Defective apoptosis and tumorigenesis: role of p53 mutation and Fas/FasL system dysregulation

Eur J Histochem. 2002;46(3):199-208. doi: 10.4081/1680.

Abstract

The transcription factor p53 and the cytokine receptor FasL are two of the most famous regulators of cell life, and their alterations can cause a large number of pathologies, including cancer. In this review, we focused on how they can determine defective apoptosis, one of the causes of tumorigenesis and tumor progression. The importance of this knowledge lies in the new perspectives that gene therapy can offer to cure cancer.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Fas Ligand Protein
  • Free Radicals
  • Genes, bcl-2 / genetics
  • Genes, p53 / genetics*
  • Genetic Therapy
  • Humans
  • Membrane Glycoproteins / genetics*
  • Neoplasms / genetics*
  • Neoplasms / pathology
  • fas Receptor / genetics*

Substances

  • FASLG protein, human
  • Fas Ligand Protein
  • Free Radicals
  • Membrane Glycoproteins
  • fas Receptor