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Cancer due to bad luck? Comment by Prof Gilles-Eric Séralini

Tuesday 6 January 2015

Cancer due to bad luck?

Comment by Prof Gilles-Eric Séralini (January 2015) on "The role of chance reassessed in cancers" (article in the newspaper Le Monde, January 3, 2015, p.5)

A number of questions were raised in the media after the publication of the article by Tomasetti and Vogelstein, based in Baltimore, MD, USA (Science 347, 6217, 78-81, 2015), on the alleged role of chance (or “bad luck”) in cancer. This article actually shows a strong correlation between the number of cell divisions found in an organ to renew the tissues and the number of cancers, as reflected in the title of the study: "Variation in cancer risk among tissues can be explained by the number of stem cell divisions".

 

This result is not surprising. To register and reproduce a mutation, including a cancer-causing mutation, a cell must multiply. The authors suggest that this is due to chance, but that hypothesis is not studied in the article. The ubiquitous impregnation of DNA by pollutants (known as adducts) from the fetal period and constantly renewed in our body throughout life1 may just as well explain this result. A staggering number of carcinogens, hormone disrupters or neuro-disrupters have been authorized for release in the order of billions of tonnes everywhere on the planet since the World War II, while almost nobody cares about the laxity of the tests approved by experts in regulatory bodies, nor their transparency.

 

To say that the chances of road accidents (by analogy, likening this to cancer) are correlated to the number of crossings (cell divisions) would not be surprising either, but that would not exclude the effect of the intensity of traffic (pollutants) on “chance”. In other words, the more traffic there is, the more accidents will occur, even if we choose to call that rise in accidents “chance” or “bad luck”. Reductionist and ignorant thinking about the ubiquitous presence of environmental pollutants, even among scientists, can only make us underestimate the growing influence of these substances on chronic diseases.

 

 

1. Documented in the book, Culinary Delights or Hidden Poisons? by GE Séralini and J Douzelet (Actes Sud, 2014).


 

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Science. 2015 Jan 2;347(6217):78-81. doi: 10.1126/science.1260825.

Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions.

Tomasetti C1, Vogelstein B2.

 

Author information
1. Division of Biostatistics and Bioinformatics, Department of Oncology, Sidney Kimmel Cancer Center, Johns Hopkins University School of Medicine and Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, 550 North Broadway, Baltimore, MD 21205, USA. ctomasetti@jhu.edu vogelbe@jhmi.edu.
2. Ludwig Center for Cancer Genetics and Therapeutics and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, 1650 Orleans Street, Baltimore, MD 21205, USA. ctomasetti@jhu.edu vogelbe@jhmi.edu.


Abstract
Some tissue types give rise to human cancers millions of times more often than other tissue types. Although this has been recognized for more than a century, it has never been explained. Here, we show that the lifetime risk of cancers of many different types is strongly correlated (0.81) with the total number of divisions of the normal self-renewing cells maintaining that tissue's homeostasis. These results suggest that only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to "bad luck," that is, random mutations arising during DNA replication in normal, noncancerous stem cells. This is important not only for understanding the disease but also for designing strategies to limit the mortality it causes.
Copyright  2015, American Association for the Advancement of Science.