PATHOLOGY OF CANCER. 
BY H. E. MUNN, M. D., 
PROFESSOR HISTOLOGY AND DERMATOLOGY 
IN TOLEDO MEDICAL COLLEGE. 
Read before the Northwestern Ohio Medical Association, at Van Wert, 0., June 29, 1894, 
REPRINT FROM TOLEDO MEDICAL COMPEND, JULY, 1894. 
•AM8EY A FI8TER PRINT PATHOLOGY OF CANCER. 
BY H. E. MUNN, M. D.f 
PROFESSOR HISTOLOGY AND DERMATOLOGY 
IN TOLEDO MEDICAL COLLEGE. 
Read before the Northwestern Ohio Medical Association, at Van Wert, 0., June 29, 1894 
The essential histological elements of cancer consist of various 
forms of cells of epithelial character. The cells constitute larger or 
smaller spherical or elongated masses in alveolar or interstitial spaces 
of the part in which they grow. Accompanying ths growth of these 
cells, and the continuous penetration of them into such spaces, is an in- 
crease, more or less proportionate, of the fibrous tissue stroma. 
In many cases the new tissue is, evidently, an inflammatory hyp- 
erplasia, produced by the irritating invasion of the epithelium. In 
other cases or forms, the stroma and vessels therein appear to be of new, 
embryonic formation, and while not of due proportion, as in surrounding 
tissues, yet not bearing evidence of inflammatory origin. Medullary or 
encephaloid. and the glandular varieties belong to this latter group, and 
scirrhous and epithelioma to the former. The cells filling the alveoli, 
to a greater or less degree, resemble normal epithelial forms found on 
such surtaces, or in such masses where the growth originated. Condi- 
tions of rapid growth, of age, of degenerative changes, and of pressure, 
determine the shape, size and other attributes of the cells. 
If the theory or hypothesis rather, of Cohnheim, that tumors arise 
from the inclusion of embryonic cells or collections of cells, which, after 
complete evolution of the tissues, are by some stimulus excited to growth 
and development, unrestrained and undirected by co-ordinate or co- 
operative growth and development of the whole—if this be true, which 
seems not improbable, then the embryonic cells or bits of tissue from 
which the carcinomata arise, must have undergone evolution up to the 
stage of differentiation of the germinal layers In fact this must be 
true also of all tumor pathogenesis, except, perhaps, for the so-called 
“dermoid cysts.” For, leaving out these last, we find no abstractly 4 
heterologous tumors; but those of mesoblastic character takiug rise from 
tissue of mesoblastic origin, and the epithelial from hypo- and epiblastic 
sites only. 
What a matter of interest, perhaps of conjecture only, to look down 
along the path of tissue evolution, to see where nature’s emigration train 
has, unnoticed, dropped the undeveloped, imperfect seed here and there 
along the way, to lie unseen, perchance to spring into luxuriant and 
noxious growth long afterwards. 
Away down in the scale of development, probably from among the 
mass of cells, having common and undifferentiated proteneies, was left 
aside from the current of evolution’s tide a cell or two, before the ger- 
minal layers had begun to form. From these we get all sorts of tissues, 
epithelial and mesoblastic, in the “dermoid cyst ” Further up, where 
the ways divide apart, we have the separation into three classes of cells, 
and across the line our growths cannot pass, but just this side of the 
line we have those abandoned orphans of nature who have all the pos- 
sibilities of the mesoblast in its infancy. 
Here the sarcomata spring, up; and soon, and on, coming down to 
those which must have been passed by, just before the final completion 
of tissue, to give rise to tumors much like the normal forms. Curiously 
enough, we get no true nervous tissue turner growth, except in “der- 
moids” and the sustentacular tissue, neurogliar gliomata. 
So these cancerous tumors also show their ancestral traits, for, not 
only do they arise from epithelial structures solely, but they exhibit in 
morphology a similarity, more or less distinctly expressed, to the epi- 
thelium of the organ or surface, in which their parent cell was included. 
Thus, the epitheliomata or epidermic origin have more or less squamous 
cells, as also the more massive and even semi-columnar ones, which 
show degenerative changes similar to stratum corneum, lucidum and 
the malpighiau layer. Cells like those in concentric nests and “pearls” 
staining like similar cells in stratum lucidum and corneum. Those of 
internal passages, of hypoblastic deriviation have cells of columnar form 
with other distorted shapes. So, also, those of glandular site present 
forms similar to those of the mature gland, or to those of general embryonic 
gland form. 
The development of normal cells, from the oosperm through all its 
progeny up to the fully matured individual living organism, show a 
purposive tendency, a disposition even through many metamorphoses to 
arrive at definite and orderly complexity and differentiation. And, if 
abortive and monstrous forms occur, they are from interrupted and in- 
complete development, or some diversion of evolution into long obsolete 
but primeval paths. That is to say, however diverse the outcome of 
development may be, from that which now constitutes the complete and 
perfected structures or organism, the resultant parts or whole, show the -5- 
atterapt of the injured, hindered or exuberant cell to develop along the 
lines, and to ihe ends shaped by ancestral environment. Therefore, we 
are justified in believing that these pathological forms are attempts of 
the aroused embryonic cell (hitherto latent),to produce something which 
it might have completed, had it gone on in tissue construction aided and 
restrained by its fellows. 
Of epithelial tumor construction we have at the extreme two classes, 
one which is nearer maturity in embryonic ancestry, and therefore 
the main line—the benign adenomata, which frequently, in its more 
perfect forms, rather closely resembles normal glands in structure and 
function—that is. producing something resembling some of the glandu- 
lar secretions. These may be set down as the epithelial analogues of 
the more mature varieties of mesoblastic tumor formation—the benign 
fibro-, lipo-, choudro-, osteo-, myomata, etc. At the other extreme are 
the carcinomata; these are for the most part made up, as pre- 
viously stated, of masses of epitheloid cells, penetrating into the 
adjacent tissues. These may be classed as of the “cadet” line, which 
left the train of evolution farther back, and not having received the 
directing and restraining impress of orderly developement and associa- 
tion as late as the other class, produce more aberrant forms. These are 
analogous to the malignant mesoblastic tumors—those embryonic and 
immature-featured sarcomata. 
In the sarcomata we recognize the mesoblastic tissue tendencies as 
much as in those of maturer and more stable development. So it seems 
to me we may recognize in the carcinomata the tendency to glaud pro- 
duction, even though lacking most essentials of the adult organ. 
Epiblastic glands are developed by the ingrowth of solid cylinders 
of epithelial cells, which branch and ramify or remain more simple, 
with formation of lumen in ducts and acini by separation or degenera- 
tive solution and mingling in first secretion; further there is formed the 
specialized limiting basement membrane, continuous with that which 
lies beneath the malpighiau layer, and upon the vascular corium. 
In hypoblastic gland evolution, in some cases the same process 
obtains, but many of the glands are produced by tubular involu- 
tions of the mesenteron with subsequent specialization of cells into 
gland epithelium. These invaginations may remain as simple tubular 
glands or become complex. The adenomata originate in the same man- 
ner, and some of them having lumena with cystic exaggeration, while 
others persist as solid cylinders of epithelium. 
As before said, the more perfect the approximation to normal type, 
the more benign their characteristics. But these epithelial new 
growths are not all benign, many of them having distinctly glandular 
appearance, being quite malignant. Now, these go over toward the 
border line of carcinomata, and not only is there a shading off of the 6 
adenomata and carcinomata toward each other in quality, but also in 
optical appearance. And this insensible graduation goes on clear 
through the epithelial tumor growths from one extreme to the other. 
At the extreme of carcinomata, we have the attempt at the pro- 
duction of gland tissue, but it reaches only the earlier embryonic stage 
in that line of evolution; that is, the ingrowth of epithelial or epitheloid 
cells in alveolar or cylindrical masses, without orderly arrangement, 
the formation of lumen or membrana propria. 
While the most embryonic of sarcomas, those consisting of granu- 
lation cell elements, are recognized as abortive attempts at connective 
tissue construction, these epithelial ingrowths have been classed as 
“anomalous” instead of being denominated as of the type of “embryonic 
adenomatous tissue” tumors. For such they properly should be. 
The general arrangement of cancerous growths and the cell pe- 
culiarities have, without a doubt, something of ontogenous impress; that 
is, are inffnenced in this way by the characteristics of contiguous struct- 
ures. We see this quite markedly in the sarcomata, which take on 
pigmentary; or reticular, or alveolar form, if growing near or into 
structures having these qualities. Nevertheless, the phylogenous in- 
fluence, or that of ancestral cell acquirement is the major one, for these 
growths never pass over the line which has differentiated the mesoblastic 
from the epithelial, thus exemplifying the laws of the “instability of the 
homogenous” and “of increasing heterogenity,” long ago recognized by 
Von Baer and Herbert Spencer For, though we find many examples 
of tumors taking on appearances in greater or less mimicry of contiguous 
tissues, we have every year more convincing evidence that the invasion 
of tumors by peripheral extension or embolic implantation in tissues of 
a specifically different class, has no effect to render its histogenesis other 
than that produced by that of ancestral or phylogenous impress. 
The primary site of cancer, remote from some glandular structure, 
is in the nature of things almost an imposibility, except, perhaps, those 
arising from the so-called endothelial surfaces as the serious body-cavities. 
So that the phylogenous influences in cancer are not so readily dis- 
tinguishable from those strictly ontogenous. 
In tumors of mesoblastic type it is, in very many cases, much more 
readily observed,for while many are decidedly homeotopic, the heterotopic 
forms are perhaps quite as frequent. The lymph-adenomatous structure, 
and the pigmented varieties of sarcomata, when originating in or near 
normal tissues having such features, are undoubted examples of local 
influence. Growths of fat, fibrous tissue, muscle, etc., in like normal 
tissue sites, are probably examples of late developmental interruption of 
the cells of origin. Heterotopic growths as of bone, cartilage, fat and 
muscle, whether benign (and therefore of more mature type), or malig- 
nant, (and therefore more embryonic) necessarily must be interpreted as -7- 
exhibiting some directing influence other than that of contiguous normal 
tissues. 
Microscopical investigations in histology, embryology and patholo- 
gy, have demonstrated that in pathogenesis, as in normal histogenesis, 
there is, we may say, a determinate effort toward orderly and definite 
development. But the immediate cell ancestors of cancer growth, as of 
other neoplasms, lack the restraining and co-ordinating impress of the 
later stages of tissue evolution. The necessary exuberance of growth 
and deficient stability, as well as the time of appearance, verifying for 
this much at least, the aphorism of Virchow, that “disease processes con- 
sist in excess, or deficiency, or being at the wrong time, or the wrong 
place.”