Cancers are caused by mutagenic agents or mutant versions of normal genes. There is progressive growth of malignant tumors because of mutations, which are able to elevate the mutation rate. These mutations are recessive mutations in tumor-suppressor genes. These agents function normally even in DNA-repair pathways.
Mutations in these genes are not only interfere with DNA repair but also promote malignant tumor growth, which is done indirectly by elevating the mutation rate. It also corrupts the normal cell cycle regulation and programmed cell death.
Nucleotide excision repair is lacking in patients with Xeroderma pigmentosum. They are prone to pigmented skin cancers.
Individuals having hereditary non-polyposis colorectal cancer lose the mismatch repair system and are prone to colorectal cancer.
Cells having one functional copy of the mismatch repair genes have normal mismatch-repair activity.
But tumor cell lines arise from such cells are mismatch deficient. These cells show high mutation rates because they are incapable of correcting indels in replication.
Individuals that are homozygous for mutations in BRCA1 and BRCA2 are prone to breast cancer. This is because they are incapable of doing double-stranded break repairing. Here the strands of DNA break in some of the sites in which they are close to each other.