Radiation induced cancer arises from a somatic mutation

Abstract

Experimental data from the literature are presented to create a chain which links radiation induced cancer in animals to cell reproductive death and then to chromosomal aberrations and somatic mutations. The cancer data reveal the same peak value of cancer induction following different radiation exposures which leads to an association between cancer induction and cell killing. Other data show a direct correlation between cell survival and chromosomal aberration yield independent of whether a sensitiser is used or not. Data on the induction of somatic mutations in mammalian cultured cells show the same direct relationship between mutation frequency and cell killing following neutron and gamma ray exposures. Taken as a whole, the experimental data provide convincing evidence that radiation induced cancer arises from chromosomal damage.

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“…This is the same form as Chadwick and Leenhouts (2011) derive for their special case (see equation ( 3)).…”

“…The same peak height implication is important because it allows the experimental data on radiation induced cancer in animals to be used to conclude that the lesions involved are the same type. It does not say anything about the nature of the lesions but, using correlations of cell sterilisation with chromosome aberrations and somatic mutations in cellular radiobiological data and that shown in our paper (Chadwick and Leenhouts (2011)), we can conclude with some confidence that radiation-induced cancer arises from a somatic mutation.…”

“…In a recent paper, Chadwick and Leenhouts (2011) utilise linear-quadratic dose kinetics to demonstrate that the maximum value of cancer incidence, CI m , is independent of the linear and quadratic coefficients of the dose-response relationship. In brief, they assume that the lesions responsible for cell sterilisation and cancer induction follow the same kinetics such that:…”

“…I consider this extension of the argument of Chadwick and Leenhouts (2011) to be of some importance because it emphasises that the peak incidence is not only independent of the coefficients in the underlying dose-response relationship, but is independent of the form of that dose-response relationship. Specifically, it applies whether the relationship f (D) is sub-linear, linear or supra-linear in D. This strengthens the conclusion drawn by Chadwick and Leenhouts (2011) that the data shown in their figures 1 to 4 imply that the same type of lesion is responsible for cancer induction and cell killing, but that the data say nothing about the nature of that lesion. We like the demonstration by Thorne that the same peak height of cancer incidence implies that the lesions responsible for cancer induction and cell sterilisation are the same type, irrespective of the dose effect function for monotonically increasing functions of dose.…”

Integrated Molecular Analysis Indicates Undetectable Change in DNA Damage in Mice after Continuous Irradiation at ~ 400-fold Natural Background Radiation

“…Carcinogenic radiation exposures are known to induce DNA strand breaks and chromosomal rearrangements (Bekker-Jensen and Mailand 2010; Chadwick and Leenhouts 2011; Holland et al 2011). Importantly, a single acute dose of radiation can give rise to cancer over a decade later, which is consistent with DNA damage being predictive of downstream cancer risk (Ron 1998).…”