Clinical Lymphoma, Myeloma & Leukemia, Vol.23, Suppl.1 - September 2023

Abstracts Clinical Lymphoma, Myeloma & Leukemia September 2023 S260 before full-count recovery. Opportunities to decrease length of care could include increased utilization of providers closer to the patients’ homes after hospital discharge. Keywords: length of stay, leukemia, utilization AML-021 Expression of the Ten‑Eleven Translocation 1 Gene (TET1) in Acute Myeloid Leukemia Eman Nagiub PhD1, Hosni Badrawi PhD2, Mohammad Galal PhD2, Monica Metry MS3 1Assiut university, Assiut, Egypt. 2SECI, Assiut, Egypt. 3SECI, Assiut, Egypt Background: The ten-eleven translocation 1 gene (TET1) is a member of the TET methyl cytosine dioxygenase family of enzymes (TET1, TET2, and TET3). TET1 has a role in various physiological and pathological processes. It is an epigenetic regulator of the DNA and RNA demethylation processes. Therefore, it regulates gene expression at both the transcriptional and post-transcriptional levels. Objective: We studied the expression levels of the TET1 gene in patients with acute myeloid leukemia (AML) and its correlation with their clinical and pathological criteria. Methods: This study was done in 37 patients who were newly diagnosed with AML. Bone marrow (BM) samples were analyzed using real-time PCR 7500s. Twenty subjects, apparently healthy, were included as a control group and matched by age and sex. Results: There was a significant correlation between the expression levels of the TET1 gene in patients with AML and their clinical and pathological criteria. It has been found that expression levels of the TET1 gene were higher in patients with AML than in the control group. Our study reported a significant TET1 gene upregulation in 62.2% of the patients with AML. Significantly higher TET1 levels were found in 66.7% of patients with AML not otherwise specified (NOS), 66.7% of patients with AML without maturation, 83.3% of patients with AML with maturation, and 61.9% of patients with AML with monocytic differentiation. Regarding AML with recurrent cytogenetic abnormalities, 100% of patients with AML carrying t(8;21) showed TET1 downregulation, but there was no difference in TET1 expression levels among AML patients with t(15;17). This study showed a significant relationship between TET1 gene levels and the percentage of blast cells in peripheral blood (PB). In BM, the higher percentage of blast cells was associated with the upregulated TET1 gene. Conclusion: TET1 exerts an oncogenic role in AML and is upregulated in patients with the disease. A relationship was found between TET1 expression levels and blast percentages in the PB and BM of patients with AML. The higher percentage of blast cells was associated with the upregulated TET1 gene. Keywords: AML, TET1, DNA demethylation, real-time PCR AML-025 Clinical Relevance of the RUNX1 Mutation in Egyptian Patients With Primary Refractory Acute Myeloid Leukemia Nahed Moawad Rakha MD, Shaza Ahmed MD, Hanaa A.elsamee MD, Reham Mousa MD Internal Medicine Department, Clinical Hematology Division, Faculty of Medicine, Ain Shams University, cairo, Egypt Background: Primary refractory acute myeloid leukemia (AML) represents a continuing obstacle in clinical management. The Runtrelated transcription factor 1 (RUNX1) gene is a relatively uncommon mutational target in AML cases. This study aims to investigate the role of the RUNX1 mutation in newly diagnosed refractory AML patients receiving first-line induction chemotherapy. Methods: This study involved 50 Egyptian patients with newly diagnosed AML. The control group included 20 patients with newly diagnosed AML who received the conventional first induction chemotherapy with complete remission (CR). The cases group included 30 patients with newly diagnosed AML who received the same conventional first induction chemotherapy protocols but did not respond to the treatment. Results: RUNXI mutations were found in 13.3% of the examined cases group compared to 5% of the control group. In the cases group, the RUNXI mutation was found to be statistically significant (P=0.01). The RUNX1 mutation and OS were significantly correlated (P=0.05). Conclusion: RUNX1 mutations may play a role in resistance to treatment and prognosis in AML. Therefore, measuring the RUNX1 level provides a new strategy for developing more aggressive treatments for primary refractory AML cases. Keywords: AML, RUNX1, genetic mutations, primary refractory AML AML-027 The LD‑VenEx Phase II Clinical Trial: An ex Vivo Flow Cytometry Based‑Drug Screening of AML Patient Samples Niveditha Umesh Katyayini PhD1, Sandra Leigh Gordon PhD2, Heikki A Kuusanmäki PhD2,3, Pilar Ayuda Durán PhD1, Jorrit Martijn Enserink PhD1, Krister Wennerberg PhD2 1Department of Molecular Cell Biology, Institute for Cancer Research, Oslo University Hospital, The Norwegian Radium Hospital, Oslo, Norway. 2University of Copenhagen, Biotech Research and Innovation Centre, Copenhagen, Denmark. 3Institute of Molecular Medicine Finland (FIMM), Helsinki, Finland Acute myeloid leukemia (AML) is a hematological malignancy distinguished by the accumulation of clonal, proliferative, poorly differentiated cells in bone marrow and peripheral blood. Cancer cells harbour druggable alterations at the genetic level, but genetic diagnostics fail to predict effective treatments for a majority of AML patients. Therefore, it is important to predict treatment response through identification of predictive molecular markers. The low-dose

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