Towards a better understanding of the molecular mechanisms involved in sunlight-induced melanoma

Mandy Williams, Allal Ouhtit

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Although much less prevalent than its nonmelanoma skin cancer counterparts, cutaneous malignant melanoma (CMM) is the most lethal human skin cancer. Epidemiological and biological studies have established a strong link between lifetime exposure to ultraviolet (UV) light, particularly sunburn in childhood, and the development of melanoma. However, the specific molecular targets of this environmental carcinogen are not known. Data obtained from genetic and molecular studies over the last few years have identified the INK4a/ARF locus as the "gatekeeper" melanoma suppressor, encoding two tumour suppressor proteins in human, p16INK4a and p14ARF. Recent developments in molecular biotechnology and research using laboratory animals have made a significant gene breakthrough identifying the components of the p16INK4a/Rb pathway as the principal and rate-limiting targets of UV radiation actions in melanoma formation. This review summarizes the current knowledge of the molecular mechanisms involved in melanoma development and its relationship to sunlight UV radiation.

Original languageEnglish
Pages (from-to)57-61
Number of pages5
JournalJournal of Biomedicine and Biotechnology
Volume2005
Issue number1
DOIs
Publication statusPublished - Jan 18 2005

Fingerprint

Sunlight
Ultraviolet radiation
Melanoma
Skin
Skin Neoplasms
Tumor Suppressor Protein p14ARF
Environmental Carcinogens
Tumor Suppressor Proteins
Biotechnology
Research laboratories
Animals
Genes
Radiation
Sunburn
Laboratory Animals
Ultraviolet Rays
Epidemiologic Studies
Molecular Biology
Research

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Genetics
  • Applied Microbiology and Biotechnology

Cite this

Towards a better understanding of the molecular mechanisms involved in sunlight-induced melanoma. / Williams, Mandy; Ouhtit, Allal.

In: Journal of Biomedicine and Biotechnology, Vol. 2005, No. 1, 18.01.2005, p. 57-61.

Research output: Contribution to journalArticle

@article{d1d652fc5d2b4cdb861370c07c0a128d,
title = "Towards a better understanding of the molecular mechanisms involved in sunlight-induced melanoma",
abstract = "Although much less prevalent than its nonmelanoma skin cancer counterparts, cutaneous malignant melanoma (CMM) is the most lethal human skin cancer. Epidemiological and biological studies have established a strong link between lifetime exposure to ultraviolet (UV) light, particularly sunburn in childhood, and the development of melanoma. However, the specific molecular targets of this environmental carcinogen are not known. Data obtained from genetic and molecular studies over the last few years have identified the INK4a/ARF locus as the {"}gatekeeper{"} melanoma suppressor, encoding two tumour suppressor proteins in human, p16INK4a and p14ARF. Recent developments in molecular biotechnology and research using laboratory animals have made a significant gene breakthrough identifying the components of the p16INK4a/Rb pathway as the principal and rate-limiting targets of UV radiation actions in melanoma formation. This review summarizes the current knowledge of the molecular mechanisms involved in melanoma development and its relationship to sunlight UV radiation.",
author = "Mandy Williams and Allal Ouhtit",
year = "2005",
month = "1",
day = "18",
doi = "10.1155/JBB.2005.57",
language = "English",
volume = "2005",
pages = "57--61",
journal = "BioMed Research International",
issn = "2314-6133",
publisher = "Hindawi Publishing Corporation",
number = "1",

}

TY - JOUR

T1 - Towards a better understanding of the molecular mechanisms involved in sunlight-induced melanoma

AU - Williams, Mandy

AU - Ouhtit, Allal

PY - 2005/1/18

Y1 - 2005/1/18

N2 - Although much less prevalent than its nonmelanoma skin cancer counterparts, cutaneous malignant melanoma (CMM) is the most lethal human skin cancer. Epidemiological and biological studies have established a strong link between lifetime exposure to ultraviolet (UV) light, particularly sunburn in childhood, and the development of melanoma. However, the specific molecular targets of this environmental carcinogen are not known. Data obtained from genetic and molecular studies over the last few years have identified the INK4a/ARF locus as the "gatekeeper" melanoma suppressor, encoding two tumour suppressor proteins in human, p16INK4a and p14ARF. Recent developments in molecular biotechnology and research using laboratory animals have made a significant gene breakthrough identifying the components of the p16INK4a/Rb pathway as the principal and rate-limiting targets of UV radiation actions in melanoma formation. This review summarizes the current knowledge of the molecular mechanisms involved in melanoma development and its relationship to sunlight UV radiation.

AB - Although much less prevalent than its nonmelanoma skin cancer counterparts, cutaneous malignant melanoma (CMM) is the most lethal human skin cancer. Epidemiological and biological studies have established a strong link between lifetime exposure to ultraviolet (UV) light, particularly sunburn in childhood, and the development of melanoma. However, the specific molecular targets of this environmental carcinogen are not known. Data obtained from genetic and molecular studies over the last few years have identified the INK4a/ARF locus as the "gatekeeper" melanoma suppressor, encoding two tumour suppressor proteins in human, p16INK4a and p14ARF. Recent developments in molecular biotechnology and research using laboratory animals have made a significant gene breakthrough identifying the components of the p16INK4a/Rb pathway as the principal and rate-limiting targets of UV radiation actions in melanoma formation. This review summarizes the current knowledge of the molecular mechanisms involved in melanoma development and its relationship to sunlight UV radiation.

UR - http://www.scopus.com/inward/record.url?scp=22544441863&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=22544441863&partnerID=8YFLogxK

U2 - 10.1155/JBB.2005.57

DO - 10.1155/JBB.2005.57

M3 - Article

VL - 2005

SP - 57

EP - 61

JO - BioMed Research International

JF - BioMed Research International

SN - 2314-6133

IS - 1

ER -