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Cited by 280

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

DNA Repair: Enzymatic Mechanisms and Relevance to Drug Response

Chaney, Stephen G., Sancar, Aziz·1996·JNCI: Journal of the National Cancer Institute

Abstract

A number of chemotherapeutic agents, such as platinum drugs, nitrogen mustards, and chloroethylnitrosoureas, act by forming bifunctional DNA adducts. It is likely that abortive attempts to replicate and/or repair the damaged DNA cause chromosome aberrations and breakage, leading to cell death. Any substantial increase in cellular capacity to repair damaged DNA may result in resistance to chemotherapeutic agents. In this review, we examine the types of DNA adducts formed by the major classes of chemotherapeutic agents, the enzymatic pathways that play a role in the repair of those adducts, the evidence that DNA repair is enhanced in drug-resistant cell lines and tumors, and strategies for utilizing selective inhibition of DNA repair to overcome resistance.

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Crossref · 10.1093/jnci/88.19.1346

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Metadata

Authors
Chaney, S. G., & Sancar, A.
Venue
JNCI: Journal of the National Cancer Institute
Published
1996-10-02
Volume
88
Issue
19
Pages
1346-1360
ISSN
  • 0027-8874 (ISSN-L)
  • 1460-2105
OpenAlex
W2096535852
Cited by
280
References
3
FWCI
4.70
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: DNA Repair: Enzymatic Mechanisms and Relevance to Drug Response. https://app.cochat.ai/papers/10.1093/jnci/88.19.1346
The paper
Chaney, S. G., & Sancar, A. (1996). DNA Repair: Enzymatic Mechanisms and Relevance to Drug Response. JNCI: Journal of the National Cancer Institute. https://doi.org/10.1093/jnci/88.19.1346

Data sources

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.