The lack of clear understanding of the cause of the cancer has led to billions of dollars spent on treatments, which on the average, have not improved cancer survival. This fact has been documented by my colleague and former thesis advisor, John Bailar, M.D., Ph.D., in the paper above. A brilliant scientist and MacArthur Fellow, in his spare time, Dr. Bailar was the statistician for the New England Journal of Medicine for over a decade and much of the modern medical literature has been published only after his careful review and approval of its accuracy, methodology, and method of inference.
Several people have asked me to post some of my research, largely done under the guidance of Dr. Bailar, from eight years of funding by the National Cancer Institute focused on cancer epidemiology and treatment. I scanned in a good summary paper that shows an elegant way to model the risk of cancer with a specific example applied to radiation risk and breast cancer. You could use these data to estimate risk of mammography induced cancer, for example.
Sutherland JV (1984) Estimates of cancer risk associated with radiation exposure. In Health Effects of Low Level Radiation. Hendee WR (Ed) Norwalk: Appleton-Century-Crofts, pp 93-117.
Of immediate interest is the fact that cancer appears to be the result of triggering programs in normal DNA. It is not a “disease” in the sense of an infectious disease caused by pathogens, although these genetic programs may be triggered by pathogens, particularly by Baccilus Licheniformis, the so-called “cancer germ” or Rife virus mentioned elsewhere on this site. The initial insults may be due to mutations caused by pathogens, radiations, chemicals, or other insults. However, the triggering process of DNA programs causing uncontrolled growth may be caused by extensive DNA repair mechanisms as cells attempt to correct these mutations.
Excerpts from my paper estimating cancer risk reinforce comments above:
The Multihit Model of Carcinogenesis
…The multiple mutation theory or multihit model of carcinogenesis was originally proposed by Muller in 1951. An extensive literature has developed from this idea during the past 30 years. In the past decade, the multihit model has gained dramatically increased acceptance due to (1) Fialkow’s demonstration that virtually all cancers arise from a single cell and (2) Ames’ demonstration that almost all carcinogens are mutagens.
The present conception of this model assumes that a normal cell is initiated (rendered potentially malignant) through alteration of cellular DNA by radiation, chemical, viruses, or other factors. Initiation may be retarded by DNA repair or accelerated by promoting agents. Farber suggested that a malignant cell is the result of an evolutionary process in which a normal cell and/or its progeny pass through several rate-limiting steps, someof which may be mutations. From a mathematical standpoint, “hits” may be either mutations or nonmutational rate-limiting events and the terms may be used interchangeably. Breast cancer may be viewed as a four-hit process. The first and third hits may be mutations. The second and fourth hits could be epigenetic events that cause proliferation of clones of cells.
Recently, Holliday unraveled two puzzling phenomena that lend greater credence to the model. Many researchers have viewed carcinogenesis as an epigenetic process since programs embedded in cellular DNA, which cause rapid prenatal cellular proliferation and which are normally dormant, could give rise to malignancy if triggered by mutation or other factors in the cellular environment. In addition, if hits cause malignancy, it was not clear why animals with short life spans are prone to tumor incidence similar to humans who have an extensive life span. Holliday proposed that “damage to DNA followed by repair can trigger epigenetic changes in gene expression which are responsible for malignancy. Since DNA repair is more efficient in large long-live animals, tumors occur over a more extended time span.