Though the roles of some specific DNA lesions in the production of chromosomal 
aberrations is clearly established, those of others remain unclear. While the 
study of aberration production in human genetic DNA repair deficiency diseases 
has been extremely rewarding already, eukaryotic repair systems are obviously 
complex, and one is tempted to feel that such studies may have raised as many 
questions as they have provided answers. For example, the "standard" sort of 
xeroderma pigmentosum is chromosomally sensitive to ultraviolet light and to 
those chemical agents inducing ultraviolet-type DNA repair. But both it and the 
variant form have been reported to also be sensitive to the crosslinking agent 
mitomycin C in one study [18], implying a common step or steps in the repair of 
pyrimidine cyclobutane dimers and DNA crosslinks. However, just to complicate 
matters, another study of chromosomal aberration production in xeroderma 
pigmentosum cells had found them no more sensitive to mitomycin C than normal 
cells [50]. Similarly, Fanconi's anemia cells, which are chromosomally sensitive 
to crosslinking agents, and appear to be defective in the "unhooking" of linked 
polynucleotide strands [15, 16, 49, 51], are reported to be chromosomally 
sensitive to ethyl methanesulfonate as well [29], and to be sensitive to 
ionizing radiation [7, 19, ]0], again implying overlapping repair systems. It 
seems certain that further study of chromosomal aberration production in repair 
deficient cells by agents inducing various DNA lesions will reveal even greater 
complexity in eukaryotic DNA repair systems and their role in chromosomal 
aberration production. Nevertheless, there seems hope, at least, that such 
studies may also ultimately lead to a complete understanding of the molecular 
mechanisms involved.