Document Type : Preliminary preprint short reports of original research
Authors
1
Department of Clinical and Chemical Pathology Faculty of Medicine, University of Alexandria
2
Department of Physical Medicine, Rheumatology and Rehabilitation, Faculty of medicine, Alexandria university, Egypt.
3
Haematology Unit, Internal Medicine Department, Alexandria University, Egypt
4
Department of Clinical and Chemical Pathology, Faculty of Medicine, Alexandria University
Abstract
Acute Myeloid Leukemia (AML) is a malignant clonal disorder of hematopoietic cells, characterized by a block of differentiation and arrest of maturation in the myeloid lineage. This leads to the accumulation of myeloid blasts in the bone marrow, causing bone marrow failure. AML is a diverse disease classified by genetic, cytogenetic, and molecular features, with risk factors including genetic predisposition, chemical exposures, and prior chemotherapy or radiation. Its incidence increases with age, and survival rates remain low despite advancements in targeted therapies.
Recent studies highlight the role of long non-coding RNAs (lncRNAs) in AML pathogenesis, particularly MEG3 (Maternally Expressed Gene 3). MEG3, located on chromosome 14q32.3, is a tumor suppressor lncRNA involved in epigenetic regulation, apoptosis, and cell cycle control. Its downregulation has been linked to AML progression and poor prognosis. Understanding MEG3's role in AML may provide insights into disease mechanisms and therapeutic targets, emphasizing the importance of epigenetic regulation in leukemia development.
AIM:
The aim of the present work was to study the expression of lncRNA MEG3 in a cohort of Egyptian newly diagnosed patients with acute myeloid leukemia and its relation with other clinical and laboratory parameters.
Keywords
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