ABSTRACT
Drugs developed for diseases caused by pathogenic infections have the advantage that there are numerous physical and functional differences between the pathogens and the cells of their human host. As a result, most of these therapeutic agents can be administered chronically at relatively high doses with typically few side effects. This is not the case in diseases such as cancer, which arise from transformed or dysregulated growth/function of the body’s own cells. Here, the differences between healthy and diseased tissues are often quite subtle and rarely are cellular features truly disease specific. It is not surprising then that for these diseases a very narrow window exists between drug doses that are effective and drug doses that are toxic. Although our increased understanding of the genetic alterations associated with diseases such as cancer will no doubt improve our ability to design better drugs, it is likely that we will continue to be faced with therapeutic targets that are differentially expressed in disease cells rather than
* Current affiliation: Bristol-Meyers Squibb, Princeton, New Jersey
uniquely expressed. This suggests that manipulating drug pharmacology/distribution to enhance tumor selectivity will continue to be an important feature in the development of new anticancer drugs.
