Molecular pathogenesis of AML
United States of America
63 slide(s) – 00:28:45 – English – 2011-06-10
Understand Molecular Genetics of AML
Understand How Some Properties of AML Can be mapped to molecular Defects
Understand Therapeutic Implications of Molecular Defects
Acute myeloid leukemia (AML) is a clonal/oligoclonal malignancy distinguished from normal hematopoietic cells by key properties including differentiation block, and enhanced self-renewal, increased proliferation, decreased cell death, dissemination and genomic instability. Modern research into the pathogenesis of AML involves the elucidation of the role of aberrant chromosomal rearrangements amplifications and deletions, point mutations and aberrant regulation of gene expression, governed in part by changes in chromatin. New technologies have accelerated the ability to sub-classify AML based upon mutation and gene expression status and many of the phenotypic properties of AML can be mapped onto underlying genetic lesions. Within several years, a near complete categorization of AML will be achieved and a variety of new therapeutic targets will be identified. Remaining challenges will be to understand the molecular mechanisms linking genetic and epigenetic changes to leukemia cell growth and the translation of these findings into robust agents designed to target specific mutant or deregulated proteins.