Reply to Ian Morison

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Infantile acute leukemia (IAL) with 11q23 abnormality is an extremely rare event1 and therefore to prove an ultimate cause epidemiologically often encounters difficulties.23 Since recent reports have not clearly demonstrated any agent with a causal relationship to IAL, I wonder why Dr Ian Morison stated that ‘epidemiological evidence is clearly against an association between genistein ingestion and infant leukemia’. On the other hand, the potential implication of naturally occurring or endogenous substances in carcinogenesis has recently been increasingly emphasized.4 Although we have suggested the possibility of soybeans, which contain genistein acting as a leukemogen for IAL, this is not a reason for anxiety because of IAL's extremely low incidence in the population, nor should anyone take it too seriously, since the benefits for human beings derived from isoflavone-containing foods including soybeans are well known. Unfortunately, however, there is always the possibility that individuals will use any suggestion of scientific evidence as absolute proof in support of their views. As professionals, we must be on the alert for such abuse of experimental data, and Dr Morison should be congratulated on his prompt and eloquent action to suppress such abuse.

At present, IAL is the focus of scientific concern, and I am sure that we are now approaching an answer to Rowley's basic question ‘do human tumors show a chromosome pattern specific for each etiologic agent?’5 Even more important, however, is to elucidate the extent of individual genetic variation underlying the metabolism of xenobiotics. Further advances in pharmacogenomics6 will undoutedly provide us with insights into in utero leukemogenesis. As for IAL, Wiemels et al7 recently found a genetic variant of NAD(P)H: quinone oxidoreductase that detoxifies quinones. They suggested that the risk of IAL may link to polymorphism in this drug-metabolizing enzyme.


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Correspondence to T Abe.

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