Further evidence on the homogeneity of the resistance to the implantation of malignant new growths / by E.F. Bashford and B.R.G. Russell ; [communicated by J. Rose Bradford].

  • Bashford, Ernest Francis, 1873-
Date:
1910
Catalogue details

Licence: In copyright

Credit: Further evidence on the homogeneity of the resistance to the implantation of malignant new growths / by E.F. Bashford and B.R.G. Russell ; [communicated by J. Rose Bradford]. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    agreement. These difficulties are associated more especially with the results following upon the secondary inoculation of animals already bearing tumours as the result of primary inoculation. Some authors have succeeded where others have failed to obtain secondary tumours in this way. The methods by which secondary inoculations can be successfully carried out, the import- ance of dosage,* and other technical details, have been fully explained in a series of papers, and the contradictory results harmonised (3, 4, 5). It is however, necessary to meet hypothetical explanations of the reasons why a secondary inoculation may fail, by recording the results of actual observation of the processes responsible and comparing them with those following the induction of active resistance in normal animals. Therefore, the histological details of the process have been ascertained by examining the site of re-inoculation at definite intervals. This method is conveniently called the examination of “ early stages.”f By its means the true nature of the trans- plantation of cancer was demonstrated (6, 7), and later it revealed how important for the implanted cancer-cells was the provision of a specific supporting and nutritive scaffolding by the tissues of the new host (8). It also demonstrated, that in mice rendered resistant to carcinomata, there was a failure to supply this specific scaffolding, and hence the conclusion was arrived at that actively resistant animals robbed the cancer-cells of the chemiotactic powers they exercise on the connective tissues of the host (4). This failure of the specific stroma reaction was seen both when resistance was induced by the previous absorption of tumour tissue, and by the previous absorption of normal tissue—whether adult or embryonic—of the s^rne species. For the elucidation of the mechanism of resistance there is, at present, no alternative to actual observation of the site of the inoculation of cancer-cells in living animals. Without resort to this laborious method the hypothetical assumption of an atreptic immunity was advanced to explain why a secondary inoculation may fail in an animal already bearing a tumour. By employing it the facts recorded in this paper have been elicited; they harmonise with what has been stated elsewhere on the successful re-inoculation of animals already bearing tumours, and show that the resistance which may exist to re-inoculation under these circumstances is identical in its nature and mechanism with that which can be induced in normal animals, i.e., in the absence of a tumour. It is immaterial which of the 65 tumour-strains growing in the laboratory * It is impossible to compare the rate of growth of the tumours following inoculation if the amount of material inoculated as the starting point of growth is not stated. This factor still continues to be neglected, even in the most recent investigations of tumour growth. Cf. Moreschi, ‘ Zeitschrift f. Immunitatsforschung,’ 1909. f Fully described in the Scientific Reports of the Imperial Cancer Research Fund.
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