Is cancer theory incomplete?

According to one physicist, major advances in science arise from two sources. The first is the introduction of new data and the second is the study of inconsistencies in established knowledge. Has cancer research missed the boat? Classically, experimental carcinogenesis is a complex, multi-stage process including initiation, promotion, and malignant progression in which the failure of DNA repair mechanisms and the subsequent clonal expansion of mutated cells play a pivotal role. However, more recently, it has become apparent that the pathogenesis of all cancers cannot be explained by this doctrine. Firstly, there is new data to suggest that cancer can be closely connected with aberrantly regulated apoptotic cell death and the resulting deregulation of cell proliferation. In fact, uncontrolled apoptosis has been directly linked to carcinogenesis. Scientific animal studies have shown that simply increasing the basal frequency of apoptosis in murine skin cells can be linked to the rapid development of squamous cell carcinomas in transgenic mice. Moreover, repeated apoptosis in human skin cells can result in tumour formation within a matter of months. Secondly, not all carcinogens are mutagens, so the assumption that mutations are always the core cause of carcinogenesis appears to be a fatal flaw in original cancer theory, especially since they are not known to occur within a short time. This suggests that there may be other alternate trigger mechanisms leading to carcinogenesis that must be considered. Various laboratory studies on animals and certain human data are suggestive that tumour formation requires at least two discrete events to take place in response to a carcinogen according to the apoptotic model of carcinogenesis. The first involves an elevation of apoptosis in a particular tissue due to a genetic predisposition, stress, or mutation. The second confers resistance to apoptosis in that same tissue resulting in the formation of an abnormal growth due to a dysregulation of cell number homeostasis. Furthermore, there is preliminary evidence to suggest that both these events may be reversible when treated with a selective apoptotic agent and, hence, they may be either genetic or epigenetic in nature.    

Chanda Siddoo-Atwal, completed her B.Sc. in Biochemistry from the University of London. Her Ph.D. was taken in Applied Sciences from Simon Fraser University in Burnaby (her research conducted at the BC Cancer Research Centre) and she did a Post-doctoral fellowship in the Biochemistry Department at the Medical College of Wisconsin. Cancer is her subject of specialization and has focussed mainly on mechanisms of carcinogenesis in various models, especially radiation-induced cancers. She is the President and Primary Biochemist of Moondust Cosmetics Ltd. (moondustcosmetics.com) and her research includes the formulation of a novel sunscreen to combat apoptotic sunburn that has been associated with skin cancer. She has authored books on cancer, contributed chapters to textbooks by various international publishers including Springer, and co-authored clinical oncology medical texts. A Facebook page presents her research in a popular way to the public (www.facebook.com/DrMoondust/).