Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2006 Aug 7;25(34):4798-811.
doi: 10.1038/sj.onc.1209608.

Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy

Affiliations
Review

Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy

S Fulda et al. Oncogene. .

Abstract

Apoptosis or programmed cell death is a key regulator of physiological growth control and regulation of tissue homeostasis. One of the most important advances in cancer research in recent years is the recognition that cell death mostly by apoptosis is crucially involved in the regulation of tumor formation and also critically determines treatment response. Killing of tumor cells by most anticancer strategies currently used in clinical oncology, for example, chemotherapy, gamma-irradiation, suicide gene therapy or immunotherapy, has been linked to activation of apoptosis signal transduction pathways in cancer cells such as the intrinsic and/or extrinsic pathway. Thus, failure to undergo apoptosis may result in treatment resistance. Understanding the molecular events that regulate apoptosis in response to anticancer chemotherapy, and how cancer cells evade apoptotic death, provides novel opportunities for a more rational approach to develop molecular-targeted therapies for combating cancer.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Science. 2000 May 12;288(5468):1053-8 - PubMed
    1. J Biol Chem. 2004 Nov 26;279(48):49575-8 - PubMed
    1. Mol Cancer Ther. 2005 Nov;4(11):1689-98 - PubMed
    1. Nat Med. 1998 Feb;4(2):232-4 - PubMed
    1. Nat Cell Biol. 2002 Nov;4(11):842-9 - PubMed

Publication types

Substances

LinkOut - more resources