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Wu D.,Beihua Affiliated Hospital | Wu Y.,Shenyang University | Zhang X.,Beihua Affiliated Hospital | Cong P.,Beihua Affiliated Hospital | Lv X.,Beihua Affiliated Hospital
Gene | Year: 2013

Emerging evidence showed that the common polymorphism (+. 61A>G, rs4444903) in the promoter region of epidermal growth factor (EGF) gene might be associated with melanoma susceptibility in humans. But individually published results are inconclusive. The aim of this Human Genome Epidemiology (HuGE) review and meta-analysis is to derive a more precise estimation of the association between EGF +. 61A>G polymorphism and melanoma risk. The PubMed, Embase, Web of Science and CBM databases were searched for all articles published up to July 1st, 2012. Seven case-control studies were included with a total of 2367 melanoma cases and 4184 healthy controls. Meta-analysis results showed that there was no significant relationship between EGF +. 61A>G polymorphism and the risk of melanoma (G vs A: odds ratio [OR]. =. 1.08, 95% confidence interval [CI]: 0.91-1.28, P=. 0.386; GG. +. AG vs AA: OR. =. 1.05, 95%CI: 0.88-1.26, P=. 0.580; GG vs AA. +. AG: OR. =. 1.10, 95%CI: 0.81-1.49, P=. 0.552; GG vs AA: OR. =. 1.06, 95%CI: 0.80-1.41, P=. 0.700; GG vs AG: OR. =. 1.12, 95%CI: 0.81-1.56, P=. 0.494). Further subgroup analyses based on source of controls, country, detection samples, genotype methods, and Breslow thickness of tumor, we also found no significant association between EGF +. 61A>G polymorphism and melanoma risk. In conclusion, this meta-analysis indicates that EGF +. 61A>G polymorphism might not be a primary determinant in melanoma development and progression; EGF gene might be expected to interact with other genes in different signaling pathways to initiate and promote the carcinogenic process. © 2012.

Wu D.,Beihua Affiliated Hospital | Wu Y.,Shenyang University | Liu J.L.,Shenyang University | Wang B.,Shenyang University | Zhang X.D.,Beihua Affiliated Hospital
Genetics and Molecular Research | Year: 2011

Numerous studies have evaluated the association between human leukocyte antigen (HLA) Cw*0602 polymorphism and psoriasis risk. However, the results have been inconsistent. We made a meta-analysis of the association between HLA-Cw*0602 polymorphism and psoriasis risk. Eighteen studies were retrieved, reporting a total of 3419 psoriasis patients and 3297 healthy controls. The associations between HLA-Cw*0602 polymorphism and psoriasis risk were estimated by pooled odds ratio (OR) and 95% confidence interval (95%CI). We found significant associations between HLA-Cw*0602 polymorphism and psoriasis risk in the comparisons of positive versus negative alleles (OR = 4.55, 95%CI = 3.65-5.67, P < 0.00001); positive homozygote versus negative homozygote combined with heterozygote (OR = 14.00, 95%CI = 8.47-23.15, P < 0.00001); positive homozygote combined with heterozygote versus negative homozygote (OR = 5.11, 95%CI = 3.86-6.76, P < 0.00001); positive homozygote versus negative homozygote (OR = 23.03, 95%CI = 13.95-38.00, P < 0.00001), and positive homozygote versus heterozygote (OR = 4.21, 95%CI = 2.35- 7.00, P < 0.00001). In conclusion, the positive allele of HLA-Cw*0602 polymorphism appears to be a risk factor for psoriasis. © FUNPEC-RP www.funpecrp.com.br.

Chang Z.,Beihua Affiliated Hospital | Shi G.,Jilin University | Jin J.,Second Group of Oncology | Guo H.,Beihua Affiliated Hospital | And 4 more authors.
International Journal of Molecular Medicine | Year: 2013

Dysregulation of the phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling has been found in several types of human cancer, including hepatocellular carcinoma (HCC). NVP-BEZ235 is a novel, orally bioavailable dual PI3K/mTOR inhibitor that has exhibited promising activity against HCC in preclinical models. Autophagy is a cellular lysosomal degradation pathway essential for the regulation of cell survival and death to maintain homeostasis. This process is negatively regulated by mTOR signaling and often counteracts the efficacy of certain cancer therapeutic agents. In this study, we explored the role of autophagy in apoptosis induced by NVP-BEZ235 in two HCC cell lines, Hep3B and PLC/PRF/5, and identified the mechanism of combinatorial treatment. NVP-BEZ235 was effective in inhibiting the growth of the two HCC cell lines possibly though induction of apoptosis. NVP-BEZ235 also potently increased the expression of LC3-II and decreased the expression of p62, indicating induction of autophagy. When NVP-BEZ235 was used in combination with Atg5 siRNA or the autophagy inhibitor 3-methyladenine (3-MA), enhancement of the inhibitory effects on the growth of HCC cells was detected. In addition, enhanced induction of apoptosis was observed in cells exposed to the combination of NVP-BEZ235 and Atg5 siRNA or 3-MA. Thus, induction of autophagy by NVP-BEZ235 may be a survival mechanism that counteracts its anticancer effects. Based on these data, we suggest a strategy to enhance the anticancer efficacy of BEZ235 by blockade of autophagy. Thus, our study provides a rationale for the clinical development of combinations of NVP-BEZ235 and autophagy inhibitors for the treatment of HCC and other malignancies.

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