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  • Küçük Resim
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    Association Between Survivin Gene Polymorphisms and the Susceptibility to Colon Cancer Development in the Turkish Population
    (Asian Pacific Organization Cancer Prevention, 2014) Yamak, Nesibe; Yaykaşlı, Kürşat Oğuz; Yılmaz, Ümit; Eröz, Recep; Uzunlar, Ali Kemal; Ankaralı, Handan; Baltacı, Davut
    Background: Colon cancer is one of the most common cancers worldwide. Apoptosis is a necessary physiological process for cell elimination which is very important both cellular homeostasis and cell proliferation and differantiation. Dysregulation can lead to uncontrolled cell growth and tumor development. Survivin, a member of the IAP family, plays a key role in promotion of cell proliferation as well as inhibition of apoptosis in cancer cells. The aim of this study was to investigate whether specific genetic polymorphisms of survivin could be associated with colon cancer development and progression in a Turkish population. Our study is the first to our knowledge to investigate the relationship between colon cancer risk and survivin gene polymorphisms. Materials and Methods: The relation between colon cancer and survivin -31 G/C (rs9904341), -241 C/T (rs17878467) and -625 C/G (rs8073069) polymorphism in promotor site of survivin gene associated with apoptosis was investigated using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Results: Individuals with -31C allele and CC genotype were found to have a higher risk of developing colon cancer (OR=13.4, p=0.01). The -241 CT genotype considerably increased the risk of colon cancer (OR=12.0, p=0.0001). However, there was no significant varaition of the survivin -625 C/G polymorphism among colon cancer patients and controls in our study. Conclusions: This study provides the first evidence that survivin -31 G/C and -241 C/T SNP significantly contribute to the risk of colon cancer in the Turkish population.
  • Küçük Resim
    Öğe
    Kolon kanseri hastalarında survivin gen polimorfizmlerinin incelenmesi
    (Düzce Üniversitesi, 2012) Yamak, Nesibe; Yaykaşlı, Kürşat Oğuz
    Kolon kanseri dünya çapında görülen en yaygın kanserlerden biridir. Kanserlerin patogenezi hücrelerin çoğalması, farklılaşması ve sağ kalımı gibi genel gereksinimlerin düzenlenmesinde anahtar görev üstlenen genlerin mutasyonlarından etkilenmekte ve hastalık bir seri somatik mutasyonun birbirini izlemesiyle gelişmektedir. Apoptozis ise, hem hücresel homeostazisin devamlılığı hem de hücre çoğalması ve farklılaşmasında çok önemli olan hücre eliminasyonu için gerekli fizyolojik bir işlemdir. Apoptozis, genetik işlergelerle düzenlenmekte ve malign hücrelerde bu işlergelerin denetimi bozulabilmektedir. Bu da kontrolsüz hücre büyümesine ve tümör gelişimine neden olmaktadır. Bu çalışmada apoptozisle ilişkili olan Survivin geninin promotör bölgesindeki -31 G/C, -241 C/T, -625 C/G ve -1547 A/G polimorfizmlerin kolon kanseri ile ilişkisi PCR-RFLP yöntemi kullanılarak incelendi. Yapılan çalışma sonucunda survivin -31C alleli ve CC genotipine sahip bireylerin kolon kanserine yakalanma riskinin yüksek olduğu bulundu. -241 CT genotipinin kolon kanseri riskini önemli derece arttırdığı bulundu (OR=12.0, p=0.0001). -625 C/G polimorfizmi ile kolon kanseri arasında istatistiksel olarak anlamlı bir fark yoktu. Survivin -1547AG genotipi AA' ya göre 3.383 kat daha fazla hastalık riski taşıdığı bulundu (p=0.026). Ayrıca GG genotipine sahip olanlarda da hastalık riski anlamlı düzeyde yüksek bulundu (p<0.05). Anahtar sözcükler: Kanser, Kolon, Polimorfizm, RFLP, Survivin
  • Küçük Resim
    Öğe
    Mide kanseri hastalarında survivin gen polimorfizmi araştırılması
    (2012) Yamak, Nesibe; Yaykaşlı, Kürşat Oğuz; Soğuktaş, Hatice; Yaykaşlı, Emine; Oktay, Murat; Erdem, Havva; Kurman, Yener
    Amaç: Dünya genelinde mide kanserinin insidansı düşmesine rağmen hala önemli bir sağlık problemidir. Türkiye’de ise yılda 30.000 yeni mide kanseri vakasıyla 2. en sık görülen kanserdir. Mide kanseri genetik ve çevresel faktörlerin etkileşimiyle ortaya çıkan çok faktörlü karmaşık bir hastalıktır. Kanserli dokuda aşırı ifade edilen survivin, apoptozis inhibe edici proteinlerdendir. Bu çalışmada Survivin -31 G/C polimorfizmi ile mide kanseri arasındaki ilişki araştırıldı. Gereç ve yöntem: Çalışma Düzce Üniversitesi Araştırma ve Uygulama Hastanesi Patoloji Laboratuvarına gelen mide kanseri tanısı konmuş 46 hasta ve sağlıklı bireylerin oluşturduğu 42 kişilik kontrol grubu ile gerçekleştirildi. Bu bireylerin genotipi Düzce Üniversitesi, Tıp Fakültesi, Tıb- bi Genetik Anabilim Dalı Laboratuvarlarında PCR-RFLP yöntemiyle tayin edildi. Bulgular: Hasta grubunda, GG genotipi 16 (% 34,8), GC genotipi 21 (% 45,7) ve CC genotipi ise 9 (% 19,6) olguda saptandı. Kontrol grubunda ise, genotip dağılımı sırasıyla 13 (% 31), 26 (% 61,9) ve 3 (% 7,1) bulundu. Hasta ve kontrol grubu karşılaştırıldığında istatistiksel olarak anlamlı bir fark saptanamadı. Fakat CC genotipine sahip bireylerin mide kanserine yakalanma riskinin GG (OR1,52) daha fazla risk oluşturduğu bulundu. Sonuç: Bu çalışma bildiğimiz kadarıyla Türk toplumunda mide kanseri ile Survivin -31G/C polimorfizmini araştıran ilk çalışmadır. Elde ettiğimiz sonuçlar hasta ve kontrol gruplarımızın temsil ettiği toplum kesitinde mide kanseri ile Survivin -31 G/C polimorfizmi arasında anlamlı bir ilişki olmadığını göstermekle birlikte CC genotipinin mide kanserine yatkınlık oluşturduğu düşünülebilir.
  • Küçük Resim
    Öğe
    Polymorphisms in MMP-2 and TIMP-2 in Turkish patients with prostate cancer
    (2014) Yaykaşlı, Kürşat Oğuz; Kayıkçı, Muhammet Ali; Yamak, Nesibe; Soğuktaş, Hatice; Düzenli, Selma; Arslan, Ali Osman; Hatipoğlu, Ömer Faruk
    Aim: Prostate cancer is the most commonly diagnosed malignancy and the second most common cause of cancer deaths in the Western male population. Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) modulate the remodeling of the extracellular matrix (ECM). The imbalance between MMPs and TIMPs may lead to an emergence of pathological processes such as cancer. In this study, the association between TIMP-2 (418 G/C) and MMP-2 (1306 C/T) polymorphisms and prostate cancer in the Turkish population was investigated. Materials and methods: Sixty-one prostate cancer patients and 46 healthy subjects were included in the study. DNA was isolated from 2 mL of peripheral blood taken from subjects, and genotypes were analyzed by the polymerase chain reaction-restriction fragment length polymorphism method. Results: The TIMP-2 418 (GC) genotype was found in 15 cases (32.6%) in the control group and in 9 cases (14.8%) in the patients group, and statistical significance was determined (P 0.037, OR 0.346). The MMP-2 1306 (CT) genotype was found 2.17 times more in the patient group than in the control group (P 0.149, OR 2.17). Conclusion: Our results show that the TIMP-2 418 (GC) genotype had a putative protective effect against prostate cancer.
  • Küçük Resim
    Öğe
    Polymorphisms in MMP-2 and TIMP-2 in Turkish patients with prostate cancer
    (Tubitak Scientific & Technical Research Council Turkey, 2014) Yaykaşlı, Kürşat Oğuz; Kayıkçı, Muhammet Ali; Yamak, Nesibe; Soğuktaş, Hatice; Düzenli, Selma; Arslan, Ali Osman; Hatipoğlu, Ömer Faruk
    Aim: Prostate cancer is the most commonly diagnosed malignancy and the second most common cause of cancer deaths in the Western male population. Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) modulate the remodeling of the extracellular matrix (ECM). The imbalance between MMPs and TIMPs may lead to an emergence of pathological processes such as cancer. In this study, the association between TIMP-2 (-418 G/C) and MMP-2 (-1306 C/T) polymorphisms and prostate cancer in the Turkish population was investigated. Materials and methods: Sixty-one prostate cancer patients and 46 healthy subjects were included in the study. DNA was isolated from 2 mL of peripheral blood taken from subjects, and genotypes were analyzed by the polymerase chain reaction-restriction fragment length polymorphism method. Results: The TIMP-2 418 (GC) genotype was found in 15 cases (32.6%) in the control group and in 9 cases (14.8%) in the patients group, and statistical significance was determined (P = 0.037, OR = 0.346). The MMP-2 1306 (CT) genotype was found 2.17 times more in the patient group than in the control group (P = 0.149, OR = 2.17). Conclusion: Our results show that the TIMP-2 418 (GC) genotype had a putative protective effect against prostate cancer.
  • Küçük Resim
    Öğe
    The Effect of BRAF T1799A Mutation on Tumor Size of Papillary Thyroid Cancer
    (Düzce Üniversitesi, 2013) Yamak, Nesibe; Oktay, Murat; Yaykaşlı, Emine; Önder, Elif; Oktay, Nilay Aydin; Aydın, Yusuf; Devlet, Düzce Atatürk
    Objective: The incidence of thyroid cancer, the most common endocrine malignancy isincreasing in all populations. Papillary thyroid cancer constitutes approximatelly 80 % of thethyroid cancers and several BRAF gene mutations escpecially T1799A are involved in theetiology of papillary thyroid cancer. The aim of this study was to investigate the frequency ofBRAF T1799A mutation in thyroid cancer and the possible association between BRAFT1799A mutation and tumor size.Methods: The study was conducted with 58 cases with thyroid cancer and 52 cases with nocancer in totally 108 cases. DNA isolated from paraffin-embedded tissues of cases, and thegenotypes were analyzed by PCR-RFLP method. Statistical analyses were performed usingSPSS 17.0 software. P values less than 0.05 were accepted as statistically significant.Results: There was no statistically significant association between patient and control groupsin term of the AA genotype. However TA genotype was significantly higher in patient groupthan control group (p=0.0001, OR=7.089 (2.7-18.6)). When comparing less and more than 1cm tumor size groups in papillary thyroid cancer cases, there was no statistically significantassociation for TA genotype (p=0,51, OR=0,641 (0,1-2,4)) and AA genotype (p=0,67,OR=0,694 (0,1-3,8)).Conclusion: Thyroid cancer has the most increasing rate among all cancers types in the world.So, the elucidation of the molecular basis in detail has gained the great importance. In thisstudy, it was concluded that BRAF T1799A mutation has no effect on tumor size. However,this study should be repeated with larger population to get more confident results