In a large, population-based case–control study in New England, we recently reported a positive exposure-response relationship between cumulative arsenic intake from drinking water and bladder cancer risk (odds ratio [OR] for quartile 4 vs quartile 1 = 1.32, 95% confidence interval [CI] = 1.02 to 1.72; OR = 1.37, 95% CI = 1.03 to 1.82, for exposure lagged 40 years) (Supplementary Table 1, available online) (1). The mechanism by which arsenic induces bladder cancer is not well understood, although several studies have suggested arsenic may target important tumor-suppresser genes (p16, Rb) and disrupt cell cycle control (2). Here, we show heterogeneity in the arsenic–bladder cancer risk relationship by tumor expression of these cell cycle proteins.

中文翻译：

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RE：新英格兰北部膀胱癌升高：饮用水和砷的作用。


在新英格兰的一项大型人群病例对照研究中，我们最近报告了饮用水中累积砷摄入量与膀胱癌风险之间存在正暴露-反应关系（第 4 分位数与第 1 分位数的比值比 [OR] = 1.32， 95% 置信区间 [CI] = 1.02 至 1.72；OR = 1.37，95% CI = 1.03 至 1.82，暴露时间滞后 40 年）（补充表 1 ，可在线获取）(1)。尽管一些研究表明砷可能以重要的肿瘤抑制基因 (p16、Rb) 为目标并破坏细胞周期控制 (2)，但砷诱发膀胱癌的机制尚不清楚。在这里，我们通过这些细胞周期蛋白的肿瘤表达来显示砷与膀胱癌风险关系的异质性。