Shared pathways

Death receptors and cytotoxic drugs in cancer therapy

I. Peták, J. A. Houghton

Research output: Contribution to journalArticle

124 Citations (Scopus)

Abstract

Death ligands (TNF, FasL, TRAIL) and their respective death receptor signaling pathways can be used to induce tumor cells to undergo apoptosis. Chemotherapeutic drugs can induce apoptosis and the upregulation of death ligands or their receptors. Downstream events following cytotoxic stress-induced DNA damage and the signaling pathways that lead to the induction of apoptosis may be either dependent or independent of death receptor signaling. The involvement of the Fas signaling pathway in chemotherapy-induced apoptosis has been the most extensively studied, with the current emergence of information on the TRAIL signaling pathway. Fas-mediated and chemotherapy-induced apoptosis can converge at the level of the receptor, FasL, DISC formation, activation of the initiator caspase-8, at the level of the mitochondria, or at the level of downstream effector caspase activation. Convergence is influenced by the specific form of DNA damage, the cellular environment, and the specific pathway(s) by which death receptor-mediated or drug-mediated apoptosis are induced. This review discusses the different levels of interaction between signaling pathways in the different forms of cell death.

Original languageEnglish
Pages (from-to)95-106
Number of pages12
JournalPathology and Oncology Research
Volume7
Issue number2
Publication statusPublished - 2001

Fingerprint

Death Domain Receptors
Apoptosis
Pharmaceutical Preparations
Neoplasms
DNA Damage
Therapeutics
Initiator Caspases
Effector Caspases
Ligands
Drug Therapy
Caspase 8
Mitochondria
Cell Death
Up-Regulation

Keywords

  • Apoptosis
  • Death receptor
  • Drug
  • Fas
  • p53
  • Tumor

ASJC Scopus subject areas

  • Cancer Research
  • Oncology
  • Pathology and Forensic Medicine

Cite this

Shared pathways : Death receptors and cytotoxic drugs in cancer therapy. / Peták, I.; Houghton, J. A.

In: Pathology and Oncology Research, Vol. 7, No. 2, 2001, p. 95-106.

Research output: Contribution to journalArticle

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