Induction of apoptosis in cancer: New therapeutic opportunities

Han Fei Ding, David E. Fisher

Research output: Contribution to journalReview article

45 Scopus citations

Abstract

Autonomous cell proliferation is one of the hallmarks of cancer cells, driven by activated growth-promoting oncogenes. However, deregulated activation of these oncogenes also triggers apoptosis via multiple pathways. Among them, the ARF-p53 pathway appears to play a major role in mediating oncogene-induced apoptosis. Consequently, suppression of apoptosis by inactivation of p53 and other tumor suppressors is central to tumor development. These findings have broad implications in understanding cancer genetics and therapy. They help define the roles for oncogenes and tumor suppressor genes in tumorigenesis. Furthermore, the notion that cancer cells often carry specific defects in apoptotic pathways but are inherently sensitive to apoptosis as a result of deregulated proliferation, offers numerous opportunities for manipulating apoptosis in directions of clinical application.

Original languageEnglish (US)
Pages (from-to)451-469
Number of pages19
JournalAnnals of Medicine
Volume34
Issue number6
DOIs
StatePublished - Dec 1 2002
Externally publishedYes

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Keywords

  • Apoptosis
  • Cancer therapy
  • Oncogene
  • Tumor suppressor gene
  • Tumorigenesis

ASJC Scopus subject areas

  • Medicine(all)

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