"Bad luck" hypothesis and cancer prevention: translating the debate to more actions.
"Bad luck" hypothesis and cancer prevention: translating the debate to more actions.
复制标题
“坏运气”假说和癌症预防：将辩论转化为更多行动。
DOI：
10.1007/s10654-019-00489-3
复制
发表时间：
2019
影响因子：
13.6
通讯作者：
Song,Mingyang
中科院分区：
文献类型：
--
作者：
Song,Mingyang
病原学研究是生物学和流行病学的重要组成部分。对于癌症，在过去的几十年里，我们对癌症根本原因的生物学理解已经通过遗传研究得到了显着推进。现在人们普遍认为，癌症是基因突变积累的结果，这些突变连续增加细胞增殖[1]。另一方面，以人群为基础的流行病学研究集中在癌症的外在和遗传原因，并确定了各种可改变的风险因素。这些数据已被转化为有效的预防策略（如烟草控制），在很大程度上促成了近几十年来癌症死亡率的下降（如1991年至2016年美国癌症死亡率下降27%）。虽然癌症研究的两个主要分支-分子生物学和流行病学-都对癌症病因学做出了重大贡献，但它们在很大程度上是独立发展的，并且连接它们的线程通常很薄[3]。2015年，由Tomasetti和Vogelstein领导的一篇科学论文中的广泛争议直截了当地揭示了这种微弱的联系[4]。研究发现，（r= 0.81），得出结论，组织中癌症风险的变化只有三分之一可归因于环境因素（E）或遗传倾向（H），而大多数是由于干细胞分裂期间产生的随机突变（R），所谓的坏运气
Etiologic research constitutes an essential part of both biology and epidemiology. For cancer, our biological understanding about its root cause has been significantly advanced by genetic research in the past few decades. It is now widely accepted that cancer is the result of accumulation of gene mutations that successively increase cell proliferation [1]. On the other hand, population-based epidemiologic studies have focused on extrinsic and hereditary causes of cancer and identified a variety of modifiable risk factors. These data have been translated into effective prevention strategies (eg, tobacco control) that have largely contributed to the decline in cancer mortality in the recent decades (eg, 27% decrease between 1991 and 2016 in the United States)[2]. While each of the two major branches of cancer research—molecular biology and epidemiology—has made substantial contributions to cancer etiology, they have developed largely independently and the threads that connect them are often thin [3]. This thin connection is bluntly unfolded by the widespread controversies on a Science paper led by Tomasetti and Vogelstein in 2015 [4]. The study found a high correlation (r= 0.81) between the number of stem cell divisions of a given tissue and the lifetime risk of cancer in that tissue, leading to the conclusion that only a third of the variation in cancer risk among tissues is attributable to environmental factors (E) or hereditary predispositions (H), while most is due to random mutations (R) arising during stem cell divisions, so-called bad luck.