Yazan: admin Tarih: Tem 23rd, 2010 | Kategori::
Prostate cancer(Prostat Kanseri)
Cancer Invest. 2006 Feb;24(1):41-5.
Silig Y, Pinarbasi H, Günes S, Ayan S, Bagci H, Cetinkaya O.
Cumhuriyet University, Science and Art Faculty, Department of Biochemistry, Sivas, Turkey. ysilig@cumhuriyet.edu.tr
Abstract
Prostate cancer is the most common cancer among men in many countries. Although the etiology of prostate cancer largely is unknown, both genetic and environmental factors may be involved. Advanced age, androgen metabolism, and heredity-race have been reported to be possible risk factors. On the other hand, several studies indicate that genetic polymorphisms in biotransformation enzymes play a role in prostate cancer development. In this study, association of the prostate cancer risk with genotype frequencies of the Phase I (CYP1A1) and Phase II (GSTM1 and GSTT1) biotransformation enzymes was investigated in 321 Turkish individuals (152 prostate cancer patients and 169 age-matched male controls). The presence or absences of the GSTM1 and GSTT1 genes were determined by a PCR-based method. Genotypes of CYP1A1 were determined by MspI-RFLP. The prevalence of GSTM1 null genotype in the cases was 64 percent, compared to 31 percent in the control group, indicating a strong association (OR = 4.08, 95%CI = 2.50-6.69). No association was observed between either GSTT1 null genotype or CYP1A1 polymorphism and prostate cancer incidence. No statistically significant association was observed between smoking status of the patients and any of the polymorphisms studied. In conclusion, results of this study indicate that only the GSTM1 null genotype may play an important role as a risk factor for prostate cancer development in Turkish population.
Yazan: admin Tarih: Tem 23rd, 2010 | Kategori::
Gene polymorphisms
Cell Biochem Funct. 2010 Jun;28(4):274-7.
Büyük U, Ates O, Dalyan L, Müsellim B, Ongen G, Topal-Sarikaya A.
Department of Molecular Biology and Genetics, Istanbul University, Turkey. atopal@istanbul.edu.tr
Systemic sclerosis (SSc) is an autoimmune disease characterized by inflammation and fibrosis of the skin and visceral organs. Fibrosis associated with SSc is characterized by an increased synthesis of a wide range of extracellular matrix (ECM). TGF-beta is a pluripotent cytokine in a wide range of cell types. In particular it has been found to be a potent inducer of ECM protein synthesis and fibroblast migration. The TGF-beta1 gene is highly polymorphic and two signal sequence polymorphisms at codon 10 and codon 25 are linked to disease outcomes. In this study, we analysed two polymorphic sites of the TGF-beta1 gene, codon 10 and codon 25, in 43 Turkish SSc female patients with interstitial lung involvement and in 75 healty individuals by ARMS-PCR. In our study no significant difference was found in codon 10, codon 25 genotype frequencies between patient with SSc and the control group (p = 0.676, 0.375, respectively). Our findings suggest that codon 10 and 25 polymorphism cannot be related with SSc for Turkish population. 2010 John Wiley & Sons, Ltd.
Yazan: admin Tarih: Tem 23rd, 2010 | Kategori::
Lung cancer (AkciÄŸer Kanseri)
Med Oncol. 2010 Jul 20.
Coskunpinar E, Eraltan IY, Turna A, Agachan B.
Department of Molecular Medicine, Institute of Experimental Medicine Research, Istanbul University, Vakif Gureba cad, Capa, 34093, Istanbul, Turkey.
Abstract
In this study, we aimed to investigate a possible association of the COX-2 polymorphisms with the risk of developing lung carcinoma. COX-2 (-765G–>C; -1195A–>G) gene polymorphisms were performed by polymerase chain reaction (PCR) and restriction fragment length polymorphism in 118 healthy individuals and 231 patients with lung carcinoma. The present study was the first that addressed the role of the COX-2-765G–>C and -1195A–>G polymorphisms in lung carcinoma in Turkish population. In the present study, we found that the frequencies of GG, CC, and CG genotypes of COX-2-765G–>C and AA, GG, and AG genotypes of -1195A–>G in our control group were 0.22, 0.22, 0.55 and 0.59, 0.0, 0.40, respectively. These frequencies in patient group were 0.34, 0.07, 0.58 and 0.74, 0.04, 0.24, respectively. There were statistically significant differences in COX-2-765G–>C (P = 0.0002) and -1195A–>G genotypes (P = 0.007) between the controls and patients. We found that individuals carrying -765 GG genotype and -765 G allele of COX-2 or 1195 AA genotype of COX-2 and -765G: -1195A haplotype had an increased risk for the development of lung carcinoma. In contrast, individuals with -765 CC, -1195 AG genotypes and -1195 G allele of COX-2 seem to be protective from lung carcinoma. We suggest that the COX-2-765G–>C and -1195A–>G genotypes may be a risk factor for lung carcinoma.
