الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Acute myeloid leukemia (AML) is a disease characterized by uncontrolled proliferation of clonal neoplastic hematopoietic precursor cells. This leads to the disruption of normal hematopoiesis and bone marrow failure. Major breakthroughs in the past have contributed to our understanding of the genetic failures and the changed biology in AML cells that underlie the initiation and progression of the disease.
It is now recognized that not only genetic but also epigenetic alterations are similarly important in this process. Since these alterations do not change the DNA sequences and are pharmacologically reversible, they have been regarded as optimal targets for what is now known as epigenetic targeted therapy.
Epigenetic modifications are heritable changes in gene expression not encoded by the DNA sequence. In the past decade, great strides have been made in characterizing epigenetic changes during normal development and in disease states like cancer. However, the epigenetic landscape has grown increasingly complicated, encompassing DNA methylation, the histone code, noncoding RNA, and nucleosome positioning, along with DNA sequence.
Overexpression of the Wilms tumor 1 gene (WT1) is implicated in the prognosis of leukemia with high expression predicting disease progression in (AML), as well as being intensively studied as a potential molecular marker for minimal residual disease (MRD) and treatment response.