首页膀胱肿瘤诊断证据详情

A network meta-analysis of the PD(L)-1 inhibitors in the salvage treatment of urothelial bladder cancer

原文: 2018 年 发布于 Immunotherapy 10 卷 第 6 期 E113-E117 浏览量:302次

作者: Rassy E. E. Bakouny Z. Aoun F. Haddad F. G. Sleilaty G. Assi T. Kattan J.

作者单位: Cancer Survivorship and Treatment Late Effects, Department of Oncology, Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark. Department of Oncology, 5073, Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark. Department of Midwifery, Physiotherapy, Occupational Therapy and Psychomotor Therapy. University College Copenhagen, Faculty of Health, Copenhagen, Denmark. Geriatric Research Unit, Department of Geriatric and Palliative Medicine, Bispebjerg and Frederiksberg Hospital-Bispebjerg, Copenhagen, Denmark Geriatric Research Unit, Department of Medicine, Herlev and Gentofte Hospitals, Herlev Denmark CopenAge-Copenhagen Center for Clinical Age Research, University of Copenhagen, Copenhagen, Denmark. Cancer Survivorship and Treatment Late Effects, Department of Oncology, Rigshospitalet, University Hospital of Copenhagen, Copenhagen, Denmark. Electronic address: bolette.skjoedt.rafn@regionh.dk.

归属分类: 膀胱肿瘤诊断证据

DOI: 10.1080/0284186x.2021.1880025

关键词: *Health Status Humans *Life Style *Quality of Life Survivors/*psychology Urinary Bladder Neoplasms/*psychology/therapy Bladder cancer Diet Exercise Lifestyle factors Quality of life Smoking Urothelial carcinoma

文献简介

N-acetyltransferase 1 (NAT1), a polymorphic Phase II enzyme, plays an essential role in metabolizing heterocyclic and aromatic amines, which are implicated in urinary bladder cancer (BCa). This systematic review investigates a possible association between the different NAT1 genetic polymorphisms and BCa risk. Medline, PubMed, EMBASE, Scopus, Web of Science, OpenGrey, and BASE databases were searched to identify eligible studies. The random-effect model was used to calculate pooled effects estimates. Statistical heterogeneity was tested with Chi-square and I(2). Twenty case-control studies, including 5606 cases and 6620 controls, met the inclusion criteria. Pooled odds ratios (OR) analyses showed a statistically significant difference in NAT1*10 versus non-NAT1*10 acetylators in the total sample (OR: 0.87; 95% CI: 0.79-0.96) but was borderline among Caucasians (OR: 0.88 with 95% CI: 0.77-1.01). No statistically significant differences in BCa risk were found for: NAT1*10 versus NAT1*4 wild type (OR: 0.97; 95% CI: 0.78-1.19), NAT1 'Fast' versus 'Normal' acetylators (OR: 1.03; 95% CI: 0.84-1.27), and NAT1 'Slow' versus 'Fast' (OR: 2.32; 95% CI: 0.93-5.84) or 'Slow' versus 'Normal' acetylators (OR: 1.84; 95% CI: 0.92-3.68). When stratifying by smoking status, no statistically significant differences in BCa risk were found for NAT1*10 versus non-NAT1*10 acetylators among the different subgroups. Our study suggests a modest protective role for NAT1*10 and a possible risk contributory role for slow acetylation genotypes in BCa risk. Further research is recommended to confirm these associations.

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