Evidence for immune facilitation of breast cancer growth and for the immune promotion of oncogenesis in breast cancer.
Autoimmune diseases have been extensively studied in man and experimental animal models and salient points are reviewed, as a clear understanding of the immune mechanisms involved is essential if one is to understand the potential of immune interactions with established cancer cells or in the premalignant period of hyperplasia. Such reactions may be of benefit to the host, with down regulation of tumor growth, or unfavourable, with facilitation of oncogenesis and cancer growth. In particular, evidence is cited that supports a beneficial effect of the host response to non-small-cell lung cancer and the association of a poor prognosis in established breast cancer caused by a heightened immune response to the tumor. Histologic evidence supports these conclusions, as do studies of specific and nonspecific immune reactivity in breast cancer patients. The potential for cytokines to stimulate breast cancer growth, increase angiogenesis and decrease cell adhesion is reviewed, also recent evidence for autologous lymphocyte stimulation of breast cancer. Parallels between immune promotion of breast cancer in mice, caused by the mouse mammary tumor virus, and the development of breast cancer in women are also reviewed. If the mouse model has relevance for human breast cancer, one could predict that there would be a reduced incidence of breast cancer in a population of chronically immunosuppressed women following organ transplantation. Such is the case. This finding, plus the fact that all treatments that have shown efficacy in breast cancer have one thing in common, they are immunosuppressive, strongly support the role of immune facilitation of breast cancer growth and immune promotion of oncogenesis in breast cancer in a substantial number of growth.
Stewart
T H
TH
Department of Medicine, Ottawa General Hospital, Canada.
D000818:Animals; D001943:Breast Neoplasms / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D002455:Cell Division / Q000276:immunology; D002471:Cell Transformation, Neoplastic / Q000276:immunology*; D005260:Female; D006801:Humans; D051379:Mice