Unresolved Inflammation and Cancer: Loss of Natural Immune Surveillance as the Correct ‘Target’ for Therapy! Seeing the ‘Elephant’ in the Light of Logic
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To begin this commentary, it is appropriate to remember the 1959 statement made by Peyton Rous (Nobel Laureate in Physiology or Medicine 1966) that “A hypothesis is best known by its fruits. What have been those of the somatic mutation hypothesis? It has resulted in no good thing as concerns the cancer problem, but in much that is bad… Most serious of all the results of the somatic mutation hypothesis has been its effect on research workers. It acts as a tranquilizer on those who believe in it.” This statement was made over 50 years ago and well before the genetic study of cancer was put on steroids!
As Americans observe the 40th anniversary of the institution of President Nixon’s war on cancer, a sobering fact is that, despite heavy public investment for more than four decades on cancer research, progress in understanding the biology of cancer and how to control it has been extremely slow and fragmentary like identifying an ‘Elephant’ in the dark. Few, if any of the data emanating...
KeywordsCancer Immune surveillance Yin and Yang Acute and chronic inflammation Oxidative stress Targeted therapy Tumoricidal Tumorigenic Neurodegenerative Autoimmune Immune-privileged Immune-responsive Aging
Selected References by the Author
- 4.Khatami, M. (2011). Inflammation, aging and cancer: Friend or foe? In M. Khatami (Ed.), Inflammation, aging and cancer. Croatia: InTech Publishing (in press).Google Scholar
- 6.Khatami, M. (2005). Developmental phases of inflammation-induced massive lymphoid hyperplasia and extensive changes in epithelium in an experimental model of allergy. Implications for a direct link between inflammation and carcinogenesis. American Journal of Therapeutics, 12, 117–128.PubMedCrossRefGoogle Scholar
- 7.Khatami, M. (2005). Cyclooxygenase inhibitor Ketorolac or mast cell stabilizers: Immunological challenges in cancer therapy. Letters to the Editor. Clinical Cancer Research, 11, 1350–1352.Google Scholar