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Rheumatology 2002; 41: 361-364
© 2002 British Society for Rheumatology

Editorials

Progress and problems in defining susceptibility genes for rheumatic diseases

J. Lanchbury, M. Hall and S. Steer

Molecular Immunogenetics Unit, Department of Rheumatology, Division of Medicine, 5th Floor, Thomas Guy House, Guy's Hospital Campus, Guy's, King's and St Thomas’ Hospitals School of Medicine, London SE1 9RT, UK

It is thought with some reason that there is no more dreadful punishment than futile and hopeless labour.

Albert Camus

Hypothesis-free genetic mapping of complex disease genes has been relatively unsuccessful to date and the rheumatic diseases are no exception. Weiss and Terwilliger in a recent article asked how many diseases it took to map a gene using single nucleotide polymorphisms (SNPs) [1; see also 2]. This ironic comment was directed at the raising of the SNP to the status of icon and saviour of human genetics. Behind the jibes lies very real disappointment at the inability of current technology and approaches to deliver verifiable linkages and consequent associations between genetic markers and diseases or intermediate disease phenotypes. If the disillusionment is palpable in the academic sector, it has been crippling for the private and publicly quoted specialized human genetics companies. In this short article we will . . . [Full Text of this Article]

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