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JNCI Journal of the National Cancer Institute 1999 91(19):1604-1605; doi:10.1093/jnci/91.19.1604
© 1999 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 91, No. 19, 1604-1605, October 6, 1999
© 1999 Oxford University Press

EDITORIALS

Lung Resistance-Related Protein: Determining Its Role in Multidrug Resistance

William S. Dalton, Rik J. Scheper

Affiliations of authors: W. S. Dalton, H. Lee Moffitt Cancer Center, University of South Florida, Tampa; R. J. Scheper, Free University Hospital, Amsterdam, The Netherlands.

Correspondence to: William S. Dalton, M.D., Ph.D., H. Lee Moffitt Cancer Center, University of South Florida, 12902 Magnolia Dr., Tampa, FL 33612.

Resistance to cytotoxic drugs remains a major obstacle for the successful treatment of cancer (1). Over the past two decades, a great deal of information has emerged that elucidates how cancer cells become drug resistant. At least one prominent drug-resistance mechanism in cancer cells is the reduction of intracellular drug concentration at the putative drug target. There are at least two mechanisms capable of reducing drug concentration at the target site. The most obvious mechanism involves an overall reduction in intracellular drug concentration by reducing drug uptake or enhancing drug efflux. A second mechanism could be a redistribution of drug . . . [Full Text of this Article]

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