PROLIFERATIVE DISEASES 



in that there is usually neither gross controlled local pro- 

 liferation nor any invasion of tissues of a malignant type. Any 

 invasion is simply of the character of normal leucocytic entry 

 into the tissues. 



Chronic myeloid leukaemia may persist in its quiescent 

 form for several years. On the average, death takes place 

 about three years after the first recognition of the disease, 

 the final episode being due to a switch to a myeloblastic 

 blood picture. On the evidence given by Scott (1957), the 

 use of modern methods of treatment has had no beneficial 

 effect whatever on the duration of life, although the remis- 

 sions induced may be of real psychological and social value 

 to the patient. When X-radiation therapy is used it is the 

 normal finding that each remission is less easy to produce and 

 lasts a shorter time until the final myeloblastic crisis closes 

 the story. With myeleran therapy the leucocyte count can be 

 kept under control without much change until the final phase 

 develops, apparently with equal inevitability. 



Here there is definite evidence of changes most readily 

 interpreted as secondary somatic mutations. It is absolutely 

 certain that acute leukaemia is enormously more likely to 

 occur in a patient with chronic myeloid leukaemia than in 

 a normal individual. The common-sense interpretation is 

 that the primary mutant provides a necessary basis on which 

 a further mutation can induce the myeloblastic behaviour. 

 The behaviour of leukaemia under deep X-ray therapy 

 suggests again a common-sense explanation, that in addition 

 to its lethal effect on large numbers of leukaemic cells the 

 radiation {a) induces mutations of various types, and 

 {b) provides a selective survival for cells relatively resistant 

 to the lethal effect of X-rays. With the reduction in the 

 average number of leukaemic cells present, one would expect 

 a delay in the appearance of the terminal mutation and its 

 manifestation as a myeloblastic crisis. 



Some other aspects of myeloid leukaemia may be relevant 

 to the present theme. There are rare examples of neutrophil 



176 



