Abstract
One of the major challenges for the earliest forms of life was to protect the cellular DNA from the highly mutagenic solar ultraviolet and from exposure to environmental mutagens. The nucleotide excision repair (NER) pathway is responsible for the removal of a large variety of lesions, including those induced by ultraviolet light and bulky adduct-forming chemicals. The NER mechanism consists of two major steps. The incision step involves introduction of dual incisions flanking the DNA lesion and subsequent removal of the damage-containing oligonucleotide. The next repair synthesis step restores the damaged site by filling in the gap created by the incision step. Humans with NER deficiencies suffer from the DNA repair syndrome, xeroderma pigmentosum (XP) with manifestations of both acute sunlight sensitivity and profoundly elevated occurrence of skin cancer. XP is a classical example of the direct relationship between genomic instability and cancer development. This chapter highlights the molecular mechanism of NER and its impact on human cancers.
Original language | English (US) |
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Title of host publication | DNA Repair, Genetic Instability, and Cancer |
Publisher | World Scientific Publishing Co. |
Pages | 65-85 |
Number of pages | 21 |
ISBN (Electronic) | 9789812706782 |
ISBN (Print) | 9789812700148 |
DOIs | |
State | Published - Jan 1 2007 |
ASJC Scopus subject areas
- General Agricultural and Biological Sciences
- General Biochemistry, Genetics and Molecular Biology
- General Medicine