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Insulin - Sniffing for Jabbing

group suggesting a locus on chromosome 911. Unfortunately not all TS families seem to have a mutation in a chromosome 9 gene and the identification of two cases of TS with chromosomal alterations involving chromosomes 11 and 12 have provided evidence for loci on these chromosomes. There has been some evidence from genetic linkage studies to support these suggestions. Are there therefore at least three different TS genes? It seems possible that this is the case on current evidence and if so it will make the finer mapping of these loci and subsequent isolation of the genes a very difficult task. The development of more informative DNA polymorphisms and a strong international collaborative research strategy means that the situation should become clearer in the next couple of years. It will be fascinating to see whether there is any correlation between the clinical phenotype and the genetic locus. Some researchers have claimed that their 'chromosome 9' families tend to have a milder phenotype in terms of mental retardation than the 'non-9' families but the data are very limited and such is the variability within families that I remain sceptical. The isolation of the genes responsible for TS would also allow more reliable carrier detection and prenatal diagnosis. There would probably be a considerable demand for prenatal diagnosis given the highly distressing nature of the disorder with many of the affected children being mentally retarded, having seizures that are difficult to control and showing hyperactive and autistic behaviour. Some of these children die prematurely in prolonged seizures or from brain tumours. Mildly affected individuals usually have a normal lifespan, although some patients have died from renal failure or brain tumours. The mentally normal adult with TS can be reassured that the risks of developing such complications is low though they Journal of the Royal Society of Medicine Volume 84 December 1991 701