Baran, Yusuf
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Baran, Y.
Baran, Y
Baran, Y
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ybaran@gmail.com
yusufbaran@iyte.edu.tr
yusufbaran@iyte.edu.tr
Main Affiliation
04.03. Department of Molecular Biology and Genetics
Status
Current Staff
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Sustainable Development Goals
1NO POVERTY
0
Research Products
2ZERO HUNGER
2
Research Products
3GOOD HEALTH AND WELL-BEING
125
Research Products
4QUALITY EDUCATION
1
Research Products
5GENDER EQUALITY
2
Research Products
6CLEAN WATER AND SANITATION
1
Research Products
7AFFORDABLE AND CLEAN ENERGY
1
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8DECENT WORK AND ECONOMIC GROWTH
1
Research Products
9INDUSTRY, INNOVATION AND INFRASTRUCTURE
12
Research Products
10REDUCED INEQUALITIES
0
Research Products
11SUSTAINABLE CITIES AND COMMUNITIES
1
Research Products
12RESPONSIBLE CONSUMPTION AND PRODUCTION
1
Research Products
13CLIMATE ACTION
4
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14LIFE BELOW WATER
0
Research Products
15LIFE ON LAND
1
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16PEACE, JUSTICE AND STRONG INSTITUTIONS
2
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17PARTNERSHIPS FOR THE GOALS
0
Research Products
Documents
103
Citations
4761
h-index
36
Documents
163
Citations
4265
Scholarly Output
185
Articles
94
Views / Downloads
460540/177056
Supervised MSc Theses
13
Supervised PhD Theses
3
WoS Citation Count
3977
Scopus Citation Count
4300
Patents
0
Projects
11
WoS Citations per Publication
21.50
Scopus Citations per Publication
23.24
Open Access Source
146
Supervised Theses
16
| Journal | Count |
|---|---|
| Haematologica | 34 |
| Leukemia Research | 9 |
| Hematology | 8 |
| Tumor Biology | 6 |
| Leukemia and Lymphoma | 4 |
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185 results
Scholarly Output Search Results
Now showing 1 - 10 of 185
Article Citation - WoS: 20Citation - Scopus: 23Apoptotic Effects of Non-Edible Parts of Punica Granatum on Human Multiple Myeloma Cells(SAGE Publications Inc., 2016) Kiraz, Yağmur; Neergheen-Bhujun, Vidushi S.; Rummun, Nawraj; Baran, YusufMultiple myeloma is of great concern since existing therapies are unable to cure this clinical condition. Alternative therapeutic approaches are mandatory, and the use of plant extracts is considered interesting. Punica granatum and its derived products were suggested as potential anticancer agents due to the presence of bioactive compounds. Thus, polypenolic-rich extracts of the non-edible parts of P. granatum were investigated for their antiproliferative and apoptotic effects on U266 multiple myeloma cells. We demonstrated that there were dose-dependent decreases in the proliferation of U266 cells in response to P. granatum extracts. Also, exposure to the extracts triggered apoptosis with significant increases in loss of mitochondrial membrane potential in U266 cells exposed to the leaves and stem extracts, while the flower extract resulted in slight increases in loss of MMP. These results were confirmed by Annexin-V analysis. These results documented the cytotoxic and apoptotic effects of P. granatum extracts on human U266 multiple myeloma cells via disruption of mitochondrial membrane potential and increasing cell cycle arrest. The data suggest that the extracts can be envisaged in cancer chemoprevention and call for further exploration into the potential application of these plant parts.Master Thesis Activated Signaling Pathways and Apoptotic Mechanisms in Resveratrol Applied Chronic Myeloid Leukemia Cells and the Involvement of Ceramide Metabolizing Genes on These Mechanisms(Izmir Institute of Technology, 2010) Kartal Yandım, Melis; Baran, Yusuf; Baran, YusufResveratrol, an important phytoalexin in many plants, has cytotoxic effects on several cancer cells. Ceramide is a significant sphingolipid which affects many signaling pathways regulating cell senescence, migration, and cell cycle arrest. Intracellular ceramide level is balanced by glucosylceramide synthase (GCS), the converter of ceramide to glucosylceramide, and sphingosine kinase-1 (SK-1) that convert ceramide to sphingosine 1-phosphate (S1P). Ceramide functions as an apoptotic molecule whereas glucosylceramide S1P function as anti-apoptotic. An important cell-permeable analogue of natural ceramides, C8:ceramide, increases intracellular ceramide levels significantly, while 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) and SK-1 inhibitor increase accumulation of ceramides by inhibiting GCS and SK-1, respectively. Chronic myelogenous leukemia (CML), a hematological disorder, results from the generation of BCR/ABL oncogene. In this study, we examined the roles of ceramide metabolizing genes in resveratrol-induced apoptosis, and the expression profiles of 84 genes underlying apoptosis, cell cycle control, DNA damage repair, and invasion and metastasis in human K562 CML cells treated with resveratrol. There were synergistic cytotoxic and apoptotic effects of resveratrol with coadministration of C8:ceramide, PDMP and SK-1 inhibitor. We observed significant increases in expression levels of LASS genes, and decreases in expression levels of GCS and SK-1 in K562 cells in response to increasing concentrations of resveratrol. There were also significant increases in the expression levels of SERPINB5, FAS, TNFRSF, MTSS that are related with tumor suppression, and decreases in Myc expression. Our data, in total, showed for the first time that resveratrol might kill CML cells through increasing intracellular generation and accumulation of apoptotic ceramides.Conference Object Expression Analysis of 84 Genes Involved in Different Signalling Pathways of Cancer in Chronic Myeloid Leukemia Cells in Response To Nilotinib(Ferrata Storti Foundation, 2010) Baran, Yusuf; Camgöz, Aylin; Can, Geylani[No abstract available]Article Citation - WoS: 10Citation - Scopus: 14Enalapril-Induced Apoptosis of Acute Promyelocytic Leukaemia Cells Involves Stat5a(International Institute of Anticancer Research, 2012) Purçlutepe, Özlem; İskender, Güniz; Kiper, Hatice Demet; Tezcanlı, Burçin; Selvi, Nur; Biray Avcı, Çığır; Kosova, Buket; Adan Gökbulut, Aysun; Şahin, Fahri; Baran, Yusuf; Saydam, GürayBackground: In this study, we aimed at evaluating the cytotoxic and apoptotic effects of enalapril on human HL60 acute promyelocytic leukaemia cells and at clarifying the roles of signal transducers and activator of transcription proteins (STATs) on enalapril-induced cell death. Materials and Methods: Cell viability and cytotoxicity tests were conducted by Trypan blue dye exclusion and 2,3-Bis[2-methoxy-4-nitro-5-sulphophenyl]-2H-tetrazolium-5- carboxanilide inner salt (XTT) assays, respectively. Apoptotic analyses were performed by the AnnexinV-enhanced green fluorescent protein (EGFP) staining method and by fluorescence microscopy. Expression levels of STAT3, -5A and -5B genes were analysed by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Results: The results showed that enalapril reduced viability and proliferation, and induced apoptosis in HL60 cells in a dose-and time-dependent manner as compared to untreated controls. The expression levels of STAT5A gene were significantly reduced in enalapril-treated HL60 cells as compared to untreated controls. Conclusion: Taken together, all data showed for the first time that enalapril has significant anticancer potential for the treatment of acute premyelocytic leukaemia.Article Citation - WoS: 24Citation - Scopus: 24Mechanisms Responsible for Nilotinib Resistance in Human Chronic Myeloid Leukemia Cells and Reversal of Resistance(Informa Healthcare, 2013) Camgöz, Aylin; Gençer, Emel Başak; Ural, Ali Uğur; Baran, YusufMultidrug resistance remains a significant obstacle to successful chemotherapy. The ability to determine the possible resistance mechanisms and surmount the resistance is likely to improve chemotherapy. Nilotinib is a very effective drug in the treatment of imatinib-sensitive or -resistant patients. Although very successful hematologic and cytogenetic responses have been obtained in nilotinib-treated patients, in recent years cases showing resistance to nilotinib have been observed. We aimed to examine the mechanisms underlying nilotinib resistance and to provide new targets for the treatment of chronic myeloid leukemia (CML). There was an up-regulation of antiapoptotic BCR/ABL, GCS and SK-1 genes and MRP1 transporter gene and down-regulation of apoptotic Bax and CerS1 genes in nilotinib-resistant cells. There was no mutation in the nilotinib-binding region of BCR/ABL in resistant cells. Inhibiton of GCS and SK-1 restored nilotinib sensitivity. Targeting the proteins that are involved in nilotinib resistance in addition to the inhibition of BCR/ABL could be a better method of treatment in CML.Conference Object Determination of Cytotoxic and Apoptotic Effects of Caffeic Acid Phenethyl Ester and Gossypol in Combination With Fludarabine at a Molecular Level in Acute Lymphoblastic Leukemia Cells(Ferrata Storti Foundation, 2013) Baran, Yusuf; İskender, G.; Pişkin, Özden; Özcan, Mehmet Ali[No abstract available]Conference Object Suppression of STAT5A Increases Chemotherapeutic Sensitivity in Imatinib-Resistant and Imatinib-Sensitive K562 Cells(Ferrata Storti Foundation, 2010) Baran, Y.; Baran, Yusuf; Kosova, B.; Ekiz, Hüseyin Atakan; Tezcanli, B.; Ekiz, H.; Cakir, Z.; Selvi, S.Master Thesis The Mechanisms Responsible for Nilotinib Resistance in Human Chronic Myeloid Leukemia Cells(Izmir Institute of Technology, 2010) Camgöz, Aylin; Baran, Yusuf; Baran, YusufMultidrug resistance remains a significant obstacle to successful chemotherapy. The ability to determine the possible resistance mechanisms and surmount the resistance is likely to improve chemotherapy. Nilotinib is a very effective drug in the treatment of sensitive or Imatinib resistant patients. Although very successful hematologic and cytogenetics responses have been obtained in Nilotinib-treated patients, in recent years resistance cases were observed. The main objective of the project is to understand the mechanisms underlying multidrug resistance to Nilotinib to provide new targets for the treatment of chronic myeloid leukemia (CML). In this study, continuous exposure of cells to step-wise increasing concentrations of Nilotinib resulted in the selection of cells resistant to 50 nM Nilotinib and referred to as K562/NIL-50. Expression analyses of BCR-ABL gene demonstrated BCR-ABL was upregulated in resistant cells as compared to parental sensitive cells. However, nucleotide sequence analyses of ABL kinase gene revealed that there was no mutation in Nilotinib binding region of the gene in resistant cells. There was also an increase in expression levels of MRP1 gene in resistant cells, which transports the toxic substances outside of cells. Besides, Bax, which is one of the apoptosis inducing genes, was dowregulated in resistant cells. In addition to this, in resistant cells, while GCS and SK-1 genes were overexpressed, decrease in expression levels of LASS1 gene was observed. In conclusion, we determined mechanisms involved in Nilotinib resistance in CML in vitro. Targeting this mechanisms, besides inhibition of BCR-ABL may be a good way of treatment of CML.Article Citation - WoS: 28Citation - Scopus: 29Revealing Genome-Wide Mrna and Microrna Expression Patterns in Leukemic Cells Highlighted “hsa-Mir as a Tumor Suppressor for Regain of Chemotherapeutic Imatinib Response Due To Targeting Stat5a(SAGE Publications Inc., 2015) Tezcanlı Kaymaz, Burçin; Selvi Günel, Nur; Ceyhan, Metin; Bozok Çetintaş, Vildan; Özel, Buket; Kartal Yandım, Melis; Kıpçak, Sezgi; Aktan, Çağdaş; Adan Gökbulut, Aysun; Baran, Yusuf; Kosova Can, BuketBCR-ABL oncoprotein stimulates cell proliferation and inhibits apoptosis in chronic myeloid leukemia (CML). For cure, imatinib is a widely used tyrosine kinase inhibitor, but developing chemotherapeutic resistance has to be overcome. In this study, we aimed to determine differing genome-wide microRNA (miRNA) and messenger RNA (mRNA) expression profiles in imatinib resistant (K562/IMA-3 μM) and parental cells by targeting STAT5A via small interfering RNA (siRNA) applications. After determining possible therapeutic miRNAs, we aimed to check their effects upon cell viability and proliferation, apoptosis, and find a possible miRNAArticle Citation - WoS: 79Citation - Scopus: 84An Update on Molecular Biology of Thyroid Cancers(Elsevier Ltd., 2014) Ömür, Özgür; Baran, YusufDifferentiated thyroid cancer (DTC) is the most common endocrinological malignancy. There are several histological variants such as papillary and follicular thyroid carcinoma. Many patients with well-differentiated subtypes of DTC are cured by surgery alone or with radioiodine, while poorly differentiated types usually have a worse prognosis. The aggressiveness of thyroid tumors is closely linked to specific gene alterations.Several diagnostic and prognostic molecular markers such as BRAF and RAS point mutations; RET/PTC and PAX8/PPARγ gene rearrangements; MAPK, PI3K, p53, Wnt-beta catenin, HIF1α and NF-kappaB signaling pathways; microRNA profiles and aberrant methylation have been demonstrated in more than 70% of DTC. Diagnostic use of these molecular markers may be optimized for identifying higher risks of mortality, tumor recurrence and metastatic potential. Understanding the molecular biology of thyroid cancers can be an important avenue for diagnosis and treatment of radioiodine-refractory or inoperable DTC patients with novel molecular targeted therapeutic agents. © 2014 Elsevier Ireland Ltd.