Format

Send to

Choose Destination
See comment in PubMed Commons below
Int J Mol Sci. 2013 Jan 9;14(1):1132-51. doi: 10.3390/ijms14011132.

The role of altered nucleotide excision repair and UVB-induced DNA damage in melanomagenesis.

Author information

  • 1Centre for Information Based Medicine, Hunter Medical Research Institute, and School of Biomedical Sciences & Pharmacy, Faculty of Health, University of Newcastle, Newcastle, NSW 2289, Australia. nikola.bowden@newcastle.edu.au.

Abstract

UVB radiation is the most mutagenic component of the UV spectrum that reaches the earth's surface and causes the development of DNA damage in the form of cyclobutane pyrimidine dimers and 6-4 photoproducts. UV radiation usually results in cellular death, but if left unchecked, it can affect DNA integrity, cell and tissue homeostasis and cause mutations in oncogenes and tumour-suppressor genes. These mutations, if unrepaired, can lead to abnormal cell growth, increasing the risk of cancer development. Epidemiological data strongly associates UV exposure as a major factor in melanoma development, but the exact biological mechanisms involved in this process are yet to be fully elucidated. The nucleotide excision repair (NER) pathway is responsible for the repair of UV-induced lesions. Patients with the genetic disorder Xeroderma Pigmentosum have a mutation in one of eight NER genes associated with the XP complementation groups XP-A to XP-G and XP variant (XP-V). XP is characterized by diminished repair capacity, as well as a 1000-fold increase in the incidence of skin cancers, including melanoma. This has suggested a significant role for NER in melanoma development as a result of UVB exposure. This review discusses the current research surrounding UVB radiation and NER capacity and how further investigation of NER could elucidate the role of NER in avoiding UV-induced cellular death resulting in melanomagenesis.

PMID:
23303275
PMCID:
PMC3565312
DOI:
10.3390/ijms14011132
[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
    Loading ...
    Support Center