Solid-state carcinogenesis

Brand, K. G. (1976). Solid state or foreign body carcinogenesis. In Symington, T. and R. L. Carter, eds. Scientific Foundations of Oncology, pp. 490-495. Year Book Medical Fhiblishers of William Heineman Medical Books, Chicago. 

Bischoff, F. and Bryson, G., Carcinogenesis through solid state surfaces. Prog. Exp. Tumor Res. 5 85-97 (1964). 

Although much is known about the processes of cancer formation, or carcinogenesis, comparatively little is known about the processes of cancer regression. The former will be explored as an introduction to the latter, and both involve the biological and chemical functions of the body, stated in terms of normal cells vs. cancerous ones. Surgical excision and radiation treatment are excluded from the discussion, though they can be selective if, say, the solid tumor is localized and has not yet spread or metastasized — and if the operations or treatments in themselves do not cause metastasis. 

On the other hand, it is also true that human beings are being exposed to many heterocyclic amines and many other carcinogens with tumor promoters and/or suppressing factors for carcinogenesis. At this moment, it is honest to state that no solid information on the estimation of risk of heterocyclic amines has been obtained in any direction, either... 

It is important to state here that these compounds have not been found to increase communication between established tumor cells and normal cells [5] this would be consistent with their inability in the lOTl/2 system to inhibit expression of the transformed phenotype i.e. growth of tumor cells in a background of normal cells, and with the experimental animal data showing that these compounds are active in the post-initiation phase of carcinogenesis prior to the establishment of tumors. These observations would also be consistent with the lack of ability of retinoic acid to inhibit solid tumor growth in clinical trials in head and neck cancer [16]. Thus, in general, the actions of carotenoids and retinoids are considered to be preventive and not therapeutic. In a recent study of dysplastic regions of the oral cavity in patients with a prior history of oral carcinoma, we discovered that even in these pre-cancerous lesions major reductions in connexin 43 expression had occurred [17]. Studies are underway to determine if retinoids can counter this decrease. 

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