An evolutionary paradigm for carcinogenesis?

An evolutionary paradigm for carcinogenesis?
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致癌的进化范式?

DOI:
10.1136/jech.57.2.89
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发表时间:
2003
影响因子:
6.3
通讯作者:
Maurizio Manuguerra
Maurizio Manuguerra
中科院分区:
医学2区
文献类型:
--
作者:
Paolo Vineis;G. Matullo;Maurizio Manuguerra

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突变似乎只是致癌机制之一。突变克隆的选择是第二个关键机制。癌症发生的进化(达尔文)理论可用于解释流行病学的一些相互矛盾的观察结果,并为癌症发生提供一个共同的理论框架。在物种选择和致癌作用(突变细胞的选择)中,突变和选择可以被解释为必要原因和不充分原因。选择以克隆之间的竞争为前提,即突变物种的生存优势;没有选择力,突变是无声的,而缺乏突变则使选择优势变得不可能。致癌物相关指纹的识别是不明确的:它既可以表明致癌刺激物留下的真正突变热点(如烟草相关的 p53 突变),也可以表明其突变似乎不具有暴露特异性的克隆的选择性优势(如黄曲霉毒素的情况)。我们提出了几个暴露的例子,这些暴露可能增加人类患癌症的风险,不是通过突变,而是通过假定的克隆选择机制。
Mutations seem to be only one of the mechanisms involved in carcinogenesis; selection of mutated clones is a second crucial mechanism. An evolutionary (darwinian) theory of carcinogenesis can be useful to explain some contradictory observations of epidemiology, and to provide a common theoretical framework for carcinogenesis. In both the selection of species and in carcinogenesis (selection of mutated cells), mutation and selection can be interpreted as necessary and insufficient causes. Selection presupposes competition among clones—that is, survival advantage of the mutated species; without selective forces a mutation is mute, while the lack of mutations makes selective advantage impossible. The identification of carcinogen related fingerprints is ambiguous: it can suggest both a genuine mutational hotspot left by the carcinogenic stimulus (like in tobacco related p53 mutations), and selective advantage of clones whose mutations seem to be not exposure specific (like in the case of aflatoxin). We present several examples of exposures that can increase the risk of cancer in humans not via mutations but through a putative mechanism of clone selection.
DOI: 10.1093/oxfordjournals.aje.a009507
发表时间: 1998-04-01
影响因子: 5
作者:
Smith, AH;Goycolea, M;Biggs, ML
通讯作者: Biggs, ML
DOI: 10.1073/pnas.180320897
发表时间: 2000-10-24
影响因子: 11.1
作者:
Rodin, SN;Rodin, AS
通讯作者: Rodin, AS
DOI: 10.1073/pnas.93.24.14025
发表时间: 1996-11-26
影响因子: 11.1
作者:
Jonason, AS;Kunala, S;Brash, DE
通讯作者: Brash, DE
DOI: 10.1093/carcin/20.5.785
发表时间: 1999-05-01
期刊: CARCINOGENESIS
影响因子: 4.7
作者:
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通讯作者: Chapkin, RS