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P-glycoproteins and multidrug resistance
1Department of Pathology, University of Arizona, Tucson 85724, USA.
Annual Review of Pharmacology and Toxicology
|January 1, 1996
Summary
Multidrug resistance in cancer therapy is often caused by P-glycoprotein, an efflux pump. Compounds can modulate this resistance, with clinical trials exploring their effectiveness against neoplastic diseases.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Multidrug resistance (MDR) is a significant challenge in treating neoplastic diseases.
- P-glycoprotein (P-gp) acts as an energy-dependent efflux pump, removing drugs from cancer cells.
- MDR1 gene expression is linked to poor prognosis in cancer patients.
Purpose of the Study:
- To investigate the role of P-glycoprotein in multidrug resistance.
- To explore compounds that can modulate P-glycoprotein-mediated drug resistance.
- To assess the potential clinical feasibility of P-gp modulation strategies.
Main Methods:
- Studying drug resistance in cultured tumor cell lines and human cancers.
- Analyzing the function of P-glycoprotein as an efflux pump.
- Evaluating the effects of various compounds (e.g., verapamil, cyclosporin) in combination with antineoplastic agents.
Main Results:
- P-glycoprotein facilitates drug efflux, contributing to multidrug resistance.
- Compounds like verapamil and cyclosporin can decrease or eliminate P-gp-mediated resistance when used with chemotherapy.
- Clinical trials are ongoing to evaluate the therapeutic potential of P-gp modulation.
Conclusions:
- P-glycoprotein is a key factor in multidrug resistance, but not the sole mechanism.
- Modulating P-glycoprotein activity shows promise for overcoming drug resistance in cancer therapy.
- Further clinical investigation is necessary to establish the feasibility of these strategies.