American Journal of Pharmacology and Toxicology

Cancer may be caused by the Immune Reaction

Richmond T. Prehn

DOI : 10.3844/ajptsp.2008.93.99

American Journal of Pharmacology and Toxicology

Volume 3, Issue 1

Pages 93-99

Abstract

Hormesis-like effects of immunity have been documented during tumor-growth experiments in mice, quantitatively large immune-reactions have inhibited while lesser quantities of the same specific immune-reactants have been stimulatory to the growth of implanted tumors. Likewise, carcinogenesis has been inhibited by a high quantities of immune reactants, but positively stimulated by lower levels of the same reactants. One observation suggests that malignant transformation may seldom, if ever, occur in vivo if there is no immune reaction against the incipient neoplasm. These and many similar observations suggest a real danger that some vaccines might stimulate rather than inhibit tumor growth. These hormesis-like effects may help to provide explanations for a number of otherwise perplexing observations such as the following: (1): The fact that immunodepression for heart or kidney allografting results in an increased incidence of some tumors, especially leukemias and skin tumors, while others, such as those of breast and rectum, show a decreased incidence in these immunodepressed patients, (2): The possible dependency of carcinogenesis on an immune reaction, (3): The fact that adult Down’s syndrome patients are unexpectedly resistant to solid tumors, especially breast-carcinoma, but have a very high incidence of leukemia, (4): The fact that Kaposi’s sarcoma in an AIDS-patient often tends to flare as the patient’s disease is ameliorated, (5): The sneaking through phenomenon, (6): Lastly, some peculiarities in the metastatic patterns of tumors of various types.

Copyright

© 2008 Richmond T. Prehn. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.