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Öğe Aggressive clinicopathological course of myeloma with t(3;16) (q21;q22) cytogenetic abnormality(Galenos Yayincilik, 2019) Bozkurt, Süreyya; Okay, Mufide; Haznedaroğlu, İbrahimMultiple myeloma (MM) is a heterogeneous disease and patients present with a wide variety of cytogenetic anomalies reflecting the nature of the disease [1]. The aim of this letter is to report a rare karyotypic abnormality with an aggressive clinical course of MM. A 56-year-old male patient was admitted to the neurosurgery clinic with dorsal shoulder pain and inability to walk in April 2011. He underwent thoracic and lumbar spinal magnetic resonance imaging. Laminectomy was performed on the patient upon detecting masses at the levels of the first and seventh thoracic vertebrae. The patient was referred to our center when he was determined to have “lymphoma” based on the first evaluation 63 of his biopsy material. The specimen was then reevaluated in our center. A high-grade hematopoietic neoplasia was detected. Immunophenotypic findings suggested neoplasia with plasma cell origin. Immunohistochemically, neoplastic cells were positive for CD38, MUM-1, and kappa and negative for lambda. The karyotype of the patient was identified as 44,X,-Y,del(1) (p13p35),+der(1),t(3;16)(q21;q22),-4,-13,-14,+mar[8]/46,XY[42] (Figure 1).Öğe Akciğer Kanseri Kök Hücrelerinde Naked İfadesinin Düzenlenmesinde Histon Modifikasyonlarının Rolünün Araştırılması(2020) Ulukaya, Engin; Sapancı, Selin; Bozkurt, Süreyya; Aztopal, NazlıhanEpigenetik değişiklikler, geleneksel tedaviye dirençten sorumlu tutulan kanser kök hücrelerin (KKH) özelliklerinin düzenlenmesinde anahtar bir role sahiptir. Bu hücrelerde, Wnt/ ß-katenin sinyalizasyonunun yeniden/aşırı aktive olduğu ve sürecin epigenetik mekanizmalar tarafından düzenlendiği bilinmektedir. Dolayısıyla, ilgili epigenetik düzenekleri hedefleyen yaklaşımlarla KKH?lerinin terapötik olarak hedeflenebildiği gösterilmiştir. Özellikle, yolağı inaktif durumda tutan ana düzenleyicilerin aktivitesinin epigenetik modifikasyonlar aracılığıyla baskılanması kötü prognoz ile ilişkilendirilmektedir. Bu nedenle, proje önerisi kapsamında, akciğer kanseri KKH?lerinde epigenetik inhibitörlerle manipülasyon sonrası Wnt/ß-katenin sinyal yolağının negatif düzenleyici bileşeni Naked (NKD1 ve NKD2) düzeylerinde değişimin araştırılması ve sürece katkı sağlayan ilgili histon modifikasyonlarının belirlenmesi amaçlanmıştır. Öncelikli olarak, parental H1299 hücre soyu (H1299/P) içindeki KKH sayısı göreceli olarak arttırıldı (propagasyon, H1299/S) ve KKH?lere karakteristik yüzey belirteci oranları akım sitometri ile gösterildi. Ardından, histon demetilaz inhibitörü /DZNep ile ön tedavi uygulanan hücreler histon deasetilaz inhibitörü/TSA ile muamele edildi ve sitotoksik etki araştırıldı. İnhibitörlerin tek başlarına toksik etki sergilemedikleri dozların (0.1-0.25 uM) kombine kullanımında güçlü sitotoksik etki saptandı. H1299/S?in agresif karakteri ile ilişkili olarak NKD2?nin gen ve protein düzeylerinde azalma olduğu ve kombinasyon uygulaması sonrası ifadesinin yeniden düzenlendiği (artış) RT-PCR ve western blotting ile gösterildi. Wnt/ ß-katenin sinyal yolağı aktivitesi, EMT süreci ve ?stemness? ilişkili değişiklikler western blotting ile araştırıldı. NKD2 ifadesinde artışın Wnt/ ß-katenin sinyal yolağının inaktivasyonu ve agresif karakterin baskılanmasına katkı sağladığı belirlendi. Kombinasyon uygulaması sonrası global histon modifikasyon profili ELISA ile değerlendirildi ve NKD2 promotor bölgelerinde ilgili histon işaretlerinin değişimi ChIP yöntemi ile araştırıldı. Transkripsiyonel baskılanma ile ilişkili histon işareti H3K9me3 düzeylerinde gözlenen azalma ile NKD2 düzeylerindeki artış arasında doğrudan bir ilişki olmadığı saptandı. Bu kombinasyon tedavisinin, KKH?leri hedeflemedeki başarısının yeni ve umut verici bir epigenetiik tedavi seçeneği olarak kullanılabileceği öngörüsüyle ileri analizlerinin yapılması gerektiği sonucuna varılmıştır.Öğe Characterization of imatinib-resistant K562 cell line displaying resistance mechanisms(C M B Assoc, 2018) Hekmatshoar, Yalda; Özkan, Tülin; Güneş, Buket Altınok; Bozkurt, Süreyya; Karadağ, Aynur; Karabay, Arzu Zeynep; Sunguroğlu, AsumanChronic myeloid leukemia (CML) is a hematopoietic malignancy characterized by the t(9; 22) and the related oncogene, BCR-ABL. Tyrosine kinase activity of fusion protein BCR-ABL is the main cause of CML. Even if imatinib is used as a tyrosine kinase inhibitor (TKI) for CML therapy. drug resistance may occur in patients and the clinical failure of imatinib treatment in resistant patients had resulted with the use of another alternative TKIs. BCR-ABL dependent and independent molecular mechanisms have crucial roles in drug resistance. To reveal the underlying molecular mechanisms which play significant roles in imatinib resistance in CML, we established K562 imatinib-resistant cell line (K562r5) which was continuously exposed to (5 mu M) imatinib to investigate molecular mechanisms which play significant roles in drug resistance. First of all, we analyzed T315I. M351T, F315L and F359C/L/V mutations with DNA sequencing as a BCR-ABL dependent mechanism in our cell lines. Moreover, we investigated BCR-ABL independent mechanisms such as apoptosis. autophagy, drug transport and DNA repair which affect drug resistance in these cell lines. In vitro cell viability was determined by MTT assay. DNA sequencing analysis was performed to detect BCR-ABL mutations. The apoptotic effect of imatinib on CML cell lines was tested by flow cytometric Annexin V-PE staining and caspase activation assays. Apoptotic, autophagic, drug transporter and DNA repair genes expression levels were determined by RT-PCR. The conventional cytogenetic analysis was performed on K562s and K562r cells. Our results indicate that inhibition of apoptosis, induction of autophagy, overexpression of efflux gene MDR1 and down-regulation of influx gene OCT1 play crucial roles in the progression of imatinib resistance.Öğe Çocukluk cağı lösemi tanılı hastalarda sitogenetik anomaliler(2019) Bozkurt, Süreyya; Cangül, Şule Ünal; Bayhan, Turan; Gümrük, Fatma; Çetin, MuallaGİRİŞ ve AMAÇ: Konvansiyonel sitogenetik analiz, çocukluk çağında görülen akut lenfoblastik lösemi (ALL) ve akut myeloid lösemi (AML) hastalarında hem tanı hem de hastalık seyrinin izlenmesinde oldukça yol göstericidir. Bazı kromozomal anomaliler spesifik olarak belirli lösemi alt gruplarında görülebilmektedir. Ayrıca hastaların taşıdığı sayısal ve kromozomal anomalilerin bazıları iyi prognoz belirteci iken bazıları da kötü prognoz belirteçleridir. Sunduğumuz bu çalışmada kromozomal anomali tespit edilmiş 10 AML ve 16 ALL olmak üzere toplam 26 pediatrik lösemi hastasının sitogenetik analiz sonuçları ile hastaların klinik parametreleri arasındaki korelasyon araştırıldı. YÖNTEM ve GEREÇLER: Hastalara ait konvansiyonel analizler, uyarılmamış kemik iliği örneklerinden, Giemsa-tripsin (GTG bantlama) yöntemi ile elde edilmiş metafaz kromozomlarının incelenmesi ile oluşturuldu. BULGULAR: Hem AML hem de ALL hastalarında çeşitli yapısal ve sayısal anomaliler tespit edilmiştir. Bu anomaliler literatür ile uyumlu olup, hastaların lösemi tipleri ile de uyumluluk göstermiştir. Kompleks karyotipler AML hasta grubunda, ALL hasta grubundan daha fazla bulunmuştur. Ayrıca 1 ALL ve 2 AML tanılı hastada, nadir olarak görülen kromozomal anomaliler tespit edilmiştir. TARTIŞMA ve SONUÇ: Günümüzde gelişmiş moleküler sitogenetik tekniklerin varlığına rağmen, konvansiyonel sitogenetik analiz halen oldukça önemli bir yere sahiptir.Öğe Downregulation of stearoyl-CoA desaturase 1 (SCD-1) promotes resistance to imatinib in chronic myeloid leukemia(Mattioli 1885, 2022) Günes, Buket Altınok; Hekmatshoar, Yalda; Özkan, Tülin; Bozkurt, Süreyya; Aydos, Oya Sena Erdoğan; Büyükaşık, Yahya; Aladağ, Elifcan; Asuman SunguroğluChronic myeloid leukemia (CML) is a malignant hematopoietic stem cell disease resulting in the fusion of BCR and ABL genes and characterized by the presence of the reciprocal translocation t(9;22)(q34;q11). BCR-ABL, a product of the BCR-ABL fusion gene, is a structurally active tyrosine kinase and plays an important role in CML disease pathogenesis. Imatinib mesylate (IMA) is a strong and selective BCR-ABL tyrosine kinase inhibitor. Although IMA therapy is an effective treatment, patients may develop resistance to IMA therapy over time. This study investigated the possible genetic resistance mechanisms in patients developing resistance to IMA. We did DNA sequencing in order to detect BCR-ABL mutations, which are responsible for IMA resistance. Moreover, we analyzed the mRNA expression levels of genes responsible for apoptosis, such as BCL-2, P53, and other genes (SCD-1, PTEN). In a group of CML patients resistant to IMA, when compared with IMA-sensitive CML patients, a decrease in SCD-1 gene expression levels and an increase in BCL-2 gene expression levels was observed. In this case, the SCD-1 gene was thought to act as a tumor suppressor. The present study aimed to investigate the mechanisms involved in IMA resistance in CML patients and determine new targets that can be beneficial in choosing the effective treatment. Finally, the study suggests that the SCD-1 and BCL-2 genes may be mechanisms responsible for resistance.Öğe Eksozomlar ve kanserdeki rolleri(2018) Bozkurt, SüreyyaEksozomlar, vücutta bulunan hücrelerin neredeyse tamamı tarafından salgılanan, 40-100 nanometre (nm) çapında ve çift fosfolipid tabaka ile çevrili ekstrasellüler veziküllerdir. İçlerinde proteinler, lipitler, çok çeşitli RNA molekülleri ve DNA fragmenleri gibi birçok biyomolekül taşırlar. Bu biyomoleküller vasıtasıyla, alıcı hücrelerde gen ifadelerini düzenleyerek, immün regülasyon, hücre farklılaşması, hücreler arası haberleşme, hücre göçü gibi birçok biyolojik fonksiyonda rol alırlar. Tümör kökenli eksozomlar ise içlerinde taşıdıkları biyomoleküller vasıtasıyla kanserin gelişimi ve yayılımına yardım etmek için lokal ve sistemik çevreyi düzenlerler. Eksozom içeriklerinin kanserin tanısında ve hastalık seyrinin izlenmesinde biyobelirteç olarak kullanım potansiyellerini araştıran çalışmalar hızla artmaktadır. Ayrıca son yıllarda kanser tedavisinde eksozomların hedeflendiği ya da kullanıldığı yaklaşımlar da bulunmaktadır. Bu derlemenin amacı eksozomların yapısının, kanser gelişimindeki ve metastazdaki rollerinin ve kanser tedavisindeki kullanım potansiyellerinin ortaya konmasıdır.Öğe Expression analysis in the transcription level of PTGS2, CALR, MAGE-A3 genes in non-small cell lung cancer(DergiPark, 2020) Köse, Büşra; Bozkurt, SüreyyaBackground: In lung cancer, expression changes in genes that indirectly trigger carcinogenesis are a remarkable issue. In addition to mutations, detection of expression of genes that affect cell division, apoptosis, invasion and cell migration is important for studies to develop new inhibitor or monoclonal antibody drugs. Aim of this study was to investigate the mRNA expression levels of PTGS2, CALR and MAGE-A3 genes in the A549 cell line which is modeling lung adenocarcinoma compared to the BEAS-2B cell line which is modeling healthy bronchial epithelium. Materials and Methods: Quantitative Real-time PCR was performed to obtain the mRNA expression level changing. Results: In the results of the study, the mRNA level expression difference in A549 cell line compared with BEAS-2B cell line 229,13-fold increase in PTGS2 gene; 4,03-fold increase in CALR gene; 3,41- fold increase in MAGE-A3 gene were observed. These three genes are known to play roles in cancer cell division, apoptosis resistance, invasion, and angiogenesis. Conclusions: As a result of this study, these three genes are thought to have jointly effect on the NF?B signaling pathway. It may be beneficial to investigate on protein level for these three genes to illuminate at this point.Öğe First report of t(1;15)(q21;q11.2) and t(1;21)(q21;q11.2) anomalies in Burkitt Lymphoma(KUWAIT MEDICAL ASSOC, 2021) Bozkurt, Süreyya; Okay, Mufide; Haznedaroğlu, Celalettin İbrahimBurkitt lymphoma (BL) is a highly aggressive B cell neoplasm characterized by t(8;14)(q24;q32) which involves the MYC gene. Sometimes, patients have additional cytogenetic anomalies beside t(8;14)(q24;q32) and these anomalies usually lead to more aggressive phenotype. The aim of this paper is to report two novel karyotypic abnormalities which give rise to tetrasomy 1q with an aggressive clinical course of BL. We present a 41-year-old woman with BL. In this patient, the t(1;15)(q21;q11) and t(1;21)(q21;q11.2) were found in the complex karyotype with the translocation of t(8;14)(q24;q32), which is a characteristic of BL. The t(1;15)(q21;q11.2) and t(1;21)(q21;q11.2) anomalies were reported for the first time according to the databases that we have investigated. In our case, the result of t(1;15)(q21;q11.2) and t(1;21)(q21;q11.2) was tetrasomy of chromosomes of 1q. Structural anomalies of chromosomes 1q could be seen in BL patients as additional cytogenetic anomalies and gain of chromosome of 1q usually associated with disease recurrence and poor prognosis. In our case, the patient died approximately 8 months after diagnosis, so her prognosis was poor, which was consistent with the literature. The candidate genes on chromosomes 1q which could be involved in tumorigenesis remain to be identified.Öğe First report of t(1;9)(q21;q34) in Fanconi anemia as a preceeding chromosomal aberration before leukemia development(KUWAIT MEDICAL ASSOC, 2022) Bozkurt, Süreyya; Unal, Sule; Gumruk, FatmaPatients with Fanconi anemia (FA) tend to develop various hematologic and solid tumors. Cytogenetic abnormalities such as translocations of chromosome 1q, monosomy 5 and 7, trisomy 10, gains of 3q and t(8;21) have been reported in patients with FA who developed hematological malignancies. Since survival is low after the development of leukemia in FA patients, the follow-up for leukemia progression is very important. For this reason, cytogenetic anomalies that can be used as biomarkers in the development of leukemia are needed. Herein, we describe a patient with FA who developed acute myeloid leukemia with der(9)t(1;9) (q21;q34) for the first time.Öğe Hematological neoplastic disorders with chromosome 3 abnormalities(Carbone Editore, 2019) Bozkurt, Süreyya; Okay, Mufide; Sağlam Yarımcan, Filiz; Haznedaroğlu, Celalettin İbrahimIntroduction: Conventional karyotyping in the patients with haematological malignancies is very important. Because chromosomal abnormalities which detected in these patients have diagnostic and prognostic value. Aim: The aim of this study was to assess the patients with hematologic malignancy having chromosome 3 abnormalities which are rare. Method: Conventional cytogenetic analysis were done from bone marrow samples of patients. Samples were treated with trypsin and stained with Giemsa (GTG banding). 20 metaphases of each patient were examined and karyotypes were formed. Results: Among the 6865 patients analysed via conventional cytogenetic methods, 701 (10.2%) were found as pathological and 39 (5.5%) of those were found to have chromosome 3 abnormalities. The most common neoplastic diseases observed in patients which have chromosomes 3 abnormalities were Multiple Myeloma and Acute Myeloid Leukaemia (25.6% each), Myelodysplastic Syndrome (20.5%), Acute Lymphoblastic Leukaemia (12.8%), Lymphoma (12.8%) and Chronic Lymphoblastic Leukaemia (2.6%). Numerical chromosomes 3 abnormalities were 53.8% and structural chromosomal abnormalities were 43.5%. Complex karyotypes were 87.1% of all chromosome 3 abnormalities in our group. Conclusion: Chromosome 3 anomalies are seen less frequently in hematologic malignancies. Patients have both numerical and structural chromosome 3 anomalies and these anomalies are mostly found in complex karyotype. With 76.6% mortality rate, in our group chromosome 3 abnormalities were found to relate with unfavorable prognosis.Öğe MDA-MB-231 meme kanseri hücre dizisinde prostoglandin endoperoksid H sentaz 2 (PTGS2), kalretikulin (CALR) ve keratin-19 (KRT19) genlerinin transkripsiyon aşamasında anlatımlarının araştırılması(DergiPark, 2020) Bozkurt, Süreyya; Kaya Yiğit, DuyguBu çalışmada MDA-MB-231 meme kanser hücre hattında prostaglandin endoperoksid H sentaz 2 (PTGS2), kalretikulin (CALR) ve keratin-19 (KRT19) genlerinin transkripsiyon düzeyindeki gen anlatımlarının belirlenmesi amaçlanmıştır. Materyal ve metod: Kültür ortamında çoğaltılan MDA-MB-231 meme kanser hücrelerinden RNA izolasyonu yapılmış ardından cDNA sentezi gerçekleştirilmiştir. PTGS2, CALR ve KRT19 genlerine spesifik primerler ile eş zamanlı PCR yapılarak, bu genlerin ifadesi transkripsiyonel seviyede belirlenmiştir. Bulgular: MDA-MB-231 hücre hattında PTGS2 gen ifadesinde 14,92 kat; CALR gen ifadesinde 1,45 kat; KRT19 geninin ifadesinde ise 6,72 kat artış olduğu saptanmıştır. Sonuç: Farklı solid kanserlerde, apoptoz direnci, metastaz, anjiyogenez gibi biyolojik süreçlerde rol aldığı bilinen KRT19, CALR, PTGS2 genlerinin meme kanseri gelişiminde de rol alabileceği ve ileride yapılacak detaylı çalışmalarla prognostik öneme sahip olacağı ön görülmektedir.Öğe New mutations in KCNT2 gene causing early infantile epileptic encephalopathy type 57: Case study and literature review(2020) Alagöz, Meryem; Kherad, Nasim; Bozkurt, Süreyya; Yüksel, AdnanPurpose: Early infantile epileptic encephalopathy (EIEE) 57 belongs to a group of encephalopathies with early-onset and characterised by severe electroencephalogram abnormalities, seizures, developmental delay and intellectual disability. Method: We carried out Whole Exome analysis using Next Generation Sequencing (NGS) and bioinformatic analysis performed to find mutation associated with the patient phenotypes. The effect of the mutation on protein structure analysed by PolyPhen2 and Swissmodel ExPASy. Results: In this study, we evaluated two unrelated Turkish males diagnosed with EIEE type 57 to investigate the genetic cause of this disease. Whole exome sequencing revealed mutations in KCN2 gene, which is a member of Potassium channels (KCN) gene family associated with epileptic encephalopathies. Two mutations, c.545A>T (p.Asn182Ile and c.2638C>A (p.Leu880Met) were reported here as a novel mutation. Conclusions: Our findings implicate the genotype-phenotype correlation of these mutations. Furthermore, the computational analysis showed their effect on protein binding site and function suggesting their role in the development of early infantile epileptic encephalopathy 57.Öğe The novel translocation of t (1;21) in multiple myeloma with poor prognosis(DergiPark, 2019) Okay, Mufide; Bozkurt, Süreyya; Özgeyik, Mehmet; Haznedaroğlu, İbrahim CelalettinObjective: Multiple myeloma (MM) is characterized as the neoplastic proliferation of plasma cells producing a monoclonal paraprotein. The aim of this paper is to report complex karyotype that leads to a fatal clinical course in a patient with MM. Case: A 48-year-old male patient was diagnosed as MM free lambda. The karyotype of the patient was 46, XY, t(1;21) (p11;p11), del(3) (q25;q29), del(6) (q24;q26), t(11;14) (q13;q32), del(13) (q14;q21) in cytogenetic evaluation. Vincristine, doxorubicin and dexamethasone were started. The creatinine levels increased after the second course of chemotherapy, the chemotherapy protocol was switched to bortezomib and dexamethasone. Patient was admitted to the emergency department with pneumonia after the second chemotherapy cycle. Despite using broad spectrum antibiotics and oxygen support, he died after the development of sepsis syndrome. Conclusion: The anomaly of t (1;21) (p11;p11), that we detected in this case was detected in a case with MM for the first time and this anomaly has not been detected between these breaking points in any malignancies before. Although the prognostic impact of this unique anomaly may be unclear, further studies are needed to evaluate the effect of cytogenetic anomalies on prognosis of multiple myeloma.Öğe Rare cytogenetic anomalies in two pediatric patients with acute leukemia(Galenos Yayincilik, 2020) Bozkurt, Süreyya; Ünal, Şule; Bayhan, Turan; Gümrük, Fatma; Çetin, MuallaStructural chromosomal abnormalities are frequently seen in both pediatric acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) cases [1,2,3]. Although some chromosomal abnormalities are common, other abnormalities are rarely seen [4,5]. In this study two relatively rare cytogenetic abnormalities are reported. All procedures were performed in accordance with the Helsinki Declaration and approved by the local ethics committee (Approval No: GO 16/267-45).Öğe Stem cell transplantation for high-risk acute lymphoblastic leukemia in a developing country: a single-center experience(WILEY, 2020) Bozkurt, Ceyhun; Aksoy, B.; Aydoğdu, S.; Bozkurt, Süreyya; Erol Çipe, Funda; Öner, O.; Özsoy, S.; Fışgın, T.: Allogeneic stem cell transplantation in patients with a diagnosis of high-risk acute lymphoblastic leukemia results in high rates of survival in developed countries. Our aim with this presentation was to share our center’s experience on this subject. Methods: Hematopoietic stem cell transplantation was performed in a total of 69 patients with a diagnosis of high-risk acute lymphoblastic leukemia between 2015 and 2020 at our center. The demographic and treatment-related information of the patients was retrospectively evaluated.
