Tissues with high cell turnover rates do not have correspondingly high cancer rates
the verdict
SUPPORTED
the evidence backs this
refutedsupported
the weight of evidence
2 sources for · 0 against
Peer-reviewed literature indicates that simple proportional models linking high stem cell division rates to cancer risk fail because tissues utilize adaptive cancer suppression mechanisms.
Abstract Since most cancers are initiated by driver mutations arising in somatic cells, the risk of cancer should be explained by the probability of driver mutations as a function of the product of the number of stem cells and the stem cell division rate for a tissue. However, such models of driver-mutation initiated carcinogenesis fail to adequately predict cancer risk. It has been suggested that the missing component is greater adaptive cancer suppression in large tissues with high rates of stem cell division. This 8 may manifest as either a greater number of driver mutations required to initiate cancer or a lower stem cell mutation rate. These hypotheses are tested here using nonlinear regression to fit models that incorporate variation in the number of driver mutations and the stem cell mutation rate to data on the tissue-specific cancer risk, number of stem cells, and stem cell division rate. The greatest concordance between predicted and observed cancer risks is obtained by single driver mutations across tissues and stem cell mutation rates that decline with increasing lifetime numbers of stem cell divisions. This provides evidence of adaptive cancer suppression among tissues.
Compiled data for the stem cell numbers, Ns, and division rates, ms, is reanalized in order to show that we can distinguish two groups of human tissues. In the first one, there is a relatively high fraction of maintenance (stem and transit) cells in the tissue, but the division rates are low. The second group, on the other hand, is characterized by very high transit cell division rates, of around one division per day. These groups do not have an embrionary origin. We argue that their properties arise from a combination of the needs of tissue homeostasis (in particular turnover rate) and a bound on cancer risk, which is roughly a linear function of the product Ns ms. The bound on cancer risk leads to a threshold at ms = 8/year, where the fraction of stem cells falls down two orders of magnitude.
Everything we examined (2)
This check searched the claim as stated. It did not run a separate search for evidence against it.