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Hybrids were performed between cell lines derived from four patients with Fanconi's anemia in which different biochemical lesions have been postulated. Complementation studies in these hybrids based on the rate of mitomycin C-induced chromosomal damage supported the concept of allelic mutations. It was therefore concluded that intergenic heterogeneity plays a much lower role in Fanconi's anemia than in Xeroderma pigmentosum or Ataxia teleangiectasia, two other disorders with defective DNA repair.
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