Fanconi anemia (FA) is one of several genetic diseases with characteristic 
cellular hypersensitivity to DNA crosslinking agents which suggest that FA 
proteins may function as part of DNA repair processes. At the clinical level, FA 
is characterized by bone marrow failure that affects children at an early age. 
The clinical phenotype is heterogeneous and includes various congenital 
malformations as well as cancer predisposition. FA patients are distributed into 
eight complementation groups suggesting a complex molecular pathway. Three of 
the eight possible FA genes have been cloned, although their function(s) have 
not been identified. FA cells are highly sensitive to DNA crosslinking agents 
(mitomycin C (MMC) and diepoxybutane), with some variability between cell lines. 
Sensitivity to monofunctional alkylating agents has been reported in some cases, 
although these studies were performed with genetically unclassified FA cells. To 
further analyse and characterize the newly identified FA complementation groups, 
we tested their sensitivity to UV radiation, monofunctional and bifunctional 
alkylating agents and to the X-ray mimetic drug bleomycin. We found that FA 
complementation groups D to H show increased sensitivity to the X-ray mimetic 
drug bleomycin. Furthermore, the single known FA-H cell line shows increased 
sensitivity to ethylethane sulfonate (EMS), methylmethane sulfonate (MMS) in 
addition to the characteristic sensitivity to crosslinking agents, suggesting a 
broader spectrum of drug sensitivities in FA cells.