Moleküler Biyoloji ve Genetik Bölüm Başkanı
Yakın Doğu Üniversitesi Fen Fakültesi, Moleküler Biyoloji ve Genetik Bölümü
1970de Lefkoşa da doğdu. 1992 yılında İstanbul Üniversitesi Biyoloji bölümünden mezun oldu. 1993 de İstanbul Üniversitesi Çapa Tıp Fakültesi İç hastalkları Anabilim dalında master eğitimini aldı ve özel öğrenci olarak Tıp fakültesine devam etti. 1999 da Marmara Üniversitesinde Tıbbi biyoloji ve Genetik bölümünde birinci doktorasını tamamladı. 2001 de de Danimarka Aarhus Üniversitesi İnsan genetiği bölümünde telomer telomeraz biyolojisi, kanser ve kök hücre çalışmaları ile ikinci doktorasını tamamladı. 2003 te aldığı proje ve destekler ile Aarhus Üniversitesi İnsan genetiği bölümü içinde kendi bölümü “Kök Hücre ve Genetik tedavi” bölümünü kurdu. Prof. Dr. Serakıncı’nın dalı tıbbi genetiğin yanısıra ikinci çalışma ve ilgi alanı mezenkimal kök hücre biyolojisi kanser ve telomere/telomeraz biyolojisidir.2003 de Tıbbi genetik doçentliğini 2007 de ikinci çalışma alanı olan yaşlanma ve kök hücre genetiği dalında ikinci doçentliğini aldı. 2011 de tıbbi genetik ve kök hücre genetiği bölümlerinden profesorlüğünü aldı. Prof. Dr. Serakıncı’nın araştırma uzmanlığı, telomerase-immortalized mesenkimal kök hücreler, ve bunların gen terapisindeki kullanımı ve ilaç araştırması için doku modeli geliştirilmesi üzerinedir. Prof. Dr. Serakıncı'nın araştırma programı, yetişkin mezenkimal kök hücrelerin moleküler, hücresel ve gelişimsel biyolojisi üzerine odaklanmıştır. Kök hücrelerin kendi kendini yenileme ve farklılaşma sürecinin anlaşılması için gerekli stratejik ve teknik yaklaşımlarıın geliştirilmesi programın temel amacıdır. Nihai amaç ise hastalık ve hasarlanmanın hücre ve gen bazlı tedavisi için gerçekçi bir temel oluşturmaktır. Prof. Dr. Serakıncı 2 tane klas iki laboratuvarı ve 4 tane tam teşekküllü genetik çalışma ve araştırma laboratuvar ile Kök Hücre ve Genetik tedavi bölümünü kurmuş ve yönetmiştir. Çok sayıda araştırma ile dünya çapında kabul edilmiş 25’in üzerinde başarılı yayınlara imza atmış ve 5 kitab bölümü yazmıştır. Ayrica kanser kök hücre ve genetik alanındaki çalışmaları 2004, 2006 ve 2010 yıllında olmak üzere üç kez dünya literatüründe ilk 10’a girmiştir. Bunun yanisira mezenkim kök hücreleri ve kanser üzerine basta dünyanin en ileri kanser arastirma merkezi ve hastanesi olan M.D. Anderson, Houston Teksas Amerika olmak üzere bircok ülkede davetli olarak konferans ve seminerler vermistir. Bu alanda bir çok doktora ögrencisi ve uzman doktor yetiştirmistir. Bugüne dek 20’nin üzerinde proje alıp ürütmüş ve başarıyla tamalamıştır. Prof. Dr Serakıncı Ocak 2011’den itibaren Yakın Doğu Üniversitesi Tıp Fakültesi Tıbbi Genetik ve Kanser Tanı ve Araştrıma merkezi kurmuş ve yürütmektedir ayrıca bunun yanisira halen güney Danimarka üniversitesi Yaşlanma ve Telomer genetiği bölümü başkanıdır.
Yakın Doğu Üniversitesi Fen Fakültesi, Moleküler Biyoloji ve Genetik Bölümü
Yakın Doğu Üniversitesi Tıp Fakültesi, Tıbbi Genetik anabilim dalı
University of Southern Denmark, Institute for Regional Health Services ( IRS ),Department of Clinical Genetics
Aarhus University, Institute of Human Genetics
University of Southern Denmark, Department of Anatomy and Neuroscience
Aarhus University, Institute of Human Genetics
Aarhus University, Institute of Human Genetics
Aarhus University, Institute of Human Genetics
Cancercytogenetics laboratory Aarhus,Denmark, Aarhus Amtssygehus,Cancercytogenetics laboratory
Department of Cytogenetics in Aarhus, Department of Cytogenetics
Department of Cytogenetics Aarhus, Department of Cytogenetics
Maramara University/School of Medicine, Department of Medical Biology and Genetics
İstanbul School of Medicine, Department of Internal Medicine/Division of Medical GeneticsNad Prenatal Diagnosis Unit
Tıbbi Biyoloji ve Genetik
Marmara Ünivesitesi
Tıbbi Genetik
İstenbul Üniversitesi, Çapa Tıp Fakültesi
Biyoloji
İstanbul universitesi
Region Syddanmarks Forskningspulje 2008, “Telomerforkortning og DNA-skader i lungevæv ved KOL”
6th Framework Programme (shared costs) 2004-2008: “Developing Molecular Medicines For Cancer In The Post-Genome Era”. Coordinator: Rob Newbold, London, UK.
İdiyopatik tekrarlayan gebelik kayıplarında telomer uzunluk dinamiği ve TRF1, TRF2, POT1 and TPP1 genlerinin ekspresyonun belirlenmesi 2015-16, Centre of excellence Araştırma Fonu, YDÜ
CENP-A Metilasyonu ve Topoizomeraz Aktivitesinin Düşüklerdeki Rolü 2015-16 Centre of excellence araştırma fonu, YDÜ
Grosseren M Brogaard og Hustrus Mindefond. 2005: Short and long term effect of gamma irradiation of adult human mesenchymal stem cells
Højberg fonden 2007: Telomere length as prognostic marker in lung cancers,
Danish Medical Research Council: Post-doc stipendium 2001-2002, Identification and characterization of expected telomerase inhibitor,
Danish Cancer Society: 2002-2005, Junior Stipend, the double-faced role of Telomeres in the development of mesenchymal tumors,
2- 6th Framework Programme 2003-2008: DNA damage responses, genomic instability and radiation-induced cancer: the problem of risk at low and protracted doses, RISK-RAD. Coordinator: Laure Sabatier, Paris, France.
Danish Research Agency: 2005: “Forskningsprogrammet for ikke-ioniserende stråling” Effects of non-ionizing radiation on neural development and mature brain. An experimental study employing human and rodent, organotypic brain slice cultures and neural stem cells. Shared cost, partner in joint project. Coordinator Jens Zimmer Rasmussen, SDU, Denmark.
Role of Angiotensin (1-7) on Reactive Oxygen Species (ROS) Damage Induced Telomere Shortening and Repair in Cardiovascular Disease and Hypertension, 2015-2016, Centre of Excellence Araştırma Proje Destek Fonu
Telomere shortening and DNA damage in pulmonary tissue from patients with chronic obstructive pulmonary disease (COPD) 2015-16 Centre of excellence araştırma fonu , YDÜ
Danish Medical Research Council: 2004, Delivery of telomerase-targeted gene therapy vectors to sites of tumour stroma formation by tumour-homing mesenchymal stem cell based carriers.
TUBİTAK 2011, co-applicant “The effect of TRF2 knockdown on radiosensitivity of human mesenchymal stem cells”
Region Syddanmarks Forskningspulje 2009, co-applicant “Telomere shortening in lung epithelial cells in patients with chronic obstructive pulmonary disease (COPD)”
5th Framework Programme 2002-2005: Telomeres and radiosensitivity of individuals. TELOSENS. Coordinator: Laure Sabatier, Paris, France.
4- 6th Framework Programme, BIOACE, Coordinator Sukran Vardar, Izmir, Turkey
The development of normal (Caspersson et al. 1968, 1971) and “high-resolution” banding of chromosomes (Yunis et al. 1983) made it possible to identify chromo- somal anomalies like deletions, duplications, inversions and translocations with a resolution down to about 5 × 106 number of chromosome defects. However, in a number of situations, chromosome aberrations are too small or too complex to be fully diagnosed by banding techniques. Therefore, more sensitive and more refined techniques are sometimes necessary. This need has been met to some extent through the development of in situ hybridization (ISH) techniques. In addition to refining the banding technique, ISH is the only method that can simultaneously give information at both molecular and cellular levels, namely by visualizing DNA sequences on chromosomes and in cells and tissue sections, thereby enabling specific nucleic acid sequences to be visualized in their natural biological microenvironment. As a consequence, ISH has found a number of applications in clinical diagnosis and research. base pairs, and this enabled the diagnosis of a...
kitap bölümü
Over the last thirty years, the foremost inspiration for research on metastasis, cancer recurrence, and increased resistance to chemo- and radiotherapy has been the notion of cancer stem cells.The twenty-eight chapters assembled in Cancer Stem Cells - The Cutting Edge summarize the work of cancer researchers and oncologists at leading universities and hospitals around the world on every aspect of cancer stem cells, from theory and models to specific applications (glioma), from laboratory research on signal pathways to clinical trials of bio-therapies using a host of devices, from solutions to laboratory problems to speculation on cancersâ€TM stem cellsâ€TM evolution. Cancer stem cells may or may not be a subset of slowly dividing cancer cells that both disseminate cancers and defy oncotoxic drugs and radiation directed at rapidly dividing bulk cancer cells, but research on cancer stem cells has paid dividends for cancer prevention, detection, targeted treatment, and improved prognosis.
kitap bölümü
Progressive multifocal leukoencephalopathy (PML) is an infectious demyelinating disease of the central nervous system caused by the JC virus, a DNA polyomavirus. PML occurs during reactivation of the latent JC virus after long-standing immunosuppression. It is usually associated with conditions causing profound immunodeficiency, classically seen in patients with AIDS. Second commonly it has been reported in lymphoproliferative disorders like chronic lymphocytic leukemia (CLL). Here we report a case of 72 years old female patient with CLL who developed PML. Her clinical symptoms were rapid progressive slight hemiparesis of the right side and aphasia. In cranial MRI, a typical subcortical demyelinating nonenhancing lesions was shown, and JC virus DNA was positive in the CSF by PCR.
Progresif multifokal lökoensefalopati (PML), bir DNA polyomavirüs olan JC virüs tarafından oluşturulan, santral sinir sisteminin enfeksiyöz demiyelinizan bir hastalığıdır. PML, latent JC virüsün uzun süreli immünsüpresyon sonrasında reaktivasyonu sırasında oluşur. Genelde belirgin immünsüpresyona yol açan durumlar ile ilişkilidir ve klasik olarak da edinilmiş immün yetmezlik sendromu (AIDS) hastalarında görülür. İkinci sıklıkla da kronik lenfositik lösemi (KLL) gibi lenfoproliferatif hastalıklarla bildirilmektedir. Burada, 72 yaşında KLL’ye sahip olan ve PML geliştiren bir kadın hasta rapor edilmektedir. Hastanın klinik semptomları hızlı ilerleyici sağ taraflı hemiparezi ve afaziydi. Beyin manyetik rezonans görüntüleme (MRG), tipik subkortikal demiyelinizan kontrast tutmayan beyaz cevher lezyonlarını göstermekteydi ve beyin omurilik sıvısı (BOS) JC virüs DNA PCR’ı pozitif saptandı.
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A gradual shortening of telomeres due to replication can be measured using the standard telomere restriction fragments (TRF) assay and other methods by measuring the mean length of all the telomeres in a cell. In contrast, stress-induced telomere shortening, which is believed to be just as important for causing cellular senescence, cannot be measured properly using these methods. Stress-induced telomere shortening caused by, e.g. oxidative damage happens in a stochastic manner leaving just a few single telomeres critically short. It is now possible to visualize these few ultra-short telomeres due to the advantages of the newly developed Universal single telomere length assay (STELA), and we therefore believe that this method should be considered the method of choice when measuring the length of telomeres after exposure to oxidative stress. In order to test our hypothesis, cultured human mesenchymal stem cells, either primary or hTERT immortalized, were exposed to sub-lethal doses of hydrogen peroxide, and the short term effect on telomere dynamics was monitored by Universal STELA and TRF measurements. Both telomere measures were then correlated with the percentage of senescent cells estimated by senescence-associated ß-galactosidase staining. The exposure to acute oxidative stress resulted in an increased number of ultra-short telomeres, which correlated strongly with the percentage of senescent cells, whereas a correlation between mean telomere length and the percentage of senescent cells was absent. Based on the findings in the present study, it seems reasonable to conclude that Universal STELA is superior to TRF in detecting telomere damage caused by exposure to oxidative stress. The choice of method should therefore be considered carefully in studies examining stress-related telomere shortening as well as in the emerging field of lifestyle studies involving telomere length measurements.
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Objectives Leptin is a hormone secreted from adipocytes. It regulates metabolism and energy homeostasis through the leptin receptor (LEPR) which is localized centrally in hypothalamus as well as in peripheral tissues. The aim of this study was to investigate the association of leptin receptor gene Q223R polymorphism on obesity in association with body mass index (BMI), lipid parameters, plasma leptin levels and homeostasis model assessment of insulin resistance (HOMA-IR). Design and methods The study included 110 obese and 90 non-obese subjects. The LEPR Q223R polymorphism was determined by polymerase chain reaction–restriction fragment length polymorphism (PCR–RFLP). Plasma leptin levels, serum lipid and antropometric parameters were measured. Results No association was found between LEPR gene Q223R polymorphism and BMI in both study and control groups. Strikingly study group with non-obese subjects and with the RR genotype (homozygous mutant) had significantly higher serum total cholesterol (p < 0.001) and low density lipoprotein cholesterol (LDL-cholesterol) levels (p < 0.05) than QR (heterozygous) and QQ (wild type) genotypes. In obese group, subjects with the RR genotypes had significantly higher triglycerides (p < 0.05) levels, waist (p < 0.05) and hip circumferences (p < 0.001) than the QQ and QR genotypes. Conclusions Our results suggest that the LEPR gene Q223R polymorphism has an association with waist and hip circumferences in obese group but no direct association with obesity although there is a significant influence on lipid profile both in obese and non-obese subjects. Abbreviations LEPR, leptin receptor; BMI, body mass index; HOMA-IR, homeostasis model assessment of insulin resistance; PCR–RFLP, polymerase chain reaction–restriction fragment length polymorphism; LDL-C, low density lipoprotein cholesterol; SNPs, single nucleotide polymorphisms; HMG-CoA reductase, 3-hydroxy-3-methylglutaryl coenzyme reductase; VLDL, very-low density lipoprotein; TG, triglycerides; HDL-C, high-density lipoprotein cholesterol; ELISA, enzyme-linked immunosorbent assay; ANOVA, analysis of variance; ApoB, apolipoprotein B
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The health care system is negatively affected by the genetic disorders that lead to an increasing rate of morbidity and neonatal deaths and affect adults as well. These create a substantial government's psychosocial and economic burden on clinicians, patients and their families with the advancement in the field of genetics. There has been a tremendous increase in the rate in which diseases associated with variant DNA sequences are being sought and identified. The goal behind the creation of Near East University Genetic Mutation Database (NEU-GD) is to map and apprehend the patterns of common genetic diversity in the human genetic makeup in order to accelerate the search for the genetic causes of human disease. NEU-GD will allow scientists to generate extraordinarily useful information such as allelic variations among pop- ulation, and description of the genetic blueprint of mutations occurring in human beings. In this communication we report the construction of the first genetic mutation database for the people belonging to different ethnic groups living in North Cyprus (http://genetics-db.neu.edu.tr/). Therefore NEU-GD can serve as an important tool available online for molecular genetic testing of inherited disorder and persuade for further in- vestigation of novel genetic disorders in North Cyprus population.
Telomere repeat binding factor TRF2 is a member of shelterin complex with an important role in pro- tecting and stabilizing chromosomal ends. In the present study, we investigated the effect of partial knockdown of TRF2 on radiosensitivity of telomerase immortalized human mesenchymal stem cells (hMSC-telo1), which have a higher radioresistance compared to non telomerized counterpart. Partial knockdown of the protein achieved 15–20% reduction in TRF2 protein levels. The study compared the effect of 2.5 Gy radiation in two–four days after irradiation for hMSC-telo1 cells and the cells transfected with siTRF2 and null control vector. Radio-response of the cells were examined using senescence asso- ciated -Gal assay (-Gal), colony forming assay (CFU) and -H2AX phosphorylation. TRF2 deficiency substantially increased radiosensitivity of cells compared to controls in both proliferation and senes- cence assay (2.4 fold increase in -Gal, 1.6 fold decrease in CFU). In addition, it increased the -H2AX foci as revealed by both immunfluorescence and Western blot analysis. Our data suggests that partial knock- down of TRF2 in hMSC-telo1 cells cause increased -H2AX foci which led to fail TRF2 to protect telomeres from radiation thus TRF2 deficiency led to a 1,5–2 fold increase in the radiosensitivity of hMSC-telo1 cells through telomere destabilization.
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Objective: Leptin (LEP) is a metabolic and neuroendocrine hormone which is present in the circulation in amounts proportional to fat mass that acts to reduce food intake and increase energy expenditure thereby regulating body weight homeostasis. Various polymorphisms are shown to be present in LEP gene which play important roles in obesity and obesity-related metabolic biomarkers. The aim of this study was to investigate the association of one of these polymorphisms, leptin gene G-2548A polymorphism, on obesity in association with body mass index (BMI), lipid parameters, plasma leptin levels and homeostasis model assessment of insulin resistance (HOMA-IR).
Patients with Turner syndrome are generally characterized by having short stature with no secondary sexual characteristics. Some abnormalities, such as webbed neck, renal malformations (450%) and cardiac defects (10%) are less common. The intelligence of these patients is considered normal. Non-mosaic monosomy X is observed in approximately 45% of postnatal patients with Turner syndrome and the rest of the patients have structural abnormalities or mosaicism involving 46,X,i(Xq), 45,X/46,XX, 45,X and other variants. The phenotype of 45,X/ 46,X,+mar individuals varies by the genetic continent and degree of the mosaicism. The gene content of the marker chromosome is the most important when correlating the phenotype with the genotype. Here we present an 11-year-old female who was referred for evaluation of her short stature and learning disabilities. Conventional cytogenetic investigation showed a mosaic 45,X/46,X,+mar karyotype. Fluorescence in situ hybridization showed that the marker chromosome originated from the X chromosome within the androgen receptor (AR) and X-inactive specific transcript (XIST) genes. Therefore, it is possible that aberrant activation of the marker chromosome, compromising the AR and XIST genes, may modify the Turner syndrome phenotype.
Telomere repeat binding factor TRF2 is a member of shelterin complex with an important role in protecting and stabilizing chromosomal ends. In the present study, we investigated the effect of partial knockdown of TRF2 on radiosensitivity of telomerase immortalized human mesenchymal stem cells (hMSC-telo1), which have a higher radioresistance compared to non telomerized counterpart. Partial knockdown of the protein achieved 15–20% reduction in TRF2 protein levels. The study compared the effect of 2.5 Gy radiation in two–four days after irradiation for hMSC-telo1 cells and the cells transfected with siTRF2 and null control vector. Radio-response of the cells were examined using senescence associated ß-Gal assay (ß-Gal), colony forming assay (CFU) and ?-H2AX phosphorylation. TRF2 deficiency substantially increased radiosensitivity of cells compared to controls in both proliferation and senescence assay (2.4 fold increase in ß-Gal, 1.6 fold decrease in CFU). In addition, it increased the ?-H2AX foci as revealed by both immunfluorescence and Western blot analysis. Our data suggests that partial knockdown of TRF2 in hMSC-telo1 cells cause increased ?-H2AX foci which led to fail TRF2 to protect telomeres from radiation thus TRF2 deficiency led to a 1,5–2 fold increase in the radiosensitivity of hMSC-telo1 cells through telomere destabilization. © 2015 Elsevier B.V.
Telomere repeat binding factor TRF2 is a member of shelterin complex with an important role in protecting and stabilizing chromosomal ends. In the present study, we investigated the effect of partial knockdown of TRF2 on radiosensitivity of telomerase immortalized human mesenchymal stem cells (hMSC-telo1), which have a higher radioresistance compared to non telomerized counterpart. Partial knockdown of the protein achieved 15–20% reduction in TRF2 protein levels. The study compared the effect of 2.5 Gy radiation in two–four days after irradiation for hMSC-telo1 cells and the cells transfected with siTRF2 and null control vector. Radio-response of the cells were examined using senescence associated ß-Gal assay (ß-Gal), colony forming assay (CFU) and ?-H2AX phosphorylation. TRF2 deficiency substantially increased radiosensitivity of cells compared to controls in both proliferation and senescence assay (2.4 fold increase in ß-Gal, 1.6 fold decrease in CFU). In addition, it increased the ?-H2AX foci as revealed by both immunfluorescence and Western blot analysis. Our data suggests that partial knockdown of TRF2 in hMSC-telo1 cells cause increased ?-H2AX foci which led to fail TRF2 to protect telomeres from radiation thus TRF2 deficiency led to a 1,5–2 fold increase in the radiosensitivity of hMSC-telo1 cells through telomere destabilization.
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Therapeutic use of multipotent mesenchymal stromal stem cells (MSC) is a promising venue for a large number of degenerative diseases and cancer. Their availability from many different adult tissues, ease of expansion in culture, the ability to avoid immune rejection and their homing ability, are some of the properties of MSCs that make them a great resource for therapy. However, the challenges and risks for cell-based therapies are multifaceted. The blessing of cell culture expansion also comes with a burden. During in vitro expansion, stem cells experience a long replicative history and therefore, become subjected to damage from intracellular and extracellular influences. As previously shown cells that are manipulated to obtain an expanded replicative potential are prone to spontaneous transformation in culture. These manipulations help bypass the naturally built-in controls of the cell that govern the delicate balance between cell proliferation, senescence and carcinogenesis. Because of this, there is a risk for patients receiving stem cells that are in vitro expanded. Whether these cells are genetically engineered or harbouring xenogenic compounds, they cannot truly be considered "safe" unless the cells are closely monitored. In the present communication, we will focus on the therapeutic potential of the human mesenchymal stem cells (hMSC) with special focus on their use in cancer therapy. We will consider different mechanisms, by which stem cells can maintain telomeres and thereby the cell's ability to be expanded in vitro, and also focus on a new therapeutic venue that utilises hMSCs as delivery vehicles in innovative new cancer treatments.
Derleme
Human mesenchymal stem cells (hMSCs) have the ability to differentiate into several tissue types. Their use in cancer therapeutics or as therapeutic delivery vehicles has significant potential, particularly in their exosome/microvesicle–mediated tissue regeneration abilities. In this review, the potential use of hMSCs in cancer therapy is discussed.
Human papillomaviruses (HPVs); small, non-enveloped viruses with double stranded circular DNA; are believed to play a role in the progression of cancer. However, the exact mechanisms are not well established. The interference of HPV proteins, especially E6 and E7, with the cell cycle are considered to be the main pathway. It is still questioned whether the expression of these proteins or the viral load is more important in the neoplastic transformation. Furthermore, HPV is believed to adapt mechanisms to evade the host cells’ immune system and the persistent HPV infection may also play a role in oncogenic transformation by causing genomic instability and local immune suppression. These factors may cause accumulation of genomic alterations within the host cell and integration of the viral genome into the host genome. In the recent years, epigenetic modifications, such as methylation, are also believed to take a part in the neoplastic transformation. All these alterations to the genome may be favourable for the development of cancer. In this communication, we highlight the association of HPV in neoplastic transformation and progression of cancer.
The importance of human papillomavirus(HPV)infection and its role in the progress of cancer have been widely evaluated.The understanding of HPV association with certain cancers,such as cervical cancer,is very well established.A big step forward in the prevention of HPV associated cancers with the use of early detection by screening strategies has also been taken.In the last decade,development of HPV vaccination has reduced the number of cases in HPV infections and infection induced cancers.In this report,we review the HPV pathogenesis and highlight the mechanism of HPV involvement in cancer development.
Human mesenchymal stem cells (hMSCs) are multipotent non-hematopoietic precursor cells with the ability to differentiate into several tissue types. The use of hMSCs has gained significant importance in cancer therapies as well as a large number of degenerative disease therapies due to their homing abilities. However, these cells may undergo spontaneous transformation leading to them bypassing naturally built-in cell controls that could lead to senescence and carcinogenesis. Therefore, although MSCs have great potential for cancer therapy, they also risk the development of cancer, which provides them with double-faced characteristics for both cancer development and therapy. The potential use of hMSCs in therapeutics from the aspect of in vitro expansion of hMSCs and telomere dynamic is discussed.
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Bitirme tezine hazırlık
Bitirme tezine hazırlık
Bitirme tezine hazırlık
Bitirme tezine hazırlık
bitirme tezi yazılacak
bitirme tezi yazılacak
bitirme tezi yazılacak
bitirme tezi yazılacak
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THE AIM IS TO TEACH THE TECHNIQUES USED IN THE STUDY OF BIOMOLECULES,ESPECIALLY NUCLEIC ACIDS AND PROTEİNS.
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THE AIM IS TO TEACH THE INHERITANCE PATTERNS OF DISEASES AND PROVIDE EXAMPLES OF GENETIC DISORDERS.
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THE AIM IS TO TEACH THE INHERITANCE PATTERNS OF DISEASES AND PROVIDE EXAMPLES OF GENETIC DISORDERS.
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THE MAIN AIM OF COURSE IS TO REPRESENT THE PLACE AND THE IMPROTANCE OF BIOLOGY IN SCIENTIFIC CONTINUUM.
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Aims to teach human genetics and genomics in more specialized manner
İnsan genetiği ve genomik hakkında detaylı bilgi vermek
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Understand different state of the art molecular genetics applications
Moleküler biyolojideki yenilekleri öğrencilere aktarmak
Moleküler biyolojideki yenilekleri öğrencilere aktarmak
Moleküler biyolojideki yenilekleri öğrencilere aktarmak
Moleküler biyolojideki yenilekleri öğrencilere aktarmak
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Moleküler biyolojideki yenilekleri öğrencilere aktarmak
Moleküler biyolojideki yenilekleri öğrencilere aktarmak
Moleküler biyolojideki yenilekleri öğrencilere aktarmak
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Moleküler biyolojideki temel kavram ve konuları anlatmak
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Moleküler biyolojideki temel kavram ve konuları anlatmak
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Seçilen konuda literatür araştırması yaparak kişişel görüşleriyle birlikte bilimsel tartışma yetisini geliştirmek
Seçilen konuda literatür araştırması yaparak kişişel görüşleriyle birlikte bilimsel tartışma yetisini geliştirmek
Seçilen konuda literatür araştırması yaparak kişişel görüşleriyle birlikte bilimsel tartışma yetisini geliştirmek
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Seçilen konuda literatür araştırması yaparak kişişel görüşleriyle birlikte bilimsel tartışma yetisini geliştirmek
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Seçilen konuda literatür araştırması yaparak kişişel görüşleriyle birlikte bilimsel tartışma yetisini geliştirmek
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Seçilen konuda literatür araştırması yaparak kişişel görüşleriyle birlikte bilimsel tartışma yetisini geliştirmek
Seçilen konuda literatür araştırması yaparak kişişel görüşleriyle birlikte bilimsel tartışma yetisini geliştirmek
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Genetikteki temel kavram ve konuları anlatmak
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Genetikteki temel kavram ve konuları anlatmak
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