92 p. L, ILBERY, P. MOORE, S. M. WINN, AND C. E. FORD 



Research Institute. This was some years ago and they may not be the same as the ones 

 now. He found a high proportion of modes in spontaneous leukaemia that were grossly 

 abnormal, with stem hnes of 41 and higher. Hauschka, in a paper last year, quotes Stich 

 as finding that about half of a number of AK leukaemias showed abnormal karyotiy-pes. 

 So that there does seem to be quite a lot of evidence that one can get consistent abnormal 

 karyotpes if sufficient observation is made. Even in human clnronic lymphocytic leuk- 

 aemia Hausclika finds that some 40% of the mitoses examined were abnormal, which is 

 about four times higher than that for non-leukaemic individuals. It is probably not 

 unfair to recall that Bayreuther a few years ago published a paper suggesting that there 

 was no abnormality in structure or number in the metaphase cliromosomes of a large 

 variety of induced tumours of a large variety of species. Hausclika makes the comment 

 that Bayreuther's results were based on looking at more than 10,000 metaphases and that 

 his conclusion could only have been properly drawn if he'd made a detailed study of each 

 one of these. Technical considerations come into this too — it's very easy to be over- 

 enthusiastic of course, if you aren't really a cliromosome expert, and to report aU sorts 

 of abnormalities which aren't really there. To return to this point of the AK mice, Ford 

 at any rate is quite happy that in chemically mduced leukaemia, in spontaneous leukaemia 

 and in radiation-induced leukaemia abnormal karyotypes are characteristic of something 

 over 80% of the total. 



