Abstract

Studies of Fanconi's anemia (FA) have been in conflict as to the existence of a clastogenic factor. Two male FA patients who received bone marrow transplants were studied. One FA patient received a transplant from his normal sister whose engrafted lymphocytes showed spontaneous, as well as diepoxybutane (DEB)-induced chromosome breakage in the normal range. The second FA patient received a transplant from his obligate heterozygous mother whose engrafted lymphocytes exhibited increased spontaneous chromosome breakage but not in response to DEB treatment. In vitro cocultivation of FA and FA heterozygous lymphocytes and of FA and normal lymphocytes showed chromosome breakage levels consistent with their genotypes. These results suggest that no detectable clastogenic factor is produced by FA cells.

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