为进一步测试它,以预测这种具有挑战性的疾病的结果提供了基础。
更新日期:2019-11-01
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