NİTRİK OKSİT SENTAZ 3 (NOS3) GLU298ASP GEN VARYASYONUNUN MEME KANSERLİ HASTALARDA İNCELENMESİ

      Nitrik Oksit'in (NO) tümör biyolojisindeki rolü tam olarak anlaşılamamış olmasına karşın  tümörün büyümesi, gelişmesi ve metastaz gibi durumlarda  önemli rol oynayan bir serbest radikal olduğu ileri sürülmektedir.  Nitrik oksit sentaz (NOS) enzim ailesi L-sitrulinin, L-arginine dönüşümü sırasında Nitrik oksit (NO),  sentezine aracılık eden bir grup katalizörlerdir. Bu çalışmanın amacı Nitrik Oksit Sentaz (NOS3) Glu298Asp polimorfizmini meme kanserli hastalarda araştırmaktır. Bu amaçla 49 meme ve 89 sağlıklı kontrol grubu çalışmaya dahil edilmiştir. Çalışma gruplarımızda NOS3 Glu298Asp polimorfizmi periferal kan örnekleri kullanarak PCR-RFLP yöntemiyle tayin edilmiştir. Meme kanserli hastalarda NOS3 Glu298Asp genotip dağılımı [GG: 2 (4.1%), GT: 22(44.9%), TT: 25(51%)] sağlıklı kontrol grubundan [GG: 25(28.1%), GT: 34(38.2%), TT: 30(33.7%)] istatistiksel olarak anlamlı derecede farklı bulunmuştur (p=0.024). NOS3 Glu298Asp gen varyasyonu T allel frekansı meme kanserli hastalarda kontrol grubuna göre  anlamlı şekilde yüksek olarak saptanmıştır (χ2=7.229; p=0.007; OR: 1.228;%95 CI: 1.065-1.415).Çalışmamız sonucunda NOS3 Glu298Asp polimorfizminin meme kanseri riski ile ilişkili olabileceği kanısına varılmıştır.

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The role of Nitric Oxide (NO) in tumour biology is not well understood. However, it has been proposed that NO is a highly reactive free radical and plays important roles in growth, progression or metastasis of tumour. Nitric oxide synthases (NOSs) are a family of enzymes that catalyzing the production of (NO) by converting L-arginine to L-citrulline. The aim of present study was to examine Nitric Oxide Synthase 3 (NOS3) Glu298Asp polymorphism in patients with breast cancer. For this purpose, 49 patients with breast cancer and 89 healthy controls were included in the study. The NOS3 Glu298Asp polymorphism were genotyped by PCR-RFLP using peripheral blood samples in our study groups. NOS3 Glu298Asp genotype distribution in the breast cancer patients [GG: 2(4.1%), GT: 22(44.9%), TT: 25(51%)] was statistically different from the healthy control group [GG: 25(28.1%), GT: 34(38.2%), TT: 30(33.7%)] (p=0.024). NOS3 Glu298Asp gene variation T allele frequency was significantly higher in breast cancer patients that of controls (χ2=7.229; p=0.007; OR: 1.228;%95 CI: 1.065-1.415). Conclusion: Our finding suggest that NOS3 Glu298Asp might be associated with breast cancer risk.

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