Mutagenic response of Fanconi's anemia cells from a defined complementation group after treatment with photoactivated bifunctional psoralens.
The induction of mutants at the hypoxanthine-guanine phosphoribosyltransferase and Na+/K+ ATPase loci by photoaddition of two bifunctional psoralens was compared in normal and in Fanconi's anemia lymphoblasts from the genetic complementation group A. For the two loci, the frequency of mutants was significantly lower in Fanconi's anemia than in normal cells. This is true whether the data are expressed as a function of dose or as a function of survival level. It is suggested that the chromosomal instability characteristic of Fanconi's anemia is responsible for the cancer proneness rather than the mutability at the gene level.
Papadopoulo
D
D
Section de Biologie, Institut Curie, UA 1292 CNRS, Paris, France.
Porfirio
B
B
Moustacchi
E
E
D000741:Anemia, Aplastic / Q000235:genetics*; D002470:Cell Survival; D005199:Fanconi Anemia / Q000235:genetics* / Q000473:pathology; D011564:Furocoumarins / Q000494:pharmacology*; D006801:Humans; D007041:Hypoxanthine Phosphoribosyltransferase / Q000235:genetics*; D008730:Methoxsalen / Q000494:pharmacology*; D009154:Mutation; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics*; D013866:Thioguanine; D014307:Trioxsalen / Q000494:pharmacology*; D014467:Ultraviolet Therapy
D011564:Furocoumarins; D007041:Hypoxanthine Phosphoribosyltransferase; D000254:Sodium-Potassium-Exchanging ATPase; D013866:Thioguanine; D008730:Methoxsalen; D014307:Trioxsalen