Page:EB1911 - Volume 20.djvu/984

Rh the condensation of the fibrous laminae and the disappearance of the cellular character of the granulation tissue. Thus is formed in the damaged area a permanent tissue known as scar tissue (fig. 35. Pl. III.).

Fibrosis.—Where a chronic inflammatory process has taken possession of an organ, or, let us say, has been located in periosteum or other fibrous part, there is a great tendency to the production of cicatricial fibrous tissue in mass. Thus it is laid down in large quantity in cirrhosis of the liver, kidney or lung, and reacts upon these organs by contracting and inducing atrophy. The term “cirrhosis” or “fibrosis” is usually applied to such a condition of organs (figs. 36 and 37, Pl. IV.), that of “sclerosis” is used when such a deposition of fibrous tissue occurs within the central nervous system. Gull and Sutton asserted that in particular states of body, and more especially in the condition associated with cirrhotic kidney, such a fibrosis becomes general, running, as they alleged it does, along the adventitia of arteries and spreading to their capillaries. They supposed that it was accompanied by a peculiar hyaline thickening of the arterial wall, usually of the tunica intima, and hence they termed the supposed diseased state “arterio-capillary fibrosis,” and gave the fibrous substance the name “hyaline-fibroid.” They held that the cirrhotic kidney is simply a local manifestation of a general fibrous disease. Their theory, however, has fallen into disfavour of late years.

The various definitions of the term “new growth” leave us with a definite conception of it as a new formation of tissue which appears to originate and to grow independently. We have already compared the body to a social community, each constituent element of which—the cell—lives its own life but subordinates its individuality to the good of the whole organism. The essential characteristic of a new growth is that this subordination is lost and the tissue elements, freed from the normal mutual restraint of their interdependence, give way to an abnormal growth. All the hypotheses about the causation of new growths seek to explain the secret of this individuality or “autonomy,” as they recognize that the mystery of the origin of the great majority of tumours would be solved if we could trace how or why the tissue elements in which they develop first took on this abnormal growth.

Tumours are divided into two main groups—innocent and malignant. These differ only in degree and there is no hard and fast line between them. Innocent tumours are usually sharply defined from the surrounding tissues, and show no tendency to spread into them or to pass by means of lymphatics and blood vessels to neighbouring parts (fig. 38, Pl. IV.). Malignant tumours, on the other hand, invade the adjacent tissues and pass by lymphatics and blood vessels to distant parts, where they set up secondary growths (fig. 39, Pl. IV.).

Tumours appear to arise spontaneously, i.e. without evident cause; they may develop in association with prolonged irritation or injury (later referred to in more detail). To heredity, as an indirect or predisposing cause, has probably been assigned too great importance, and the many facts brought forward of the relative frequency of cancer in members of one family only justify the conclusion that the tissue-resistance of certain families is lowered.

At the present time we have still before us the question, what is the essential cause of (q.v.)? This, one of the most difficult problems of pathology, is being attacked by many able workers, who are all striving from different standpoints to elucidate the nature of these new formations, which spring from the normal tissues in which they develop and which they destroy. In spite of all the valuable research work that has been done within the last few years, the essential cause of new growths still remains unknown.

To the work carried on by the Imperial Cancer Research Fund in England, and to investigators in other countries, are due the present day scientific efforts made to systematize investigation and clear away many of the hypothetical speculations that have gathered round this most difficult subject. Their investigations on cancers found in the lower animals, and the successful transplantation of such growths into a new host of the same species (mice and rats), have greatly advanced our knowledge of the etiology of this disease.

Many of the hypotheses of the past put forward to explain cancer must be discarded, in view of the facts brought to light by the comparative and experimental research of recent times. According to the hypothesis of Waldcyer and Thiersch there is perfect equilibrium between the normal epithelium and its supporting structure, the connective tissue, but with advancing age this balance is upset

owing to the connective tissue gradually losing its restraining power. The epithehal cells are then able to pass from their normal position, in consequence of which they proliferate and at the same time revert to a more primitive type of cell. In this way they give rise to a malignant new growth.

Cohnheim's hypothesis of “embryonic residues” provides that early in the development of the embryo some of the cells, or groups of cells, are separated from their organic continuity during the various foldings that take place in the actively growing embryo. The separated cells become intermingled with other tissue elements amongst which they lie dormant with their inherent power of proliferation in abeyance. At a later date in the life of the individual, by some unknown stimuli, they resume their active power of proliferation and so give rise to new growths.

The “tissue-tension” hypothesis of Ribbert is a combination of the two foregoing. He holds that new growths arise, both before birth or at any subsequent period of life, by the separation of cells or clumps of cells from their normal position, and that in health there is a balance between the various tissues and tissue elements regulated by what he calls the “tissue-tension” of the part, i.e. that cells or groups of cells have a restraining power on one another which prevents any physiological over-activity.

From whatever cause the resisting power of the tissue elements is thus weakened, the invasion of other tissue elements is then allowed to take place. These being freed from the normal inhibiting power of the neighbouring elements, multiply and go on to the formation of a new growth. According to Ribbert it is the isolation, together with the latent capacity of isolated cells for unlimited proliferation, that gives rise to new growths.

Hansemann's “anaplasia” hypothesis seeks to find an explanation of the formation of new growths in the absence of the histological differentiation of the cell associated with a corresponding increase in its proliferative power and a suspension, or loss, of its functional activity.

The greater the degree of anaplasia the more the tumour cells conform in character and appearance to the embryonic type of cell and the more malignant is the new growth. A simple fibroma is a growth composed of fully formed fibrous tissue (fig. 40, Pl. IV.). The small round celled sarcoma is a malignant growth, and is composed of the primitive type of cell that goes to form fibrous tissue (fig. 41, Pl. IV.).

Then we have Beard's “germ-cell” hypothesis, in which he holds that many of the germ-cells in the growing embryo fail to reach their proper position—the generative areas—and settle down and become quiescent in some somatic tissue of the embryo. They may at some later date become active in some way, and so give rise to a cellular proliferation that may imitate the structure in which they grow, so giving rise to new growths.

Some workers regard certain appearances in dividing cells found in cancer as evidence of a reversion of the somatic cell to the germ-cell type (heterotypical), otherwise found only in the process which results in the formation of an embryo. These appearances are probably due to a pathological mitosis, commonly found in cancer, in which there is an irregular diminution in the number of chromosomes; some are cast out and become degenerated or some pass over to one of the daughter cells, leaving a reduced number in the other, and thus give rise to asymmetrical mitosis.

From the histological examination of tumour cells there is no evidence to show that they resemble the protozoa unicellular organisms in occasionally passing through a sexual process of reproduction, i.e. that nuclear conjugation between cells ever takes place.

In recent years the successful experimental transplantation of new growths, occurring sporadically in white mice and rats, into animals of the same species, has thrown a fresh light on all the features of malignant growths. From these experiments it is shown that cells taken from these growths and introduced into animals of the same species give rise to a cancerous growth, whose cells have acquired unlimited powers of proliferation. They are direct lineal descendants of the cells introduced, and are in no way formed from the tissue cells of the host in which they are placed and grow.

Not only is this true of epithelial cells, but the connective tissue-cells of the supporting structure of cancerous growth, after repeated transplantation, may become so altered that a gradual evolution of apparently normal connective tissue into sarcomatous elements takes place, these giving rise to “mixed tumours.” The sarcomatous development may even completely outgrow the epithelial elements and so form and continue to grow as a pure sarcoma.

The fact that it is possible to propagate these cells of one animal for years in other animals of the same species, without any loss of their vegetative vitality, suggests that this continued growth is kept up by a growth-stimulating substance present in the proper species of animal; this substance, however, has not the power of transforming the normal tissue into a cancerous one.

Henser, Bencke, Adami, Marchand and others have also put forward hypotheses to account for the origin of new growths. These observers maintain that the cells from some cause lose, or may never have had developed, their functional activity, and thus