P53 protein and pathogenesis of melanoma and nonmelanoma skin cancer

Honnavara N. Ananthaswamy, Cara Benjamin, Vladislava O. Melnikova

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

The p53 tumor suppressor gene and gene product are among the most diverse and complex molecules involved in cellular functions. Genetic alterations within the p53 gene have been shown to have a direct correlation with cancer development and have been shown to occur in nearly 50% of all cancers. p53 mutations are particularly common in skin cancers and UV irradiation has been shown to be a primary cause of specific' signature' mutations that can result in oncogenic transformatiorn. There are certain 'hot-spots' in the p53 gene where mutations are commonly found that result in a mutated dipyrimidine site. This review discusses the role of p53 from normal function and its dysfunction in precancerous lesions, nonmelanoma and melanoma skin cancers. Additionally, molecules that associate with p53 and alter its function to produce neoplastic conditions are also explored in this chapter.

Original languageEnglish
Pages (from-to)265-282
Number of pages18
JournalAdvances in Experimental Medicine and Biology
Volume624
DOIs
StatePublished - Dec 1 2008
Externally publishedYes

Fingerprint

Skin Neoplasms
Melanoma
Skin
Genes
p53 Genes
Mutation
Proteins
Tumor Suppressor Genes
Molecules
Neoplasms
Tumors
Irradiation

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

P53 protein and pathogenesis of melanoma and nonmelanoma skin cancer. / Ananthaswamy, Honnavara N.; Benjamin, Cara; Melnikova, Vladislava O.

In: Advances in Experimental Medicine and Biology, Vol. 624, 01.12.2008, p. 265-282.

Research output: Contribution to journalArticle

Ananthaswamy, Honnavara N. ; Benjamin, Cara ; Melnikova, Vladislava O. / P53 protein and pathogenesis of melanoma and nonmelanoma skin cancer. In: Advances in Experimental Medicine and Biology. 2008 ; Vol. 624. pp. 265-282.
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