Abstract

Progress in understanding the genetic changes that drive tumorigenesis has enabled the development of molecularly targeted anticancer therapy. The first small molecule targeted to a specific protein was imatinib mesylate (Gleevec, STI571), which is used to treat chronic myeloid leukemia (CML). A recent article presents a computational model with which to study the treatment response in CML patients and investigates the effect that imatinib exerts on leukemic stem cells. Here, I discuss insights derived from this study and their implications for imatinib therapy against CML.