The risk of induction of a second primary cancer after a therapeutic irradiation 
with conventional photon beams is well recognized and documented. However, in 
general, it is totally overwhelmed by the benefit of the treatment. The same is 
true to a large extent for the combinations of radiation and drug therapy. After 
fast neutron therapy, the risk of induction of a second cancer is greater than 
after photon therapy. Neutron RBE increases with decreasing dose and there is a 
wide evidence that neutron RBE is greater for cancer induction (and for other 
late effects relevant in radiation protection) than for cell killing. Animal 
data on RBE for tumor induction are reviewed, as well as other biological 
effects such as life shortening, malignant cell transformation in vitro, 
chromosome aberrations, genetic effects. These effects can be related, directly 
or indirectly, to cancer induction to the extent that they express a "genomic" 
lesion. Almost no reliable human epidemiological data are available so far. For 
fission neutrons a RBE for cancer induction of about 20 relative to photons 
seems to be a reasonable assumption. For fast neutrons, due to the difference in 
energy spectrum, a RBE of 10 can be assumed. After proton beam therapy (low-LET 
radiation), the risk of secondary cancer induction, relative to photons, can be 
divided by a factor of 3, due to the reduction of integral dose (as an average). 
The RBE of heavy-ions for cancer induction can be assumed to be similar to 
fission neutrons, i.e. about 20 relative to photons. However, after heavy-ion 
beam therapy, the risk should be divided by 3, as after proton therapy due to 
the excellent physical selectivity of the irradiation. Therefore a risk 5 to 10 
times higher than photons could be assumed. This range is probably a pessimistic 
estimate for carbon ions since most of the normal tissues, at the level of the 
initial plateau, are irradiated with low-LET radiation.