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less than the carcinazenic response in tha latter.

This argument would

appear to have merit since mitotic death of cells, cf well as reducing the

soneral viability of the tissue, would also reduce the number of irradiated
cells with carcinogenic potential.

Usually implicit in this argument is a

conceptualization of all radiation carcinogenesis as a single-cell, direc.injury process.
To confirm this argument, there is a respectable literature in
which carcinogenesis is described as occurring after doses of radiation
that are sufficiently local as to not be organism lethal, and that are

sufficiently high for the fraction of mitotically competent cells to be
greatly reduced, i.e., to 1% or less.

Unfortunately, in at least some of

these experiments, carcinogenesis is inversely related to the fraction of
mitotically competent cells, i.e., cancer induction in the regime where

_mitotic competence is greater than 1% is smal] compared with the cancer
induction in the regime where mitotic competence is much less than 1%.
There are several points to be made here.

Loss of mitotic

competence and carcinsgenesis are two indices of radiation effect in tissue.
They cannot be indeperdent, and their relationship can tell us something
about some radiation carcinogenesis.
Mitotic competence is not generally related in a linear wey to
carcinogenic response.

Moreover, it is a major anomaly that an increased

carcinogenic response is observed in dose regimes associated with greatly
reduced mitotic competence:

It is difficult to reconcile this result with

any single-cell, direct-effect origin for radiation induced cancer.
Mitotic comnetence of a cell population decreases exponentially

with increasing alpha-radiation dose and is‘a fairly ganeral index of
radiation effect in tissue.

If radiation carcinogenasis universally

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