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Cited by 295

The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.

Role of the Glutathione Redox Cycle in Acquired and de Novo Multidrug Resistance

Kramer, Robert A., Zakher, Jehane, Kim, George·1988·Science

Abstract

Drug resistance represents a major obstacle to successful cancer chemotherapy. However, the specific biochemical mechanisms responsible for clinical drug resistance are unknown. In these studies resistance to the antitumor agent adriamycin was found to involve two mechanisms, one that decreased drug accumulation by the P170 mechanism and another that altered the glutathione redox cycle, an important pathway in the detoxification of reactive oxygen. This dual mechanism of drug resistance was demonstrated in cell lines that had acquired the multidrug-resistant phenotype and in human colorectal cancer cells with de novo resistance. These studies support a model of acquired and de novo multidrug resistance that includes alterations in both drug accumulation and the glutathione redox cycle.

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Crossref · 10.1126/science.3399900

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Metadata

Authors
Kramer, R. A., Zakher, J., & Kim, G.
Venue
Science
Published
1988-08-05
Volume
241
Issue
4866
Pages
694-697
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W2012120642
Cited by
295
References
30
FWCI
16.97
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Role of the Glutathione Redox Cycle in Acquired and de Novo Multidrug Resistance. https://app.cochat.ai/papers/10.1126/science.3399900
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Kramer, R. A., Zakher, J., & Kim, G. (1988). Role of the Glutathione Redox Cycle in Acquired and de Novo Multidrug Resistance. Science. https://doi.org/10.1126/science.3399900

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

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.