As I have got older, I have become increasingly aware of how much luck plays in one’s life, both for good and bad. Looking back, I realize the many, many occasions when it was due to luck that things turned out well or badly for me and I have no reason to think that luck does not play a similar important role for other people.
This does not mean that one’s own efforts and attitudes are not important. They play a significant role mainly in not throwing away the chances that good luck hands you and enabling one to cope with, and recover from, bad luck.
One important area of luck is of course one’s health. And it turns out that when it comes to getting cancer, the role played by luck is greater than one might have thought, as the abstract from this paper suggests.
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. [My italics-MS]
In the body of the paper Variation in cancer risk among tissues can be explained by the number of stem cell divisions, the authors Cristian Tomasetti and Bert Vogelstein elaborate on their work.
The concept underlying the current work is that many genomic changes occur simply by chance during DNA replication rather than as a result of carcinogenic factors. Since the endogenous mutation rate of all human cell types appears to be nearly identical (23, 24), this concept predicts that there should be a strong, quantitative correlation between the lifetime number of divisions among a particular class of cells within each organ (stem cells) and the lifetime risk of cancer arising in that organ.
To test this prediction, we attempted to identify tissues in which the number and dynamics of stem cells have been described. Most cells in tissues are partially or fully differentiated cells that are typically short-lived and unlikely to be able to initiate a tumor. Only the stem cells—those that can self-renew and are responsible for the development and maintenance of the tissue’s architecture—have this capacity. Stem cells often make up a small proportion of the total number of cells in a tissue and, until recently, their nature, number, and hierarchical division patterns were not known.
Through an extensive literature search, we identified 31 tissue types in which stem cells had been quantitatively assessed (see the supplementary materials). We then plotted the total number of stem cell divisions during the average lifetime of a human on the x axis and the lifetime risk for cancer of that tissue type on the y axis.
The correlation between these two very different parameters—number of stem cell divisions and lifetime risk—was striking, with a highly positive correlation (Spearman’s rho = 0.81; P < 3.5 × 10-8). Pearson’s linear correlation 0.804 [0.63 to 0.90; 95% confidence interval (CI)] was equivalently significant (P < 5.15 × 10-8). One of the most impressive features of this correlation was that it extended across five orders of magnitude, thereby applying to cancers with enormous differences in incidence. No other environmental or inherited factors are known to be correlated in this way across tumor types.
The wrong lesson to draw from this study (assuming that the finding holds up in later work) is that we do not need to worry that much about carcinogens in the environment and in food and cigarettes. We should definitely continue to reduce our exposure to such things. But it does mean that those of us who try to live healthy lives and yet develop cancer may be just the victims of bad luck and there is no point wringing our hands and second-guessing ourselves by thinking that we did something wrong.
The authors say that their work may shed some light on which types of cancers are most likely to respond to preventative treatments. Jennifer Couzin-Frankel writes more about the paper.