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No Successful Treatments For Aml Essay

722 words - 3 pages

The current treatments of AML patients are considered unsuccessful. Although a complete remission of adult AML is achieved by induction therapy using anthracyclins and cytarabine, the therapy eventually fails due to disease relapse. Moreover, due to the diversity of AML cytogenetics and molecular background, there is an increasing need for targeted therapy.
A panel of inhibitors against Flt3 as well as anti-Flt3 antibodies has been developed and is at present in different phases of clinical trials [189], [190], [191] and [192]. These are all small molecule heterocyclic compounds that competitively inhibit ATP binding to Flt3, but are not considered very specific. All reduce the cell proliferation rate by up regulating pro-apoptotic proteins but have had little effect in clinical studies. The therapeutic responses are usually modest with a transient reduction of peripheral blasts, and clinical trials are currently focused on combining Flt3 inhibitors with conventional chemotherapy. Most of the Flt3 inhibitors are rather unspecific like the majority of kinase inhibitors in general, and often recognize targets like PDGFR, c-Kit and VEGFR. This not only disables the evaluation of Flt3 inhibition, but may cause toxic responses due to the multiple targets when used in patients. Recently, a novel type of kinase inhibitor LS104, competing out substrate binding to the receptor instead of inhibiting the ATP binding site, was shown to target Flt3 ITD and its downstream signaling in primary AML blasts [193]. There have been reports of anti-Flt3 neutralizing antibodies in leukemic mouse models with positive responses [194], and this approach is more specific and less toxic. The antibodies mainly interfered with the cell surface expressed Flt3, and may for this reason not be the best option for the ITD mutant, predominantly expressed as the immature intracellular receptor.
Activating mutations in c-Kit are found in AML cases with CBF abnormalities. Imatinib, best known for its function in inhibiting Bcr–Abl in CML, also inhibits c-Kit and may therefore represent a potential drug in CBF leukemias where c-Kit correlates to a worse prognosis [195]. However, in the case of CML, point mutations in the kinase domain of Bcr–Abl often result in imatinib resistance [196]....

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