The most widely accepted point of view is that cells are endowed with
the capacity to repair the primary lesions responsible for cancer indu
ction. In radiobiology, this popular belief evolved from experiments o
f the same type as those that suggested the existence of sublethal rad
iation damage repair. The central problem with such data is that the c
ell-killing component of radiation damage may mask the effects associa
ted with repair of precancerous lesions. The challenge is to separate
the two processes that contribute to the observed tumor incidence afte
r irradiation. Using a recently developed stochastic model of radiatio
n carcinogenesis allowing for cell death (see Ref. 7), we provide evid
ence that precancerous lesions are not subject to repair under certain
experimental conditions. (C) Elsevier Science Inc., 1997.