  We report on a theoretical study of point mutations effects on charge
transfer properties in the DNA sequence of the tumor-suppressor p53 gene. On
the basis of effective single-strand or double-strand tight-binding models
which simulate hole propagation along the DNA, a statistical analysis of charge
transmission modulations associated with all possible point mutations is
performed. We find that in contrast to non-cancerous mutations, mutation
hotspots tend to result in significantly weaker {\em changes of transmission
properties}. This suggests that charge transport could play a significant role
for DNA-repairing deficiency yielding carcinogenesis.
