Simple statistical considerations show that chemical carcinogens bound to DNA exert most of their effects through long-range mechanisms that can deblock an oncogene that is wound on histones. The same is true for DNA double-strand breaks caused by radiations. The latter lead to a loss of genetic information that may include also antioncogenes. Different large-range mechanisms will be shown for the effect of chemical carcinogens. Among them, the formation of conformational solitary waves caused by chemical carcinogen binding has a twofold effect: (1) The solitary wave (which has a long lifetime) can move along a DNA base stack and can break weak bonds (among others, H bonds) between DNA and proteins in a nucleoprotein. In this way they can deblock normally suppressed genetic information (activation of oncogenes). (2) Theoretical calculations show that there is a quite strong possibility for hopping conduction across the nucleotide base-pair stacks and along the protein chains. Since there is a unnegligible charge transfer from DNA and to proteins, this means that in a normal nucleoprotein there is a hole conduction along the base stacks and an electronic conduction along the protein chains. The occurrence of conformational solitons in the base-pair stacks acts as a “bulge” that hinders the conduction across it. In this way the conformational solitons interfere also in a second way with the strength with the DNA–protein interactions. Namely, it was shown a long time ago that van der Waals forces between two biopolymer chains are much smaller if in one of them no conduction occurs. To counteract these effects of chemical carcinogens, one can think to try to intercalate partially saturated (having no π electrons) molecules (like partially saturated psolarenes) between the base stacks. Such molecules would act as a block for the solitary waves. They could not move through the barrier, and at the other side of the barrier electric conduction could still occur due to charge transfer. In this way, though the conduction along the base-pair stacks would be restricted only to certain segments of DNA, they would not be completely hindered, as it is the case of a freely moving solitary wave. Finally, it was theoretically shown that DNA double-strand breaks most probably occur, if after a single-strand break, a molecule of the stack is excited far away from the point of the first break. Namely, an excited molecule in a base stack can generate again a solitary wave that could propagate until the point of the first single-strand break. Since then the wave would reach a point where the general structure of DNA is already disturbed, it would most probably give away its energy at this point causing a break also in the second strand. Against this phenomenon the intercalation into the stack of partially saturated molecules would most probably be helpful again. © 2000 John Wiley & Sons, Inc. Int J Quant Chem 78: 450–458, 2000