As one of the main pathological changes of Parkinson's disease (PD), axonal degeneration was thought to be a passive process that is secondary to the apoptosis of dopaminergic neurons and, therefore, it has been overlooked for some time. Recent research, however, has indicated that axonal injury is the first location of damage in dopaminergic neurons in PD, and that the degree of injury in axonal degeneration is higher than in neural death.

ABSTRACT. Published data regarding the association between aryl hydrocarbon receptor (Ahr) rs2066853 polymorphism and the risk of breast cancer shows conflicting results. We performed a meta-analysis on 2999 patients and 3050 controls from three related case-control studies to estimate the association between Ahr rs2066853 polymorphism and the risk of breast cancer. The protocol was approved by the Institutional Animal Care and Use Committee (IACUC) at the University of Florida (America NIH Publication No. 86-231985 Revision). According to the three eligible populations, the odds ratios (ORs), 95% confidence intervals (CIs) on the risk of breast cancer for the genotypes GA vs GG, AA vs GG, and A vs G ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 16162-16168 (2015) 16163A meta-analysis on Ahr polymorphism and breast cancer were 1.06 (0.81-1.40), 0.96 (0.81-1.13), and 1.02 (0.85-1.22), respectively. The OR (95%CI) for GA + AA vs GG was 1.05 (0.80-1.37). Furthermore, after multi-variates adjustment, the ORs (95%CIs) were 1.05 (0.80-1.38) for GA vs GG, and 0.92 (0.76-1.10) for AA vs GG. This meta-analysis suggests that Ahr (rs2066853) polymorphism would not modify the risk of breast cancer. However, further research should be conducted to provide more evidence.

MSP58, a novel oncogene, shows transforming activity in mouse embryonic fibroblasts. However, the oncogenic role of MSP58 in tumor cells has not been fully characterized. To extend understanding of how this protein operates in tumorigenesis, we aimed to identify the effect of MSP58 on neuroblastoma cell proliferation. Here, we found that MSP58 was highly expressed in neuroblastoma tumor samples and cell lines. We found that the majority of MSP58 protein can be detected in the nucleus as reported in other cells. Moreover, MSP58-targeted shRNA lentivirus attenuated neuroblastoma cell proliferation. Knockdown of MSP58 resulted in S-phase cell accumulation, which was accompanied by changes in cell cycle-related molecules. These results indicate that MSP58 plays an oncogenic role in the proliferation of neuroblastoma cells and could be a novel target for the treatment of neuroblastoma.