Abstract
Extensive studies carried out over the past decade have abundantly confirmed the supposition that human cancer cells, both in vitro and in vivo, have an enormous capacity to develop variant phenotypes which display altered degrees of drug sensitivity. (Goldie and Coldman 1984; Von Hoff 1985). Evidence is accumulating that many of the mechanisms of specific drug resistance that have been identified in experimental systems are also likely to occur in clinical situations (Fojo et al. 1987).