Titlebook: Ataxia-Telangiectasia; Richard A. Gatti,Robert B. Painter Conference proceedings 1993 Springer-Verlag Berlin Heidelberg 1993 Ataxia-Telang

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Conference proceedings 1993 cancer. All of this stems fromdefects of a singlegene.Provided here is an up-to-date review of all important workin thefield. A wide spectrum of topics is covered, namelygenetics, chromosome 11 mapping, radiobiology,complementation, heterozygote identification,clinicalvariants, biochemistry, and treatment of A-T.

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Wolfgang Asholt,Frank Baasner,Wolfram Vogel applied to identify cell clones showing increased resistance to the lethal action of the DNA damaging agent. An attempt is then made to rescue the piece of DNA responsible for this phenotypic change, which is expected to represent a candidate gene.

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Complementation of the Cellular A-T Phenotype by Gene Transfer applied to identify cell clones showing increased resistance to the lethal action of the DNA damaging agent. An attempt is then made to rescue the piece of DNA responsible for this phenotypic change, which is expected to represent a candidate gene.

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1010-8793 um of topics is covered, namelygenetics, chromosome 11 mapping, radiobiology,complementation, heterozygote identification,clinicalvariants, biochemistry, and treatment of A-T.978-3-642-78280-0978-3-642-78278-7Series ISSN 1010-8793

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How Many Ataxia-Telangiectasia Genes?In this chapter we review the evidence for genetic heterogeneity and clinical variability of A-T. Because of the existence of five complementation groups [Jasper et al. 1988], a homogeneity model is automatically suspect. There are also clinical variants of A-T, and those are discussed briefly.

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Ataxia-Telangiectasia978-3-642-78278-7Series ISSN 1010-8793

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