A new study on the “bad luck” of cancer is a wonderful contribution to science but is being severely misinterpreted by both science writers and the media.
This study is the first of its kind to accurately quantify the probability of the development of a cancer cell in any given tissue over a lifetime. It supports other hypotheses stating that increased frequency of cell division, which is also a hallmark of cellular aging, leads to increased risk of cancer. However, it is not representative of a cancer cell’s ultimate destiny. New cancer cells form in our bodies everyday and our immune system destroys them. We’ve known for 20+ years that tissues that are prone to faster cell division and turnover, like colon and skin, have a higher probability of developing cancer cells. This is why inflammation is strongly associated with the development of cancer. Inflammation from immune activity causes rapid damage and therefore places a high demand on the affected tissue for renewal by cell division. Thus, a higher frequency cell division results in a higher statistical probability that mutations will occur, cancer cells will develop and one of them might escape under the immune system’s radar. An example; we know that cigarette smoking leads to a much higher risk of developing lung cancer. There are two parts to this. One is the simple carcinogenicity of some of the chemicals in cigarette smoke. However, a much larger role is played by the fact that the body responds to cigarette smoke by launching an immune response that leads to increased inflammation, increased cellular replacement, impaired cellular death and diminished tissue cleanup,.
Most importantly, the cancer risk study excludes any statistics on breast and prostate cancers. Perhaps these were intentionally excluded from the study as edge cases since their occurrence in the general population is 300% higher than any of the cancers included in the study. Because these tissues are hormone-sensitive, they are highly susceptible to influence by external factors. Hundreds of studies have established their extreme vulnerability to chemicals that mimic estrogen and stimulate rapid growth and cell division. This parallels the theme of this recent study suggesting that faster cell division leads to a high probability of mutations and cancer cell development. Including these two types of cancer in the study’s statistics could increase their external influence factor by as much as 20%.
Although there are some correlations it is important to note that the probabilities in the study do not evenly parallel rates of cancer incidence in the US. For example the study shows, stem cell divisions in colorectal cells as being significantly higher but than in lung but cancer statistics show that the incidence of these cancers is flip flopped.
While this information is invaluable for quantifying cancer cell development, it is missing significant aspects of our basis of cancer knowledge and statistics and by no means establishes final numbers or parameters for cancer risk or its influence by external factors.
 Cristian Tomasetti, Bert Vogelstein. Variation in Cancer Risk Among Tissues can be Exlapined by the Number of Stem Cell Divisions. Science 2 January 2015 Vol. 347 no. 6217 pp. 78-81. DOI: 10.1126/science.1260825
 Steve Horvath. DNA Methylation Age of Human Tissue and Cell Types. Genome Biology 2013 12:R115 doi:10.1186/gb-2013-14-10-r115
 Naotaka Noda, Koichiro Matsumoto, Soturu Fukuyama, Yukari Asia, Hiroko Kitajima, Nanae Seki, Yuko Matsunaga, Keiko Kan-o, Atsushi Moriwaki, Konosuke Morimoto, Hiromasa Inoue and Yoichi Nakanishi. Cigarette Smoke Impairs Phagocytosis of Apoptotic Neutrophils by Alveolar Macrophages Via Inhibition of Histone Deacetylase/Rac/CD9 Pathways. Int. Immunol. (2013) 25 (11) 643-650. doi: 10.1093/intimm/dxt033
 Susan JM Hoonhorst, Wim Timens, Leo Koenderman, Adele T Lo Tam Loi, Jan-Willem J Lammers, H Marike Boezen, Antoon JM van Ossterhout, Dirkje S Postma, Nick HT ten Hacken. Increaded Activation of Blook Neutrophils After Cigarette Smoking in Young Individuals Susceptible to COPD. Respiratory Research 2014 15:121 doi:10.1186/s12931-014-0121-2