84 J. B. CLELAND. 
deficiency of the fat-forming constituents) may be unable 
to reach the cells because the vascular and lymphatic chan- 
nels, the roads by which it comes, are blocked or inefficient, 
or because the concentration of the pro-fat materials sur- 
rounding the fat cells is, for some reason, still too high in 
spite of a deficiency elsewhere. The fat cell is then in the 
position of the carpet-snake that has swallowed a china 
nest-egg—unable to split up the body distending it, and 
equally unable to disgorge it. Neighbouring pro-fat cells 
similarly form fat, store it up, and then find it cannot be 
dealt with. Finally the summation of these cells forms 
a tumour. Enzymes probably play a similar part in the 
production and absorption of fibrous and even bony material 
—witness, for instance, the absorption of callus after an 
injury to bone. A little imagination will show how this 
view can be applied to fibromata and osteotomata as well 
as lipomata. 
Malegnant growths are similarly formed of cells growing 
independently of the bodily needs. They differ from inno- 
cent growths in that their cells, to a greater or less extent, 
tend to invade the surrounding tissues and replace them, 
and even to be dislodged from the situation in which they 
‘grow, to be distributed by the vascular or lymphatic tissues 
to other parts of the body. When thus seeded they begin 
to grow in the new situation, forming fresh deposits of 
the new growth or metastases. The faculty of invasion may 
give rise to a loss in size of the invaded tissues by a process 
of erosion—when we have the anomaly of a malignant ‘‘tu- 
mour’’ which shows a shrinkage in size from the normal, 
and not an increased ‘‘swelling,’’ as the name imples—or 
to an increase in size from the number and size of the 
malignant cells more than making up for the loss of the 
normal cells. Death may result either from interference, 
22) 
by replacement, with vital tissues from the original growth 
