TP53 mutations and molecular epidemiology

Kazunori Otsuka, Chikashi Ishioka

Research output: Contribution to journalReview articlepeer-review

3 Citations (Scopus)

Abstract

Tumor suppressor p53 protein is activated by a variety of cellular stresses through several pathways and transactivates its downstream genes, including regulators of cell cycle, apoptosis and DNA repair. The loss of p53 function by TP53 gene mutations therefore fails to activate these genes and is thought to be a critical cause of carcinogenesis and/or tumor progression. TP53 is one of the most frequently mutated genes in human cancer. TP53 mutations are found in about 50% of human cancers, although the frequency of TP53 mutations differs among tumor types. However, the degree of functional disorder of mutant p53 varies according to the type of TP53 mutation. And the effects of p53 on cancer formation and/or progression are influenced by the degree of p53 dysfunction. So it is important to analyze the effects of TP53 mutations carefully according to the oncogenicity of each mutation from the molecular epidemiological point of view. Here, together with some cautions needed for analyzing and interpreting the significance of TP53 gene mutations, we present some examples of the identified specific mutation spectrum and the correlation between the prognosis and TP53 mutation in some cancers.

Original languageEnglish
Pages (from-to)683-689
Number of pages7
JournalGan to kagaku ryoho. Cancer & chemotherapy
Volume34
Issue number5
Publication statusPublished - 2007 May

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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