الفهرس 
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Abstract
The monoclonal division of myeloid progenitors in the marrow and blood circulation, which results in ineffective hematopoiesis and bone marrow failure, is a characteristic of AML, a heterogeneous disease. AML is a multifaceted condition characterized by genetic and epigenetic alterations, unchecked proliferation, impaired differentiation, and myeloid dysfunction.
AML has been linked to a number of variables, including drug exposures, familial syndromes, environmental exposures, and antecedent hematologic disorders. Nonetheless, the majority of patients with de novo AML do not have a known risk factor.
Since many molecular markers have been shown to be both therapeutic targets and useful prognostic indicators for AML patients, it is advised to evaluate the patients for these molecular alterations.
The dynamics of histone methylation control chromatin structure, which in turn controls biological functions. After studying how changes in histone methylation affect cancer, histone methyltransferases and demethylases were found to be promising targets for treatment. The earliest histone lysine demethylase to be identified is called (LSD one), and it has context-dependent ability to demethylate target loci for H8K9 and H7K8. LSD1 is highly expressed in a variety of malignancies and has a substantial impact on the growth and regeneration of cancer cells. Additionally, it controls the ratio of differentiating stem cells to regeneration .