ABSTRACT
The therapeutic index of most cytotoxic agents is still a matter of concern because drug
activity against malignant cells is associated with toxicity to normal tissues. In addition
to this, new drugs designed to inhibit specific molecular pathways critical to tumor cell
survival, such as imatinib and gefitinib (1), are susceptible to therapeutic failure due to
target mutation or downregulation with activation of alternative signal transduction
pathways. Recent progress in analytical techniques and the sequencing of the human
genome has allowed the discovery of gene variants involved in pharmacokinetic and
pharmacodynamic pathways (Fig. 1), which define cancer chemosensitivity and/or drug tolerability (2).
