Abstract
Historically, most drugs developed for treatment of leukemias, lymphomas, and myeloma had already been studied in the solid tumor setting. Nearly 10 years ago, chronic myelogenous leukemia (CML) forever changed this paradigm. Imatinib showed that it was possible to nullify the pathognomic genetic lesion in a hematologic malignancy. Since the approval of imatinib for CML, a host of new drugs active in blood cancers have emerged. This article highlights some areas of innovative drug development in lymphoma where possible; it emphasizes the biologic basis for the approach, linking this essential biology to the biochemical pharmacology. The article focuses on the many new targets including Syk, Bcl-2, CD-40, and the phosphoinositide-3 kinase/AKT/mammalian target of rapamycin pathway.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
