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Cited by 800

The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.

Cellular stress response and apoptosis in cancer therapy

Open access
Herr, Ingrid, Debatin, Klaus-Michael·2001·Blood

Abstract

Anticancer treatment using cytotoxic drugs is considered to mediate cell death by activating key elements of the apoptosis program and the cellular stress response. While proteolytic enzymes (caspases) serve as main effectors of apoptosis, the mechanisms involved in activation of the caspase system are less clear. Two distinct pathways upstream of the caspase cascade have been identified. Death receptors, eg, CD95 (APO-1/Fas), trigger caspase-8, and mitochondria release apoptogenic factors (cytochrome c, Apaf-1, AIF), leading to the activation of caspase-9. The stressed endoplasmic reticulum (ER) contributes to apoptosis by the unfolded protein response pathway, which induces ER chaperones, and by the ER overload response pathway, which produces cytokines via nuclear factor-κB. Multiple other stress-inducible molecules, such as p53, JNK, AP-1, NF-κB, PKC/MAPK/ERK, and members of the sphingomyelin pathway have a profound influence on apoptosis. Understanding the complex interaction between different cellular programs provides insights into sensitivity or resistance of tumor cells and identifies molecular targets for rational therapeutic intervention strategies.

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Metadata

Authors
Herr, I., & Debatin, K.-M.
Venue
Blood
Published
2001-11-01
Volume
98
Issue
9
Pages
2603-2614
ISSN
  • 0006-4971 (ISSN-L)
  • 1528-0020
OpenAlex
W2077754831
Cited by
800
References
13
FWCI
17.91
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Cellular stress response and apoptosis in cancer therapy. https://app.cochat.ai/papers/10.1182/blood.v98.9.2603
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Herr, I., & Debatin, K.-M. (2001). Cellular stress response and apoptosis in cancer therapy. Blood. https://doi.org/10.1182/blood.v98.9.2603

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.