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• W2009603634 abstract "A Khani-Hanjani and colleagues1Khani-Hanjani A Lacaille D Hoar D et al.Association between dinucleotide repeat in non-coding region of interferon-gamma gene and susceptibility to, and severity of, rheumatoid arthritis.Lancet. 2000; 356: 820-825Summary Full Text Full Text PDF PubMed Scopus (94) Google Scholar suggest that a simple polymorphic tandem-repeat genetic marker in the IFNG was associated with rheumatoid arthritis per se, and with severe disease in particular. The study had a casecontrol design and involved small groups, although the effect size seemed large. W E R Ollier's commentary2Ollier WER Role of interferon-μgM gene in rheumatoid arthritis?.Lancet. 2000; 356: 783-784Summary Full Text Full Text PDF PubMed Scopus (15) Google Scholar is highly sceptical of the findings and he cites his own group's work on the same marker and on other biallelic interferon gamma variants in rheumatoid arthritis that were at odds with the new findings. He drew particular attention to the frequency distributions of the IFNG alleles in patients and controls that were essentially similar if one assumed that a systematic 2 bp shift had occurred in one of the study groups, causing that group to be out of phase with its comparator. Ollier suggests that the results be treated with caution until independent confirmation obtained. We believe several lessons can be learned from the publication of this work. We assume that the replication suggested is by distinct studies of similar groups of patients and controls. Although independent replication is the essence of the scientific method, there are difficulties in comparing similar markers in independent complex-disease datasets, of which rheumatoid arthritis is just one example. The literature is becoming mired with examples of failures of replication that may merely reflect clinical, genetic or ethnic, or environmental heterogeneity.3Risch N Searching for genes in complex diseases: lessons from systemic lupus erythematosus.J Clin Invest. 2000; 105: 1503-1506Crossref PubMed Scopus (45) Google Scholar A further source of confusion is that generated by type I and type II statistical errors. Some form of genetic meta-analysis will probably be necessary eventually to extract meaning from multiple studies.4Wise LH Lanchbury JS Lewis CM Metaanalysis of genome searches.Ann Hum Genet. 1999; 63: 263-272Crossref PubMed Google Scholar However, these issues should not be confused with technical ones. Microsatellite genotyping has been extensively used in family studies of complex disease and is increasingly used in case-control studies. In our experience, absolute sizing of fluorescently labelled alleles over a time period is best done by coelectrophoresis of test alleles with differently labelled allelic ladders (figure). In our report5Fife MS Fisher SA John S et al.Multipoint linkage analysis of a candidate gene locus in rheumatoid arthritis: significant evidence of linkage and association with the CRH genomic region.Arthritis Rheum. 2000; 43: 1673-1678Crossref PubMed Scopus (47) Google Scholar cited by Ollier, genotyping of the associated corticotropin-releasing hormone locus was done independently in two laboratories (London and Manchester) with highly concordant results. Such precautions are essential to confidently detect and replicate weak but real genetic effects. If the results of Khani-Hanjani and colleagues can be explained away at a technical level, then resolution is a trivial exercise involving exchange of the study DNA with a few other laboratories. Once this possibility has been dismissed further studies are warranted to verify an effect that Ollier's group have not seen in a white UK population." @default.
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• W2009603634 date "2000-12-01" @default.
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• W2009603634 title "Interferon gamma gene in rheumatoid arthritis" @default.
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• W2009603634 doi "https://doi.org/10.1016/s0140-6736(05)67268-6" @default.
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