The compound 13-D selectively induces apoptosis in white blood cancers versus other cancer cell types

White blood cell cancers constitute a diverse array of neoplasms including leukemia, lymphoma, and myeloma. Leukemias are divided into four major types, acute myelogenous leukemia (AML), acute lymphocytic leukemia (ALL), chronic myelogenous leukemia (CML), and chronic lymphocytic leukemia (CLL). Lymphomas are divided into two major categories, Hodgkin’s and non-Hodgkin’s lymphoma, and multiple myeloma constitutes approximately 90 % of all myeloma cases. The prognosis for patients receiving one of these diagnoses is highly variable. The drug Gleevec(imatinib) has been rec ently developed based on the known chromosomal translocation (the “Philadelphia chromosome”) in patients with CML, a translocation that results in the production of the Bcr-Abl kinase fusion protein. [1] Gleevec has had widely celebrated success as a selective inhibitor of this kinase, and the patient-response rate to this drug in some studies has been a remarkable 90 %. [2] Similarly, Hodgkin’s lymphoma can be cured in > 80 % of cases. [3] In contrast, the survival of patients with CLL (the most common type of leukemia in the western hemisphere) varies widely, with many dying soon after diagnosis. [4] In addition some lymphomas, such as follicular lymphoma, are unresponsive to chemotherapeutic agents. [5] Thus, while great strides have been made in the fight against certain white blood cell cancers, others remain untreatable or are only moderately responsive to even the most potent of chemotherapeuticagents. The vast majority of anticancer agents can be classified as antimetabolites (methotrexate, fluorouracil), DNA-damaging agents (cisplatin, doxorubicin), or antimitotics (Taxol, vincristine). [6] In general, antimetabolites and DNA-damaging agents