Abstract
Tomasetti and Vogelstein recently proposed that the majority of variation in cancer risk among tissues is due to "bad luck," that is, random mutations arising during DNA replication in normal noncancerous stem cells. They generalize this finding to cancer overall, claiming that "the stochastic effects of DNA replication appear to be the major contributor to cancer in humans." We show that this conclusion results from a logical fallacy based on ignoring the influence of population heterogeneity in correlations exhibited at the level of the whole population. Because environmental and genetic factors cannot explain the huge differences in cancer rates between different organs, it is wrong to conclude that these factors play a minor role in cancer rates. In contrast, we show that one can indeed measure huge differences in cancer rates between different organs and, at the same time, observe a strong effect of environmental and genetic factors in cancer rates.
Highlights
Tomasetti and Vogelstein recently proposed that the majority of variation in cancer risk among tissues is due to “bad luck,” that is, random mutations arising during DNA replication in normal noncancerous stem cells
They conclude from this that the majority of variation in cancer risk among tissues is due to “bad luck,” that is, random mutations arising during DNA replication in normal noncancerous stem cells
The logical fallacy is to extrapolate that, because environmental and genetic factors cannot explain the huge differences in cancer rates between different organs, these factors play a minor role in cancer rates
Summary
Tomasetti and Vogelstein recently proposed that the majority of variation in cancer risk among tissues is due to “bad luck,” that is, random mutations arising during DNA replication in normal noncancerous stem cells. Correspondence Tomasetti and Vogelstein showed 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 organ-specific tissue’s homeostasis [1].
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