Apolipoprotein E Genotypes in Patients with Prostate Cancer

Yencilek, F. | Yilmaz, S.G. | Yildirim, A. | Gormus, U. | Altinkilic, E.M. | Dalan, A.B. | İşbir, Turgay

Article | 2016 | Anticancer research36 ( 2 ) , pp.707 - 711

BACKGROUND: Apolipoprotein E (ApoE) is a potential inhibitor of cell proliferation, immune regulation and modulation of cell growth and differentiation; it also has a substantial role in antioxidant activity. ApoE has a potential role in prostate cancer progression.MATERIALS AND METHODS: ApoE genotyping was performed using real-time polymerase chain reaction (RT-PCR) for blood samples from a group of patients with prostate cancer (n=68) and a control group (n=78).RESULTS: The frequency of the E3/E3 genotype was significantly higher in patients compared to controls (p=0.004). E3/E3 genotype carriers were 3.6-fold more likely to be pa . . .tients than controls (odds ratio=3.67, 95% confidence interval=1.451-9.155; p=0.004). Additionally, the patients with E3/E3 genotype had significantly higher Gleason score (p=0.017), and more patients with this genotype had a Gleason score higher than 7 (p=0.007). Individuals carrying the E4 allele were significantly more common in the control group (p=0.006). The frequency of the E3/E4 genotype was found to be significantly higher in controls compared to patients (p=0.007), and patients were significantly less likely to have this genotype than controls (odds ratio=0.89, 95% confidence interval=0.833-0.967, p=0.007). Individuals carrying the E2/E3 genotype had a significantly lower Gleason score (p=0.049)-all of the patients with this genotype had a Gleason score lower than 7 (p=0.024).CONCLUSION: E3/E3 genotype may be a potential risk factor for prostate cancer and high Gleason scoring. The E4 allele maybe a risk-reducing factor for prostate cancer. Copyright© 2016 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved Daha fazlası Daha az

Investigation of interleukin-1? Polymorphisms in prostate cancer

Yencilek, F. | Yildirim, A. | Yilmaz, S.G. | Altinkilic, E.M. | Dalan, A.B. | Bastug, Y. | İşbir, Turgay

Article | 2015 | Anticancer Research35 ( 11 ) , pp.6057 - 6061

Background: Cytokine-mediated immune and inflammatory responses are considered to play an important role in the pathogenesis of prostate cancer. The present study investigated certain interleukin-1? (IL1?) polymorphisms and their association with prostate cancer. Materials and Methods: Genotyping of the IL1B-31(rs 1143627 G>A) and IL1B-511(rs 16944 A

Effects of caspase 9 gene polymorphism in patients with prostate cancer

Yilmaz, S.G. | Yencilek, F. | Yildirim, A. | Yencilek, E. | İşbir, Turgay

Article | 2017 | In Vivo31 ( 2 ) , pp.205 - 208

Background: Prostate cancer is one of the most common solid tumors and the second leading cause of the death due to malignancy in men. Caspase 9 (CASP9) is a member of the intrinsic pathway and plays a central role in the apoptosis. Patients and Methods: Genotyping of the CASP9 (rs1052576) polymorphism were performed using realtime polymerase chain reaction for blood samples of prostate cancer patients (n=69) and controls (n=76). Results: There were no significant differences between the groups in the frequency of CASP9 genotypes (x2=1.363; p=0.506). Patients with CASP9 (rs1052576) CT genotype were 12.8 fold higher in pathological s . . .tage of pT2a compared to any other stages of cancer (OR=0.078, 95% CI= 0.009-0.062; p=0.004). Also TT genotype carriers were 11.3 times lower in pathological stage of pT2a (OR=11.33, 95% CI=2.39-53.748; p=0.000). C allele carriers were 11.36 fold higher in pathological stage of pT2a compared to any other stages of cancer (OR=0.088, 95% CI=0.019-0.418; p=0.002). Conclusion: CASP9 (rs1052576) C allele was decreasing the risk for pathological stage of patients with prostate cancer and also CT genotype had positive impact on pathological stage of patients with prostate cancer. CASP9 (rs1052576) TT genotype was seemed to be associated with higher risk of pathological stage. Those results implicated that CASP9 variations could be associated with severity of prostate cancer Daha fazlası Daha az

Dual-inhibition of mTOR and Bcl-2 enhances the anti-tumor effect of everolimus against renal cell carcinoma in vitro and in vivo

Nayman, A.H. | Siginc, H. | Zemheri, E. | Yencilek, F. | Yildirim, A. | Telci, D.

Article | 2019 | Journal of Cancer10 ( 6 ) , pp.1466 - 1478

Renal cell carcinoma (RCC) is the predominant type of kidney cancer. Mammalian target of rapamycin (mTOR) inhibitor everolimus is currently used as a second-line therapy for sorafenib or sunitinib-refractory metastatic RCC patients. The clinical limitation confronted during everolimus therapy is the onset of drug resistance that decreases the efficacy of the drug. Elevated level of anti-apoptotic Bcl-2 protein is proposed to be an emerging feedback loop for the acquired drug-resistance in various cancer types. In this study, the Bcl-2 inhibitor ABT-737 was used in combination with everolimus to enhance its anti-tumor effectiveness i . . .n everolimus-resistant RCC cell lines. Everolimus and ABT-737 combination synergistically led to a decrease in the proliferation of primary site A-498 and metastatic site Caki-1 RCC cell lines, which was accompanied by a reduction in protein levels of cell cycle and mTOR pathway proteins. In both RCC cell lines, everolimus-ABT-737 combination not only induced apoptosis, caspase and PARP-1 cleavage but also a decrease in Bcl-2 protein levels in parallel with a concomitant increase in Bim and Noxa levels. In order to confirm our in vitro findings, we have generated everolimus-resistant RenCa cell line (RenCares) to establish a RCC mouse xenograft model. Animals co-treated with everolimus and ABT-737 exhibited a complete suppression of tumor growth without any notable toxicity. This study thus proposes the everolimus-ABT-737 combination as a novel therapeutic strategy for the treatment of RCC to overcome the current clinical problem of everolimus resistance. © Ivyspring International Publisher Daha fazlası Daha az

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