Kiraz Durmaz, Yağmur
Loading...
Profile URL
Name Variants
Kiraz, Yağmur
Ki̇raz Durmaz, Yağmur
Kiraz Durmaz, Yagmur
Durmaz, Yağmur Ki̇raz
Kiraz, Y.
Kiraz, Yagmur
Ki̇raz Durmaz, Yağmur
Kiraz Durmaz, Yagmur
Durmaz, Yağmur Ki̇raz
Kiraz, Y.
Kiraz, Yagmur
Job Title
Email Address
yagmur.kiraz@ieu.edu.tr
Main Affiliation
05.08. Genetics and Bioengineering
Status
Current Staff
Website
ORCID ID
Scopus Author ID
Turkish CoHE Profile ID
Google Scholar ID
WoS Researcher ID
Sustainable Development Goals
1NO POVERTY
0
Research Products
2ZERO HUNGER
0
Research Products
3GOOD HEALTH AND WELL-BEING
14
Research Products
4QUALITY EDUCATION
0
Research Products
5GENDER EQUALITY
0
Research Products
6CLEAN WATER AND SANITATION
0
Research Products
7AFFORDABLE AND CLEAN ENERGY
0
Research Products
8DECENT WORK AND ECONOMIC GROWTH
0
Research Products
9INDUSTRY, INNOVATION AND INFRASTRUCTURE
0
Research Products
10REDUCED INEQUALITIES
0
Research Products
11SUSTAINABLE CITIES AND COMMUNITIES
0
Research Products
12RESPONSIBLE CONSUMPTION AND PRODUCTION
0
Research Products
13CLIMATE ACTION
0
Research Products
14LIFE BELOW WATER
0
Research Products
15LIFE ON LAND
0
Research Products
16PEACE, JUSTICE AND STRONG INSTITUTIONS
0
Research Products
17PARTNERSHIPS FOR THE GOALS
0
Research Products
Documents
22
Citations
1827
h-index
9
Documents
0
Citations
0
Scholarly Output
15
Articles
11
Views / Downloads
132/75
Supervised MSc Theses
2
Supervised PhD Theses
0
WoS Citation Count
10
Scopus Citation Count
8
Patents
0
Projects
6
WoS Citations per Publication
0.67
Scopus Citations per Publication
0.53
Open Access Source
9
Supervised Theses
2
| Journal | Count |
|---|---|
| Annals of Hematology | 2 |
| Discover Oncology | 1 |
| European Journal of Biology | 1 |
| Experimed | 1 |
| Febs Open Bio | 1 |
Current Page: 1 / 3
Scopus Quartile Distribution
Competency Cloud
15 results
Scholarly Output Search Results
Now showing 1 - 10 of 15
Review Citation - WoS: 1Molecular Characterization of Multiple Myeloma(Poznan univ medical sciences, 2022-07-07) Kiremitçi, B. Zeren; Gürler, Elif Serap; Kiraz, YağmurMultiple myeloma (MM) is a hematologic malignancy which occurs when plasma cells, a type of white blood cell, grow out of control and start to overproduce antibodies accumulating in the blood and bone marrow. Despite the recent advances, the survival rate for MM has not increased significantly which opens the need for identifying new molecular targets. This review article presents the most frequently observed gene mutations (KRAS (22.0%), NRAS (18.0%), DIS3 (9.3%), TTN (8.3%), ZNF717 (8.3%), TENT5C (7.3%), TP53 (7.3%) %), BRAF (6.3%), MUC16 (6.3%), RYR2 (5.4%), and LRP1B (5.4%)) in MM patients, with their rates, correlations, clinical significance, importance in the framework of MM, as well as potential novel targets collected from the literature. The genes and MM patients' dataset (211) were obtained from cBioportal. Summing up, in the study conducted in MM patients, 3 genes with the most frequent mutations were reported as KRAS, NRAS and DIS3. In addition, in the context of our literature reviews and the data obtained, it appears that the TZNF717, TTN, MUC16, RYR2 genes need further investigations within the framework of MM.Article PSMB8 as a Novel Target for AML Therapy: Uncovering Synergistic Potential with PI3K Inhibitors(2025-03-25) Kiraz, Yağmur; Ateş, OnurAkut miyeloid lösemi (AML), progenitör kan hücrelerindeki genetik mutasyonlar nedeniyle hematopoetik kök hücrelerde meydana gelen düzensizliklerden kaynaklanan bir kemik iliği hastalığıdır. Bu mutasyonlar, malign klonal miyeloid kök hücrelerin kontrolsüz çoğalmasına yol açar. Miyeloid sarkomlar ve lösemi kutisi gibi ekstramedüller belirtiler ortaya çıkabilse de, temel sorun hematolojik hücre üretimindeki bozulmalardır. Yaşlı hastalarda tam remisyon oranı yüksek olmasına rağmen, önemli sayıda hasta üç yıl içinde nüks yaşamaktadır. Bu sorunun üstesinden gelmek için yeni hedeflerin belirlenmesi gerekmektedir. Önceki çalışmamızda, AML hastalarında PSMB8’in yüksek ekspresyon seviyeleri göstermesi ve düşük ekspresyon seviyelerine sahip hastalara kıyasla daha düşük sağkalım oranları ile ilişkilendirilmesi dikkatimizi çekmiştir. Daha önceki çalışmamızda, PSMB8 hedef alınarak sanal ilaç taramaları, ADMET analizi ve ardından Moleküler Dinamik (MD) simülasyonları gerçekleştirilmiştir. Bu çalışmalar sonucunda AML tedavisi için üç potansiyel ilaç adayı belirlenmiştir: Adozelesin, Fiduxosin ve Omipalisib. PI3K/mTOR inhibitörü olarak bilinen Omipalisib, AML gelişiminde PI3K/mTOR yolak proteinlerinin aşırı ekspresyon göstermesi nedeniyle sitotoksisite analizi için dikkatimizi çekmiştir. Sonraki aşamada, HL60 hücre hattında Omipalisib’in sitotoksisitesi, PSMB8 inhibitörü olan ONX-0914 ile karşılaştırılmıştır. Bu araştırma, PSMB8'in Akut Myeloid Lösemi için olası bir hedef olabileceğini ve potansiyel bir ilacın hedefli tedavi için kullanılabileceğini gösterdi.Conference Object Increasing Treatment Efficacy by Drug Repositioning in Acute Lymphoblastic Leukemia(Wiley, 2024) Kiraz, Y.; Tukel, E. Y.; Budak, B.; Turanli, B.[No abstract available]Article Unraveling bortezomib resistance in multiple myeloma: insights from RNA-Seq and PI3K/mTOR pathway analysis(Journal of Biological Research - Bollettino della Società Italiana di Biologia Sperimentale, 2026-02-04) Ates, Onur; Kiraz, YagmurMultiple Myeloma (MM), characterized by abnormal plasma cell proliferation, lacks curative treatment due to drug resistance, notably against Bortezomib, a critical proteasome inhibitor. To elucidate resistance mechanisms, we conducted RNA sequencing on Bortezomib-sensitive and resistant RPMI-8226 MM cells, comparing them to healthy B-cells. Differential expression analysis highlighted significant alterations in immune signaling, proteasome function, and metabolism. Resistant MM cells exhibited decreased antigen-presentation genes (HLA-DRA, HLA-DPA1, CD74), indicating immune evasion. Downregulation of metabolic regulators like GLUL and MDK suggested a glycolytic metabolic shift, whereas enhanced proteasome activities and nucleocytoplasmic transport represented adaptive strategies against proteotoxic stress. Importantly, resistant cells showed notable upregulation of PRAME and FAF1 genes, as oncogenes and apoptosis-related genes linked to therapy resistance. Pathway analysis revealed enrichment in neurodegenerative disease-related pathways, suggesting common protein misfolding mechanisms in MM progression. Additionally, resistant cells displayed cross-resistance to the dual protein kinase B (AKT)/mammalian target of rapamycin (mTOR) BEZ235, with a four-fold increase in IC₅₀ values, reflecting enhanced survival signaling and metabolic flexibility. These findings underscore the multifaceted nature of Bortezomib resistance, driven by metabolic reprogramming, immune modulation, and translational regulation. Targeting these adaptive pathways through combination therapies involving proteasome inhibitors, metabolic modulators, and autophagy inhibitors may present novel strategies to overcome drug resistance in MM.Article Exploring Pi3k Pathway Inhibitors for Acute Myeloid Leukemia: a Drug-Repurposing Approach(Istanbul University Press, 2023-12-28) Ergun, Cansu; Kiremitci, Buse Zeren; Arslantas, Gizem; Bozkurt, Busenur; Duran, Gizem Ayna; Kiraz, YağmurObjective: Acute myeloid leukemia (AML) is a malignant disease characterized by the uncontrolled growth, differentiation, and proliferation of immature hematopoietic cells. Patients with AML often have poor survival rates, which are associated with specific gene mutations in FLT3, CEBPA, and NPM1. The phosphatidylinositol 3-kinase (PI3K) pathway, a lipase pathway, is activated in many malignancies, including AML. Given the low survival rates in AML, this study identified candidate drugs that could inhibit the PI3K pathway, thereby offering a potential treatment for AML, by using a drug-repurposing approach. Materials and Methods: Online bioinformatics tools were utilized to identify pathway-related genes and FDA-approved drugs. Subsequently, molecular docking was performed to determine the binding affinity values. Important genes were identified by evaluating their impact on survival and their aberrant expression in the tumor. In this study, genes such as VAV1, GSK3B, MTOR, PDPK1, PRR5, TSC2, AKT3, and CREB1 were determined and docked with their potential inhibitors. Particular attention was paid to VAV1 because there were no known potential VAV1 inhibitors used in AML. Results: The docking results were ranked, and the proposed gene–drug pairs were identified as tideglusib and fostamatinib for the inhibition of GSK3B, pimecrolimus and fostamatinib for the inhibition of MTOR, and fostamatinib for the inhibition of PDPK1. Furthermore, nebivolol, darifenacin, dihydroergotamine, libanserin and entereg were identified as potential inhibitors of VAV1 in AML. Conclusion: To sum up, most effective gene–drug pairs according to binding affinities were proposed as candidate inhibitor drugs for AML.Article Citation - WoS: 4Citation - Scopus: 4Integrated Systems Biology Analysis of Acute Lymphoblastic Leukemia: Unveiling Molecular Signatures and Drug Repurposing Opportunities(Springer, 2024-06-05) Budak, Betül; Tükel, Ezgi Yağmur; Turanlı, Beste; Kiraz, YağmurAcute lymphoblastic leukemia (ALL) is a hematological malignancy characterized by aberrant proliferation and accumulation of lymphoid precursor cells within the bone marrow. The tyrosine kinase inhibitor (TKI), imatinib mesylate, has played a significant role in the treatment of Philadelphia chromosome-positive ALL (Ph + ALL). However, the achievement of durable and sustained therapeutic success remains a challenge due to the development of TKI resistance during the clinical course.The primary objective of this investigation is to propose a novel and efficacious treatment approach through drug repositioning, targeting ALL and its Ph + subtype by identifying and addressing differentially expressed genes (DEGs). This study involves a comprehensive analysis of transcriptome datasets pertaining to ALL and Ph + ALL in order to identify DEGs associated with the progression of these diseases to identify possible repurposable drugs that target identified hub proteins.The outcomes of this research have unveiled 698 disease-related DEGs for ALL and 100 for Ph + ALL. Furthermore, a subset of drugs, specifically glipizide for Ph + ALL, and maytansine and isoprenaline for ALL, have been identified as potential candidates for therapeutic intervention. Subsequently, cytotoxicity assessments were performed to confirm the in vitro cytotoxic effects of these selected drugs on both ALL and Ph + ALL cell lines.In conclusion, this study offers a promising avenue for the management of ALL and Ph + ALL through drug repurposed drugs. Further investigations are necessary to elucidate the mechanisms underlying cell death, and clinical trials are recommended to validate the promising results obtained through drug repositioning strategies.Article Citation - WoS: 2Citation - Scopus: 2Identification of Potential Inhibitors for Drug Resistance in Acute Lymphoblastic Leukemia Through Differentially Expressed Gene Analysis and in Silico Screening(Academic press inc elsevier science, 2024-11) Özay, Başak; Tükel, Ezgi Yağmur; Ayna Duran, Gizem; Kiraz, Yağmur; Duran, Gizem AynaAcute lymphoblastic leukemia (ALL) is a disease of lymphocyte origin predominantly diagnosed in children. While its 5-year survival rate is high, resistance to chemotherapy drugs is still an obstacle. Our aim is to determine differentially expressed genes (DEGs) related to Asparaginase, Daunorubicin, Prednisolone, and Vincristine resistance and identify potential inhibitors via docking. Three datasets were accessed from the Gene Expression Omnibus database; GSE635, GSE19143, and GSE22529. The microarray data waes analyzed using R4.2.0 and Bioconductor packages, and pathway and protein-protein interaction analysis were performed. We identified 1294 upregulated DEGs, with 12 genes consistently upregulated in all four resistant groups. KEGG analysis revealed an association with the PI3K-Akt pathway. Among DEGs, 33 hub genes including MDM2 and USP7 were pinpointed. Within common genes, CLDN9 and HS3ST3A1 were subjected to molecular docking against 3556 molecules. Following ADMET analysis, three drugs emerged as potential inhibitors: Flunarizine, Talniflumate, and Eltrombopag. Molecular dynamics analysis for HS3ST3A1 indicated all candidates had the potential to overcome drug resistance, Eltrombopag displaying particularly promising results. This study promotes a further understanding of drug resistance in ALL, introducing novel genes for consideration in diagnostic screening. It also presents potential inhibitor candidates to tackle drug resistance through repurposing.Article LEP and FOXO1 Genes, as a Proposed Tumor Suppressor Autophagic Cell Death Related Genes, Can Be Targeted by Antidiabetic Therapy in Nondiabetic Breast Cancer Patients(Springer, 2025-11-10) Duran, Gizem Ayna; Kiraz, Yagmur; Baykara, DenizIntroduction Breast cancer can be treated effectively with personalized, gene-targeted therapies due to its molecular and genetic differences. Our study aims to identify breast cancer-specific tumor suppressor genes related to autophagic cell death and discover new drugs that target these mechanisms, even if they are not breast cancer-specific. Materials and methods Gene intensity values of 457 tumor and 19 healthy breast tissues were used to determine downregulated and upregulated genes related to autophagy and apoptosis using Bioconductor R program via LIMMA package. Then, genes affecting survival were identified by survival analysis via Kaplan-Meier Plotter tool. Furthermore, the signalling pathways associated with these genes and targeting candidate drug components were determined by gene enrichment analysis using "KEGG pathway option" and Drug MATADOR in "ShinyGo 0.82" web-tool, respectively. Results Breast cancer tumor tissues showed downregulation of genes related to autophagy and apoptosis (c19orf12, CRYAB, LEP, SRPX, SNCA, FOXO1) and upregulation of others (SLC7A5, ATP2A2, INHBA, ATP5IF1). Among these, SLC7A5, c19orf12, LEP, SPRX, SNCA, and FOXO1 affected patient survival and prognosis. The AMPK signaling pathway, targeting FOXO1 and LEP, was identified as key. Only the LEP gene was targeted by Metformin, Pioglitazone, Rosiglitazone, and Troglitazone. Conclusion In our study, survival associated LEP and FOXO1 genes were identified as candidate tumor suppressor genes associated with autophagic cell death in non-obese and non-diabetic breast cancer patients. Anti-diabetic drugs such as Metformin, Pioglitazone, Rosiglitazone, Troglitazone are proposed as candidate components in the treatment processes by targeting the LEP gene in nondiabetic breast cancer patients.Article In Silico Approach for Identification of PI3K/MTOR Dual Inhibitors for Multiple Myeloma Treatment(Istanbul Univ, 2023-04-14) Masalaci, Ilke; Akdogan, Yaren; Mutlu, Ozge; Eyvaz, Hande; Kiraz, YagmurObjective: Multiple myeloma is a hematologic malignancy in which targeting phosphoinositide 3 kinase (PI3K) and/or the mammalian target of rapamycin (mTOR) individually has been shown to have anti-proliferative effects, however, inhibiting both proteins simultaneously has been reported to have more effective results for its treatment. The aim of this study is to determine the molecular interactions and predicted inhibitory effects of 40 different dual inhibitors on mTOR, PI3K delta, and PI3K gamma to propose potentially the most effective dual inhibitor that targets the PI3K delta and PI3K gamma isoforms as well as the mTOR proteins since those isoforms are known to be predominant in multiple myeloma patients. Therefore, the focus in this study is built around the specific targeting of the PI3K delta and PI3K gamma isoforms from the multiple myeloma perspective. Materials and Methods: In silico docking experiments were conducted to determine the binding energies for different ligands that target mTOR, PI3K delta, and PI3K gamma. Protein-dual inhibitor complexes and the amino acids and bond types were visualized to identify molecular interactions. The absorption, distribution, metabolism, and excretion properties of dual inhibitors were analyzed and evaluated. Results: The binding affinity values were found to be between -7 and -9.9 kcal/mol. The toxicity prediction values of the selected dual inhibitors were obtained from the Pro-Tox-II web tool and classified according to the globally harmonized system of classification of labeling of chemicals. Conclusion: Correspondingly, among all dual inhibitors, Vistusertib is determined to be a promising compound against multiple myeloma cells by inhibiting both PI3K delta and PI3K gamma as well as mTORC1/2.Erratum Citation - WoS: 1Correction To: Integrated Systems Biology Analysis of Acute Lymphoblastic Leukemia: Unveiling Molecular Signatures and Drug Repurposing Opportunities (annals of Hematology, (2024), 10.1007/S00277-024-05821-w)(Springer Science and Business Media Deutschland GmbH, 2024-07-11) Budak, B.; Tükel, E.Y.; Turanlı, B.; Kiraz, Y.https://doi.org/10.1007/s00277-024-05821-w. In the published paper, Figs. 4 and 5 were mistakenly replaced with Figs. 2 and 3 during proofing stage by the production department of the journal. We sincerely apologize for the error introduced. The original article has been corrected. © The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2024.
