Some genotypic and environmental conditions of the host in cutaneous malignant melanoma.

Research output: Contribution to journalArticle

Abstract

The factors involving the development of melanoma vary according to the phenotype and environment conditions experienced by the host MC1R variant alleles that are associated with increased melanoma risk are likely to sensitize melanocytes to DNA damage by ultraviolet (UV) exposure, and the interactions between UV radiation and the genome induce melanoma. In fact, the non-functional MC1R cells have a very slow rate of cyclobutane pyrimidine dimers removal. The most significant mutations induced by UV in the skin occur in the CDKN2A gene being the major target of UV, that encodes 2 distinct proteins cell cycle regulators: p16INK4A and p14ARF. Inactivation of both tumor suppressors results in escape from cell cycle arrest because of disruption of the G1/S restriction point The outcome is premature cell cycle progression and incomplete repair of DNA damage that leads to genomic instability and mutations. In fact, the signaling pathways of UV in melanocytes reveal the complex interrelationship between the pathways that regulate survival, proliferation and melanogenesis
Original languageEnglish
Pages (from-to)465-469
Number of pages5
JournalGIORNALE ITALIANO DI DERMATOLOGIA E VENEREOLOGIA
Volume141
Publication statusPublished - 2006

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Melanoma
Melanocytes
DNA Damage
Tumor Suppressor Protein p14ARF
p16 Genes
G1 Phase Cell Cycle Checkpoints
Pyrimidine Dimers
Cell Cycle Proteins
Mutation
Genomic Instability
Cell Cycle Checkpoints
Cell Cycle
Alleles
Genome
Radiation
Phenotype
Skin
Cutaneous Malignant Melanoma
Neoplasms

All Science Journal Classification (ASJC) codes

  • Dermatology

Cite this

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title = "Some genotypic and environmental conditions of the host in cutaneous malignant melanoma.",
abstract = "The factors involving the development of melanoma vary according to the phenotype and environment conditions experienced by the host MC1R variant alleles that are associated with increased melanoma risk are likely to sensitize melanocytes to DNA damage by ultraviolet (UV) exposure, and the interactions between UV radiation and the genome induce melanoma. In fact, the non-functional MC1R cells have a very slow rate of cyclobutane pyrimidine dimers removal. The most significant mutations induced by UV in the skin occur in the CDKN2A gene being the major target of UV, that encodes 2 distinct proteins cell cycle regulators: p16INK4A and p14ARF. Inactivation of both tumor suppressors results in escape from cell cycle arrest because of disruption of the G1/S restriction point The outcome is premature cell cycle progression and incomplete repair of DNA damage that leads to genomic instability and mutations. In fact, the signaling pathways of UV in melanocytes reveal the complex interrelationship between the pathways that regulate survival, proliferation and melanogenesis",
author = "Giuseppe Pistone and Bongiorno, {Maria Rita} and Mario Arico'",
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journal = "GIORNALE ITALIANO DI DERMATOLOGIA E VENEREOLOGIA",
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T1 - Some genotypic and environmental conditions of the host in cutaneous malignant melanoma.

AU - Pistone, Giuseppe

AU - Bongiorno, Maria Rita

AU - Arico', Mario

PY - 2006

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N2 - The factors involving the development of melanoma vary according to the phenotype and environment conditions experienced by the host MC1R variant alleles that are associated with increased melanoma risk are likely to sensitize melanocytes to DNA damage by ultraviolet (UV) exposure, and the interactions between UV radiation and the genome induce melanoma. In fact, the non-functional MC1R cells have a very slow rate of cyclobutane pyrimidine dimers removal. The most significant mutations induced by UV in the skin occur in the CDKN2A gene being the major target of UV, that encodes 2 distinct proteins cell cycle regulators: p16INK4A and p14ARF. Inactivation of both tumor suppressors results in escape from cell cycle arrest because of disruption of the G1/S restriction point The outcome is premature cell cycle progression and incomplete repair of DNA damage that leads to genomic instability and mutations. In fact, the signaling pathways of UV in melanocytes reveal the complex interrelationship between the pathways that regulate survival, proliferation and melanogenesis

AB - The factors involving the development of melanoma vary according to the phenotype and environment conditions experienced by the host MC1R variant alleles that are associated with increased melanoma risk are likely to sensitize melanocytes to DNA damage by ultraviolet (UV) exposure, and the interactions between UV radiation and the genome induce melanoma. In fact, the non-functional MC1R cells have a very slow rate of cyclobutane pyrimidine dimers removal. The most significant mutations induced by UV in the skin occur in the CDKN2A gene being the major target of UV, that encodes 2 distinct proteins cell cycle regulators: p16INK4A and p14ARF. Inactivation of both tumor suppressors results in escape from cell cycle arrest because of disruption of the G1/S restriction point The outcome is premature cell cycle progression and incomplete repair of DNA damage that leads to genomic instability and mutations. In fact, the signaling pathways of UV in melanocytes reveal the complex interrelationship between the pathways that regulate survival, proliferation and melanogenesis

UR - http://hdl.handle.net/10447/28635

UR - https://www.minervamedica.it/en/journals/dermatologia-venereologia/issue.php?cod=R23Y2006N05

M3 - Article

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JO - GIORNALE ITALIANO DI DERMATOLOGIA E VENEREOLOGIA

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