الفهرس 
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Abstract
Acute myeloid leukemia is a heterogeneous group of hematologic malignancies that arise from dysfunctional proliferation of developing leukocytes resulting in accumulation of large number of clonal and abnormal immature myeloid cells in the bone marrow and peripheral blood.
Alterations in genes involved in epigenetic regulation have recently emerged as a third class of mutations, with downstream effects on both cellular differentiation and proliferation.
Polycomb repressive complex 2 comprises multiple subunits. Its core subunit is the catalytic subunit Enhancer of Zeste Homolog 2 (EZH2) which is essential for epigenetic gene silencing. EZH2 functions as a tumor suppressor in many tumors. Inactivating mutations and deletion of EZH2gene are found in patients with myeloid malignancies and EZH2 mutations are associated with poor patient survival.
PHD finger protein19 gene is PRC2 cofactor, acts as a critical mediator of tumorigenesis and functions by maintaining repressive transcriptional states of many developmental regulatory genes.
This study was conducted to investigate PHF 19 expression pattern and EZH2 gene deletion in patients with acute myeloid leukemia. The study included 60 individuals divided into 2 groups:
group I: Included 40 newly diagnosed AML patients, 23 males and 17 females, their ages ranged from 18 to 80 years who were admitted at clinical hematology unit of internal medicine department at Assiut University Hospital and oncology department of South Egypt Cancer Institute.
group II: Included 20 apparently healthy individuals as control group (13 males and 7 females) their ages ranged from 21 to 60 years.
Inclusion criteria:
• Newly diagnosed patients with acute myeloid leukemia (AML), who fullfill 2022 WHO criteria.
Exclusion criteria:
• Patients with any other type of malignant tumors.
• Therapy related AML patients.
• AML on top of myeloproliferative neoplasms or MDS.
All participants gave an informed consent prior to being included in the study. The study was approved by the ethical committee of Faculty of Medicine, Assiut University.
The following laboratory investigations were done:
• Complete blood counting and reticulocytic count.
• Examination of PB films with differential leucocytic count.
• Erythrocyte sedimentation rate (ESR).
• Prothrombin time and concentration.
• Liver function tests, kidney function tests, serum LDH enzyme, calcium and uric acid levels.
• Examination of leishman stained BMA smears.
• Flowcytometric (FCM) immunophenotypic analysis of BMA samples
• Real time polymerase chain reaction (PCR): Relative quantification of whole blood PHF 19 gene expression level was done in the Molecular Biology Unit, Clinical Pathology Department, Assiut University Hospital.
• Fluorescence in situ hybridization (FISH) for detection of EZH2 gene deletion in cytogenetic lab, Clinical Pathology Department, South Egypt Cancer Institute.
• Follow up of the patients after 6 months of therapy by BM blast cell count was done.