There is increasing evidence that most human cancers contain multiple

mutations. Genetic and environmental sources are abundant. In addition to

genetic insults caused by the environment, the very process of
DNA replication during cell division is prone to error. The rate at which DNA
polymerase adds incorrect nucleotides during DNA replication is a major
factor in determining the spontaneous mutation rate in an organism. For
example, by examining the number of individuals in a given population who
were diagnosed with neurofibromatosis , scientists determined that
the spontaneous mutation rate of the gene responsible for this disease
averaged 1 x 10-4mutations per gamete (Crowe et al., 1956). Defects in DNA
repair underlie a number of human genetic diseases that affect a wide variety
of body systems but share a common traits, most notably a predisposition to
cancer. These disorders include ataxia-telangiectasia (AT), a degenerative
motor condition caused by failure to repair oxidative damage in the
cerebellum, and xeroderma pigmentosum (XP), characterized by sensitivity to
sunlight and linked to a defect in an important ultraviolet damage repair
pathway. UV radiation causes two classes of DNA lesions which are
cyclobutane pyrimidine dimers and 6-4 photoproducts. According to Suzanne
(2008), the best known example of the link between environmental-induced
DNA damage and disease is that of skin cancer, which can be caused by
excessive exposure to UV radiation in the form of sunlight.

Clancy, S. (2008) DNA damage & repair: mechanisms for maintaining DNA
integrity. Nature Education 1(1):103

Crowe, F. W., et al. A Clinical, Pathological, and Genetic Study of Multiple

Neurofibromatosis (Springfield, Illinois, Charles C. Thomas, 1956)