ABSTRACT
Acknowledgment................................................................................................................ 455
References .......................................................................................................................... 455
Historically, drugs developed for cancer treatment have largely been cytotoxic agents with
significant toxicities related to effects on rapidly dividing cells. These drugs have mechanisms
of action that involve major disruptions in DNA and RNA synthesis or function (1,2). Early
stages of development have focused on identification of maximally tolerated doses and signals
of activity in refractory populations. Later stages of development have usually focused on
evaluation of safety and efficacy in patient populations mainly defined by clinical and
histologic criteria.
