Yazar "Bozkurt, Sureyya" seçeneğine göre listele

Listeleniyor 1 - 4 / 4
  • Küçük Resim
    Öğe
    Determining the frequency of iron overload at diagnosis in de novo acute myeloid leukemia patients with multilineage dysplasia or myelodysplasia-related changes: a case control study
    (Springer Heidelberg, 2019) Yavuz, Boran; Aydın, Seda; Bozkurt, Sureyya; Üner, Ayşegül; Büyükaşık, Yahya
    Acute myeloid leukemia (AML) with myelodysplasia-related changes (AML-MRC) is a new disease category, which was defined as a separate entity in the World Health Organization Classification of Tumours of Haematopoietic and Lymphoid Tissues. While pre-treatment iron overload in patients with myelodysplastic syndrome has been previously studied, its relationship with AML-MRC has not been studied. We aimed to investigate the relationship between serum iron tests compatible with iron overload and the diagnosis of multilineage dysplasia (MLD) and AML with myelodysplasia-related changes (AML-MRC) in AML patients diagnosed at Hacettepe University Adult Hospital between January 2002 and September 2017. Ninety-three patients who met the criteria were enrolled. Bone marrow aspirate of each patient was re-examined, and dysplasia was investigated; other data were examined from patient's records. The iron overload status at diagnosis and transferrin saturation (TS) values were compared between the groups with and without MLD and those with and without AML-MRC. When iron overload was defined as TS >= 58% and ferritin >= 500 ng/mL, iron overload was observed in 10 (37%) patients with MLD and in 4 (13%) without MLD. The difference is almost statistically significant (p = 0.053). The mean TS value and frequency of iron overload were higher in AML-MRC patients than in non-AML-MRC patients (p < 0.05 for both). A mild positive significant correlation was observed between the dysplasia severity score and TS (r = 0.317, p = 0.032). In patients with AML-MLD and AML-MRC, iron overload occurred regardless of the transfusion status at the time of diagnosis. Morphologic severity of dysplasia may be correlated with higher TS values at the time of diagnosis.
  • Küçük Resim Yok
    Öğe
    Identification of common genes and pathways underlying imatinib and nilotinib treatment in CML: a Bioinformatics Study
    (Taylor & Francis Inc, 2023) Hekmatshoar, Yalda; Rahbar Saadat, Yalda; Ozkan, Tulin; Bozkurt, Sureyya; Karadag Gurel, Aynur
    Imatinib (IMA) and nilotinib are the first and second generations of BCR-ABL tyrosine kinase inhibitors, which widely applied in chronic myeloid leukemia (CML) treatment. Here we aimed to provide new targets for CML treatment by transcriptome analysis. Microarray data GSE19567 was downloaded and analyzed from Gene Expression Omnibus (GEO) to identify common genes, which are downregulated or upregulated in K562-imatinib and K562-nilotinib treated cells. The differentially expressed genes (DEGs) were assessed, and STRING and Cytoscape were used to create the protein-protein interaction (PPI) network. In imatinib and nilotinib treated groups' comparison, there were common 626 upregulated and 268 downregulated genes, which were differentially expressed. The GO analysis represented the enrichment of DEGs in iron ion binding, protein tyrosine kinase activity, transcription factor activity, ATP binding, sequence-specific DNA binding, cytokine activity, the mitochondrion, sequence-specific DNA binding, plasma membrane and cell-cell adherens junction. KEGG pathway analysis revealed that downregulated DEGs were associated with pathways including microRNAs in cancer and PI3K-Akt signaling pathway. Furthermore, upregulated DEGs were involved in hematopoietic cell lineage, lysosome and chemical carcinogenesis. Among the upregulated genes, MYH9, MYH14, MYL10, MYL7, MYL5, RXRA, CYP1A1, FECH, AKR1C3, ALAD, CAT, CITED2, CPT1A, CYP3A5, CYP3A7, FABP1, HBD, HMBS and PPOX genes were found as hub genes. Moreover, 20 downregulated genes, YARS, AARS, SARS, GARS, CARS, IARS, RRP79, CEBPB, RRP12, UTP14A, PNO1, CCND1, DDX10, MYC, WDR43, CEBPG, DDIT3, VEGFA, PIM1 and TRIB3 were identified as hub genes. These genes have the potential to become target genes for diagnosis and therapy of CML patients.
  • Küçük Resim Yok
    Öğe
    Mediterranean Journal of Hematology and Infectious Diseases
    (Mattioli 1885, 2023) Qipa, Egzona; Acar, Muradiye; Bozkurt, Sureyya; Buyukdogan, Murat; Sonmez, Hazal B.; Sayitoglu, Muge; Erbilgin, Yucel
    Acute lymphoblastic leukemia (ALL) is a malignant disease of hematopoietic stem cells. B cell ALL (B-ALL) is characterized by highly proliferative and poorly differentiated progenitor B cells in the bone marrow. Chromosomal rearrangements, aberrant cell signaling, and mutations lead to dysregulated cell cycle and clonal proliferation of abnormal B cell progenitors. In this study, we aimed to examine hot spot genetic variations in the RUNX1, IDH2, and IL2RA genes in a group of (n=52) pediatric B-ALL. Sanger sequencing results revealed a rare RUNX1 variant p.Leu148Gln in one B-ALL patient with disease recurrence. Additionally, common intronic variations rs12358961 and rs11256369 of IL2RA were determined in two patients. None of the patients had the IDH2 variant.RUNX1, IDH2, and IL2RA variations were rare events in ALL. This study detected a novel pathogenic RUNX1 variation in a patient with a poor prognosis. Examining prognostically important genetic anomalies of childhood lymphoblastic leukemia patients and the signaling pathway components will pilot more accurate prognosis estimations.
  • Küçük Resim Yok
    Öğe
    Phenotypic and functional characterization of subpopulation of Imatinib resistant chronic myeloid leukemia cell line
    (Elsevier Urban & Partner Sp Z O O, 2023) Hekmatshoar, Yalda; Gurel, Aynur Karadag; Ozkan, Tulin; Saadat, Yalda Rahbar; Koc, Asli; Karabay, Arzu Zeynep; Bozkurt, Sureyya
    Purpose: Chronic myeloid leukemia (CML) is a hematological malignancy characterized by the presence of BCR-ABL protein. Imatinib (IMA) is considered as the first line therapy in management of CML which particularly targets the BCR-ABL tyrosine kinase protein. However, emergence of resistance to IMA hinders its clinical efficiency. Hence, identifying novel targets for therapeutic approaches in CML treatment is of great importance. Here, we characterize a new subpopulation of highly adherent IMA-resistant CML cells that express stemness and adhesion markers compared to naive counterparts.Materials and methods: We performed several experimental assays including FISH, flow cytometry, and gene expression assays. Additionally, bioinformatics analysis was performed by normalized web-available microarray data (GSE120932) to revalidate and introduce probable biomarkers. Protein-protein interactions (PPI) network was analyzed by the STRING database employing Cytoscape v3.8.2.Results: Our findings demonstrated that constant exposure to 5 & mu;M IMA led to development of the adherent phenotype (K562R-adh). FISH and BCR-ABL expression analysis indicated that K562R-adh cells were derived from the original cells (K562R). In order to determine the role of various genes involved in epi-thelial-mesenchymal transition (EMT) and stem cell characterization, up/down-regulation of various genes including cancer stem cell (CSC), adhesion and cell surface markers and integrins were observed which was similar to the findings of the GSE120932 dataset.Conclusion: Treating CML patients with tyrosine kinase inhibitors (TKIs) as well as targeting adhesion molecules deemed to be effective approaches in prevention of IMA resistance emergence which in turn may provide promising effects in the clinical management of CML patients.