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Cited by 226

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Role of the MRP1/ABCC1 Multidrug Transporter Protein in Cancer

Munoz, Marcia, Henderson, Michelle, Haber, Michelle, Norris, Murray·2007·IUBMB Life

Abstract

Multidrug resistance is a major obstacle to cancer treatment and leads to poor prognosis for the patient. Multidrug resistance‐associated protein 1 (MRP1) transports a wide range of therapeutic agents as well as diverse physiological substrates and may play a role in the development of drug resistance in several cancers including those of the lung, breast and prostate, as well as childhood neuroblastoma. The majority of patients with neuroblastoma present with widely disseminated disease at diagnosis and despite intensive treatment, the prognosis for such patients is dismal. There is increasing evidence that MRP1 is a MYCN target gene involved in the development of multidrug resistance in neuroblastoma. Given the importance of MRP1 overexpression in neuroblastoma, MRP1 inhibition may be a clinically relevant approach to improving patient outcome in this disease.

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Metadata

Authors
Munoz, M., Henderson, M., Haber, M., & Norris, M.
Venue
IUBMB Life
Publisher
Wiley
Published
2007-01
Volume
59
Issue
12
Pages
752-757
ISSN
  • 1521-6543 (ISSN-L)
  • 1521-6551
OpenAlex
W1985176138
Cited by
226
References
2
FWCI
1.81
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Role of the MRP1/ABCC1 Multidrug Transporter Protein in Cancer. https://app.cochat.ai/papers/10.1080/15216540701736285
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Munoz, M., Henderson, M., Haber, M., & Norris, M. (2007). Role of the MRP1/ABCC1 Multidrug Transporter Protein in Cancer. IUBMB Life. https://doi.org/10.1080/15216540701736285

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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.