West Andrew B, Dawson Valina L, Dawson Ted M
Institute for Cell Engineering, and Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Trends Neurosci. 2005 Jul;28(7):348-52. doi: 10.1016/j.tins.2005.05.002.
Epidemiological evidence suggests a reduced incidence of many common types of non-smoking-related cancers in individuals with Parkinson's disease (PD). Genes that underlie familial forms of PD are often abnormally expressed in cancer, owing to their differential regulation or mutation. Functional studies implicate these genes in maintenance of the cell cycle, in some cases through interaction in the ubiquitin-proteasome system. Variation in genes associated with familial-linked PD could therefore modify susceptibility to both cancer and PD, implying some degree of overlap in the underlying biochemical dysfunction. When considering the normal function of these PD-linked genes in the periphery and their potential role in cancer, further emphasis might be placed on protein handling relating to cell-cycle control in the etiology of PD.
流行病学证据表明,帕金森病(PD)患者中许多常见类型的与非吸烟相关癌症的发病率有所降低。家族性PD相关基因由于其调控差异或突变,在癌症中往往异常表达。功能研究表明,这些基因在细胞周期维持中发挥作用,在某些情况下是通过泛素-蛋白酶体系统中的相互作用实现的。因此,与家族性PD相关的基因变异可能会改变对癌症和PD的易感性,这意味着潜在的生化功能障碍存在一定程度的重叠。在考虑这些与PD相关基因在外周的正常功能及其在癌症中的潜在作用时,可能需要进一步强调蛋白质处理与PD病因中细胞周期控制的关系。