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电离辐射与血液系统恶性肿瘤:改变适应性景观。

Ionizing radiation and hematopoietic malignancies: altering the adaptive landscape.

机构信息

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

出版信息

Cell Cycle. 2010 Aug 1;9(15):3005-11. doi: 10.4161/cc.9.15.12311. Epub 2010 Aug 7.

Abstract

Somatic evolution, which underlies tumor progression, is driven by two essential components: (1) diversification of phenotypes through heritable mutations and epigenetic changes and (2) selection for mutant clones which possess higher fitness. Exposure to ionizing radiation (IR ) is highly associated with increased risk of carcinogenesis. This link is traditionally attributed to causation of oncogenic mutations through the mutagenic effects of irradiation. On the other hand, potential effects of irradiation on altering fitness and increasing selection for mutant clones are frequently ignored. Recent studies bring the effects of irradiation on fitness and selection into focus, demonstrating that IR exposure results in stable reductions in the fitness of hematopoietic stem and progenitor cell populations. These reductions of fitness are associated with alteration of the adaptive landscape, increasing the selective advantages conferred by certain oncogenic mutations. Therefore, the link between irradiation and carcinogenesis might be more complex than traditionally appreciated: while mutagenic effects of irradiation should increase the probability of occurrence of oncogenic mutations, IR can also work as a tumor promoter, increasing the selective expansion of clones bearing mutations which become advantageous in the irradiation-altered environment, such as activated mutations in Notch1 or disrupting mutations in p53.

摘要

体细胞进化是肿瘤进展的基础,它由两个基本组成部分驱动:(1)通过遗传突变和表观遗传变化使表型多样化;(2)选择具有更高适应性的突变克隆。电离辐射(IR)暴露与致癌风险增加高度相关。这种联系传统上归因于照射的诱变作用导致致癌突变。另一方面,照射对改变适应性和增加对突变克隆选择的潜在影响经常被忽视。最近的研究将照射对适应性和选择的影响作为焦点,表明 IR 暴露导致造血干细胞和祖细胞群体适应性的稳定降低。这些适应性的降低与适应性景观的改变有关,增加了某些致癌突变赋予的选择性优势。因此,照射与致癌之间的联系可能比传统上认为的更为复杂:虽然照射的诱变作用应该增加致癌突变发生的概率,但 IR 也可以作为肿瘤促进剂,增加在照射改变的环境中具有优势的携带突变的克隆的选择性扩张,例如 Notch1 中的激活突变或 p53 中的破坏突变。

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