VIRUS-INDUCED MURINE LEUKAEMIAS 101 



I960; Gross, 1961). All the 19 leukaemias analysed cytologically in the present 

 investigation, were the product of the same virus, thus the causative agent 

 being the same, uniformity in the behaviour and chromosome constitution of 

 these leukaemias might be expected. They all display a certain degree of 

 hereroploidy in their cell population; the frequency of heteroploid cells, 

 however, shows considerable variation not only between different animals, 

 but between different sites of the same animal. The difference shown by the 

 white cell comits is a further indication that the development and progression 

 of the various leukaemias follows an independent line, after the leukaemic 

 transformation of normal cell by the virus has been accomplished. 



The chromosome number of heteroploid cells in these leukaemias was 

 40+1 or 40 + 2; other chromosome numbers were very rare. Similar 

 limitation of irregular chromosome number was observed by Wakonig and 

 Stich (1960) in spontaneous AKR leukaemias, by Ford and co-workers in 

 X-ray induced leukaemias (1958), and by Stich (1960) in chemically-induced 

 leukaemia. The deviation from the 2n number is apparently a limited process, 

 only cells in which the increase is not more than 1-2 remaining functional, 

 others being eliminated by selection. Similarly the occurrence of marker 

 chromosomes (metacentrics) and the frequency of cells carrying such chromo- 

 somes is very rare. An exception to this observation is the recent finding of 

 Wakonig (1962) who observed a metacentric chromosome in 85 to 94% of 

 cells in a urethane-induced mouse leukaemia. 



Two transplanted lymphoid leukaemias provide further evidence in 

 favour of the selection theory. One (C + leukaemia) origmated in Balb/c, the 

 other (EL4) in C57BL strain of mice and maintained in our Institute for over 

 100 transplant generations. The cytological analysis of these leukaemias, 

 carried out by Dr. A. J. S. Davies, has shown that nearly 95% of the cell 

 population in C+ leukaemia is composed of cells with 40 chromosomes, 

 without evidence of structural change. The stem-line of EL4 leukaemia was 

 found to consist of cells with 39 chromosomes, one of which was metacentric. 

 The percentage of cells with 39 chromosomes is 93%; thus the frequency of 

 cells with the metacentric is about the same as reported by Wakonig (1962) 

 in her urethane-induced leukaemia [cf. Roller, 1961). 



It is interesting to note that in cases of human leukaemias, chromosome 

 heteroploidy is restricted to a small structural change in one chromosome of 

 2n complex (the Ph' chromosome in chronic myeloid leukaemia: Nowell and 

 Hungerford, 1961) or to the presence of very few extra chromosomes found 

 in a certain proportion of acute leukaemias so far studied (Baikie et at., 1961). 



The inconsistency in the chromosome composition shown by the virus- 

 induced murine leukaemias seems to suggest that heretoploidy m the leukae- 

 mic cell population is an epiphenomenon and that the limited spectrum 

 of variation in chromosome number is the result of selection. 



