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将癌症与其病因联系起来需要考虑对组织微环境的影响。

Connecting Cancer to Its Causes Requires Incorporation of Effects on Tissue Microenvironments.

作者信息

DeGregori James

机构信息

Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Aurora, Colorado.

出版信息

Cancer Res. 2017 Nov 15;77(22):6065-6068. doi: 10.1158/0008-5472.CAN-17-1207. Epub 2017 Jul 28.

DOI:10.1158/0008-5472.CAN-17-1207
PMID:28754675
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5690828/
Abstract

In a recent article in , Tomasetti and colleagues present an expanded model for cancer risk, which they claim demonstrates the relative contribution of mutations caused by replication errors, environment, and heredity. The foundation of this model is the theory that the overwhelming driver of cancer risk is mutations. This perspective will present experimental evidence and evolutionary theory to challenge the basis of this underlying theory. An argument will be presented that the mutation-centric model of cancer suggests unrealistic solutions to cancer and distracts the research community from more promising approaches that consider tissue context. .

摘要

在最近发表于《》的一篇文章中,托马塞蒂及其同事提出了一个扩展的癌症风险模型,他们声称该模型展示了由复制错误、环境和遗传导致的突变的相对贡献。这个模型的基础理论是,癌症风险的主要驱动因素是突变。本文将提供实验证据和进化理论来挑战这一基础理论。我们将论证,以突变为中心的癌症模型提出的癌症解决方案不切实际,并使研究界偏离了更有前景的考虑组织背景的方法。