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Can RGS4 polymorphisms be viewed as credible risk factors for schizophrenia? A critical review of the evidence.

ABSTRACT: There has been a recent explosion in the list of putative susceptibility genes for schizophrenia (SZ). These genes have been identified on the basis of presumed pathogenesis, linkage, and genetic association studies. While several promising candidates have arisen, identification of a conclusive genetic risk factor has remained elusive. The proof would be most compelling if it stemmed from all three of these domains. In this review, we consider such evidence in relation to the regulator of G-protein signaling 4 (RGS4), a gene localized to chromosome 1q23. Disorder-specific changes in RGS4 mRNA levels have been observed in post-mortem brain samples; linkage has been reported at chromosome 1q23; and several association studies have concluded that significant associations exist. The latter are supported by a recently conducted meta-analysis. Thus, there is suggestive evidence in each of these domains implicating a role for RGS4 in SZ susceptibility. However, analogous to other promising susceptibility candidates, the nature of the genetic association, the precise polymorphism(s) conferring risk, and the functional implications of sequence variation at this gene are unclear. We review the published data and place them in the context of suggested criteria for establishing a candidate gene as a credible susceptibility factor for disorders with non-Mendelian patterns of inheritance.

SUBMITTER: Talkowski ME

PROVIDER: S-EPMC2632201 | biostudies-literature | 2006 Apr

REPOSITORIES: biostudies-literature

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Can RGS4 polymorphisms be viewed as credible risk factors for schizophrenia? A critical review of the evidence.

Talkowski Michael E ME Chowdari Kv K Lewis David A DA Nimgaonkar Vishwajit L VL

Schizophrenia bulletin 20060209 2

There has been a recent explosion in the list of putative susceptibility genes for schizophrenia (SZ). These genes have been identified on the basis of presumed pathogenesis, linkage, and genetic association studies. While several promising candidates have arisen, identification of a conclusive genetic risk factor has remained elusive. The proof would be most compelling if it stemmed from all three of these domains. In this review, we consider such evidence in relation to the regulator of G-prot ...[more]

PMID: 16469939

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Project description:BackgroundEpstein Barr Virus (EBV) infects 90%-95% of all adults globally and causes ~ 1% of all cancers. Differing proportions of Burkitt's lymphoma (BL), gastric carcinoma (GC), Hodgkin's lymphoma (HL) and nasopharyngeal carcinoma (NPC) are associated with EBV. We sought to systematically review the global epidemiological evidence for risk factors that (in addition to EBV) contribute to the development of the EBV-associated forms of these cancers, assess the quality of the evidence, and compare and contrast the cancers.MethodsMEDLINE, Embase and Web of Science were searched for studies of risk factors for EBV-associated BL, GC, HL and NPC without language or temporal restrictions. Studies were excluded if there was no cancer-free comparator group or where analyses of risk factors were inadequately documented. After screening and reference list searching, data were extracted into standardised spreadsheets and quality assessed. Due to heterogeneity, a narrative synthesis was undertaken.Results9916 hits were retrieved. 271 papers were retained: two BL, 24 HL, one GC and 244 NPC. The majority of studies were from China, North America and Western Europe. Risk factors were categorised as dietary, environmental/non-dietary, human genetic, and infection and clinical. Anti-EBV antibody load was associated with EBV-associated GC and BL. Although the evidence could be inconsistent, HLA-A alleles, smoking, infectious mononucleosis and potentially other infections were risk factors for EBV-associated HL. Rancid dairy products; anti-EBV antibody and EBV DNA load; history of chronic ear, nose and/or throat conditions; herbal medicine use; family history; and human genetics were risk factors for NPC. Fresh fruit and vegetable and tea consumption may be protective against NPC.ConclusionsMany epidemiological studies of risk factors in addition to EBV for the EBV-associated forms of BL, GC, HL and NPC have been undertaken, but there is a dearth of evidence for GC and BL. Available evidence is of variable quality. The aetiology of EBV-associated cancers likely results from a complex intersection of genetic, clinical, environmental and dietary factors, which is difficult to assess with observational studies. Large, carefully designed, studies need to be strategically undertaken to harmonise and clarify the evidence.RegistrationPROSPERO CRD42017059806.

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Can RGS4 polymorphisms be viewed as credible risk factors for schizophrenia? A critical review of the evidence.

Publications

Can RGS4 polymorphisms be viewed as credible risk factors for schizophrenia? A critical review of the evidence.

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