Abstract
Acute Myeloid Leukemia as a Model for Cancer Therapy
Highlights
A notable exception has been in the treatment of patients with acute promyelocytic leukemia (APL) with the introduction of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), drugs targeted at the specific molecular aberration causative of the disease [the PML-RARA fusion product of t(15;17) translocation, pathognomonic for the disease]
One of the best examples of this is the identification of the mutated form of FLT3 tyrosine kinase which confers a worse outcome in the 30% of patients whose leukemic cells bear this abnormality
Other potential targets include NPM1, c-KIT in CBF leukemias, the JAK-STAT signaling pathway in post-MPN AML, the MAPK pathway in RAS mutated leukemias and various cellular signaling components which include a number of tyrosine and serine/threonine kinases
Summary
Up to 85% of adult patients with AML achieve complete response (CR) using current standard regimens and depending on pre-treatment characteristics. These data support the notion that neoplastic change is the culmination of a number of molecular events that result in deregulated cellular pathways with more molecular aberrations leading to diseases that are more resistant to traditional cancer therapeutics.
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