1.Mineralocorticoid receptor gene - 2G/C polymorphism in central serous chorioretinopathy and relation of polymorphism with plasma cortisol levels
Yazici ALPER ; Sari Sogutlu ESIN ; Eser, BETUL ; Sahin, GOZDE ; Alpdemir MEDINE ; Kilic, ADIL ; Erol Kazim MUHAMMET ; Ermis Samet SITKI
International Eye Science 2016;16(7):1203-1206
AIM:To evaluate the mineralocorticoid receptor ( MR) gene - 2G/ C single nucleotide polymorphism in central serous chorioretinopathy ( CSCR ), polymorphism and plasma cortisol level relationship.
METHODS: Sixty CSCR patients and 50 controls were included in the study. Inclusion criteria for patients were acute manifestation of CSCR characterized by serous retinal detachment, RPE detachment or dysfunction without evidence of any other possible cause of fluid exudation, such as choroidal neovascularization, inflammation or infiltration. Peripheric blood sample was collected from the participants between 8 and 10 a. m. to avoid the diurnal changes of cortisol levels. MR (NR3C2) gene polymorphism ( rs2070951 ) and plasma cortisol levels sere studied.
RESULTS: The genotype frequencies in CSCR group were G/ C (46. 6% ), G/ G (26. 7%) and C/ C (26. 7%). There was no statistically significant difference in terms of genotype distribution among groups ( P = 0. 96 ). The plasma cortisol levels were also studied and the results were 401. 2±162. 1 nmol/ L in the CSCR group and 296. 8±130. 1 nmol/ L in the control group and the difference was statistically significant ( P < 0. 01 ). The plasma cortisol levels also did not differ between G/ C (345.0±137.0 nmol/ L), G/ G (369.2±165. 3 nmol/ L) and C/ C (395. 3±188. 8 nmol/ L) genotypes (P= 0. 50).
CONCLUSION: The MR (NR3C2) gene polymorphism is not associated with CSCR and the plasma cortisol levels.
2.Lycopene Protects Against Spontaneous Ovarian Cancer Formation in Laying Hens
Kazim SAHIN ; Engin YENICE ; Mehmet TUZCU ; Cemal ORHAN ; Cengizhan MIZRAK ; Ibrahim H OZERCAN ; Nurhan SAHIN ; Bahiddin YILMAZ ; Birdal BILIR ; Bulent OZPOLAT ; Omer KUCUK
Journal of Cancer Prevention 2018;23(1):25-36
BACKGROUND: Dietary intake of lycopene has been associated with a reduced risk of ovarian cancer, suggesting its chemopreventive potential against ovarian carcinogenesis. Lycopene's molecular mechanisms of action in ovarian cancer have not been fully understood. Therefore, in the present study, we investigated the effects of lycopene on the ovarian cancer formation using the laying hen model, a biologically relevant animal model of spontaneous ovarian carcinogenesis due to high incidence rates similar to humans. METHODS: In this study, a total of 150 laying hens at age of 102 weeks were randomized into groups of 50: a control group (0 mg of lycopene per kg of diet) and two treatment groups (200 mg or 400 mg of lycopene per kg of diet, or ~26 and 52 mg/d/hen, respectively). At the end of 12 months, blood, ovarian tissues and tumors were collected. RESULTS: We observed that lycopene supplementation significantly reduced the overall ovarian tumor incidence (P < 0.01) as well as the number and the size of the tumors (P < 0.004 and P < 0.005, respectively). Lycopene also significantly decreased the rate of adenocarcinoma, including serous and mucinous subtypes (P < 0.006). Moreover, we also found that the serum level of oxidative stress marker malondialdehyde was significantly lower in lycopene-fed hens compared to control birds (P < 0.001). Molecular analysis of the ovarian tumors revealed that lycopene reduced the expression of NF-κB while increasing the expression of nuclear factor erythroid 2 and its major target protein, heme oxygenase 1. In addition, lycopene supplementation decreased the expression of STAT3 by inducing the protein inhibitor of activated STAT3 expression in the ovarian tissues. CONCLUSIONS: Taken together, our findings strongly support the potential of lycopene in the chemoprevention of ovarian cancer through antioxidant and anti-inflammatory mechanisms.
Adenocarcinoma
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Birds
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Carcinogenesis
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Chemoprevention
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Diet
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Hemeproteins
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Humans
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Incidence
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Malondialdehyde
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Models, Animal
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Mucins
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Ovarian Neoplasms
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Oxidative Stress
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Transcription Factors