The pathogenesis of Vogt-Koyanagi Harada disease (VKH) has not yet been fully defined. Current studies mainly suggest that VKH is actually an autoimmune disease, especially related to the immune response mediated by various signal transduction pathways involved in the function of T cells. In recent years, the influence of the balance imbalance of various T cell subsets in cellular immunity on the pathogenesis of VKH has been a hot research direction. Currently, T helper cell 17/T regulatory cells, balance is the focus of clinical research, meanwhile, new discoveries and potential clinical treatment schemes have been made for related cellular pathways, particularly the Janus kinase/signal transducers and activators of transcription pathway and NF-kappa B pathway. The exploration of B cells in the pathogenesis of VKH has also achieved initial results through the successful application of various targeted drugs. In the future, further screening and localization of genes or proteins that are abnormally regulated or expressed in VKH, for which early comprehensive and in-depth exploration will be helpful, thus improve the efficacy of clinical treatment programs and develop new therapeutic targets.
Objective To investigate the correlation between MDM2 SNP309 and gastric cancer (GC) risk in Eastern Asian population. Methods Two reviewers independently searched MEDLINE, EMbase and CBM (from January 1st, 1990 to October 23rd, 2012) for case-control studies on the correlation between MDM2 SNP309 and GC risk in Eastern Asian population. Two reviewers independently screen literature, extracted the data, and assessed the methodological quality. Then meta-analysis was performed using RevMan 5.0 software. Results 5 case-control studies were finally included involving 1 621 GC cases and 2 639 controls. The pooled results showed that the variant homozygote (309GG genotype) was significantly associated with an increased risk of GC as compared to wild-type homozygote (309TT genotype: OR=1.54, 95% CI 1.04 to 2.29, P=0.02). Nevertheless, no association was found in comparison of variant heterozygote (309TG genotype) between wild-homozygote (309TT genotype: OR=1.03, 95% CI 0.75 to 1.42, P=0.006). A significantly increased risk of GC was observed for the recessive model (GG vs. TT/TG: OR=1.49, 95% CI 1.20 to 1.84, P=0.07). While in the dominant model (GG/TG vs. TT), non-significant association was observed (OR=1.18, 95% CI 0.84 to 1.65, P=0.001). Conclusion The MDM2 309GG may be significantly associated with an increased risk of GC among Eastern Asians.