[nonbel]

>"The original implementation of the Armitage-Doll model contains simplifications made for computational reasons"

Quoting myself rather than editing...Actually, I forgot they come right out and say it:

"This result will be valid for large values of t (of the order of a human lifetime) provided that p1t, p2t, y, prt are all sufficiently small (as could be assumed in an application of this theory to human cancer)." http://www.nature.com/bjc/journal/v91/n12/pdf/6602297a.pdf

But with low probability of mutation at a given site p, how can you get their model to turnover (as is seen in the age specific incidence data)? I don't think you can, however the turnovers easily appear if you allow high mutation rates along with high clearance rates. But those high mutation rates are inconsistent with the estimated mutation rates in human cells.

Anyway, I hope someone checks into it because something is wrong with the mainstream model of carcinogenesis.

Edit:

It is also possible the data used to give the age-specific incidence (ie SEER) is fatally flawed and those turnovers are artefacts.