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PATHOLOGY: E. F. SMITH 
cerous growth. The other phenomena are subsidiary and may be left 
out of account in this brief abstract. 
3. Earlier discoveries in plants. — In 1907 the author and his colleagues 
(Townsend and Brown) proved that a common hyperplasia of various 
cultivated plants which had been for many years under observation 
in this country and in Europe and for which various causes had been 
inconclusively assigned (frosts, physiological disturbances, mites, myxo- 
mycetes, etc.) was really due to a polar flagellate schizomycete, named 
by us Bacterium tumefaciens. This was first cultivated from tumors on 
the Paris daisy in 1906, but afterwards it was obtained from various 
other plants, in several distinct strains (daisy strain, hop strain, etc.) and 
shown to be cross-inoculable on a variety of plants with resultant 
tumors in which no bacterial cavities or bacterial occupation of cells, 
vessels, or intercellular spaces could be seen in fresh material or demon- 
strated in serial sections by stains, and yet from which the causal organ- 
ism was readily cultivable in small numbers by the common methods 
of the bacteriologist. 
4. Further discoveries —In 1911 I discovered in inoculated Paris 
daisies a parenchymatous tumor-strand connecting the primary stem 
tumors with deep-seated secondary tumors which had developed in the 
leaves some weeks after the stem inoculations. I also showed these 
secondary leaf-tumors to be possessed of stem structure, i.e., to have the 
structure of the primary tumor, thus following the law of cancer in 
man and animals. These discoveries were fully illustrated and described 
at that time in United States Department of Agriculture bulletins^ and 
elsewhere. From the origin, structure and general appearance of these 
tumors I likened them to sarcomata. 
5. Other resemblances of crown gall to cancer in man and animals. — 
Without entering into details which may be found elsewhere a few 
other resemblances are here summarized: (1) No parasite visible; (2) 
Embryonic character and rapid multiplication of the proliferating cells; 
(3) Loss of polarity in the proliferating tissues; (4) Invasive surface 
growth of the tumor and absence of a capsule; (5) Non-granulomatous 
development of secondary tumors; (6) Growth in autonomous species 
from grafts; (7) Presence of degenerative changes in the proliferating 
cells as shown by behavior toward stains, by lobed and cleft nuclei, 
polynuclear cells, etc.; (8) Destruction of surrounding tissues; (9) 
Defective vascularization and early central necrosis with invasion of the 
open wounds by secondary parasites and by saprophytes; (10) Fre- 
quent return after excision; (11) Presence of atrophy and cachexia. 
