Cancer risk: Role of environment

作者: N. A. Ashford , P. Bauman , H. S. Brown , R. W. Clapp , A. M. Finkel

DOI: 10.1126/SCIENCE.AAA6246

关键词:

摘要: The Report “Variation in cancer risk among tissues can be explained by the number of stem cell divisions” (C. Tomasetti and B. Vogelstein, 2 January, p. [78][1]) is dangerously misleading because it understates role prevention causation. It widely acknowledged that many cancers a two-step process: initiation one or series mutations, followed promotion genetic “mistake” to recognizable tumor blood disease ([ 1 ][2]). observation replication mistake may proceed at different rates no doubt correct. However, some mutations are initiated chemical viral exposures, others occur without known cause. ![Figure][3] ILLUSTRATION: G. GRULLON/ SCIENCE Promotion DNA damage occurs both cases. conclusion “stochastic effects be…distinguished from external environmental factors” an inaccurate statement rests on false dichotomy. An influence fact create change which, if present when copied, subsequently “fixed” into genome as permanent change. more replications, less time there for repair take place before next copying/fixation event. Thus, correlation between frequency copying events lifetime risks does not imply influences play lesser causation those same mutations. age-adjusted vary substantially countries where statistics kept, workplaces communities differ demonstrates large fraction influenced factors ][4]). What authors' work suggests stochastic differences occurrence distinguished factors. This distinction far trivial. Furthermore, “[t]he concept underlying current genomic changes simply chance during rather than result carcinogenic ignores event must have taken mutation replicated. paper obscures incidence initiating leading cancer. 1. [↵][5] 1. D. Hanahan, 2. R. A. Weinberg , Cell 144, 646 (2011). [OpenUrl][6][CrossRef][7][PubMed][8][Web Science][9] 2. [↵][10] IARC, Cancer Incidence Five Continents, Vol. X (International Agency Research Cancer, Lyon, France, 2013). [1]: /lookup/doi/10.1126/science.1260825 [2]: #ref-1 [3]: pending:yes [4]: #ref-2 [5]: #xref-ref-1-1 "View reference text" [6]: {openurl}?query=rft.jtitle%253DCell%26rft.stitle%253DCell%26rft.aulast%253DHanahan%26rft.auinit1%253DD.%26rft.volume%253D144%26rft.issue%253D5%26rft.spage%253D646%26rft.epage%253D674%26rft.atitle%253DHallmarks%2Bof%2Bcancer%253A%2Bthe%2Bnext%2Bgeneration.%26rft_id%253Dinfo%253Adoi%252F10.1016%252Fj.cell.2011.02.013%26rft_id%253Dinfo%253Apmid%252F21376230%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [7]: /lookup/external-ref?access_num=10.1016/j.cell.2011.02.013&link_type=DOI [8]: /lookup/external-ref?access_num=21376230&link_type=MED&atom=%2Fsci%2F347%2F6223%2F727.1.atom [9]: /lookup/external-ref?access_num=000288007100007&link_type=ISI [10]: #xref-ref-2-1 text"

参考文章(2)
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Douglas Hanahan, Robert A. Weinberg, Hallmarks of cancer: the next generation. Cell. ,vol. 144, pp. 646- 674 ,(2011) , 10.1016/J.CELL.2011.02.013