A progressively better understanding of the genetic and epigenetic abnormalities underlying acute myeloid leukemia has changed clinical practice and affected the outcome of thousands of patients. Over the past decades, approaches focused on cloning, sequencing, and functional characterization of one or a few genes were the preferred (and the only possible) modality of investigation. The advent of disruptive new sequencing technologies brought about an unprecedented acceleration in our learning curve. Our view of the abnormalities required to generate and sustain leukemia is evolving from a piecemeal account based on individual lines of research into a comprehensive view of how all the important components (eg, transcriptional program, chromatin modifications, DNA sequence, alterations in noncoding genome) interact, in each patient and each leukemic cell. In this article, we provide an overall look at this complicated landscape and highlight outstanding issues for future research.
|Number of pages||14|
|Journal||Seminars in Hematology|
|Publication status||Published - Oct 1 2014|
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