Is Cancer Really What We Think It Is?

The time has come to shift the conceptual framework away from the idea that cancer is something bad that happens to the body, to something the body does in order to survive vis-à-vis an increasingly toxic and nutrient-deprived environment. Only then we will begin to unravel the mystery behind the colossal failure of the conventional medical system and why the ‘war against cancer’ will only be successful when we embrace our enemy with greater compassion and understanding, instead of blasting it (and ourselves) into oblivion.

For the past half century, the “Mutational Theory” has provided the prevailing explanation for the cause of most cancers, where, as the story goes, accumulated mutations to the DNA within the nucleus of our cells lead some to “go berserk,” their “insane” behavior a result of multiple destructive events to the intelligent code within the cell (DNA) that keep them acting in a ‘civilized’ manner relative to the larger bodily whole. In this view, these rogue cells clone themselves inordinately, spreading outward in a characteristically cancerous manner (cancer = Greek for “crab”), not unlike the characteristics of an infectious process within the host, eventually obstructing vital processes, resulting in morbidity and death. One paper summarizes this view as follows:

Cancer is derived from a single somatic cell that has accumulated multiple DNA mutations.

The default state of cell proliferation in metazoan (animal life) is quiescence

Cancer is a disease of cell proliferation caused by mutations in genes that control proliferation and the cell cycle.

The problem with this view is that over 100 cancer-promoting genes (oncogenes) have already been discovered nested deep within our genome – hardly a byproduct of chance mutation within individual cells. Proliferation may very well be the default state of all cells, and much of the behavior of healthy, well-differentiated cells in higher animals is a regulatory overlay (suppressing ancient genes) on top of a far more ancient program which becomes unmasked during carcinogenesis. Cancer, therefore, may be an “evolutionary throwback” to a time before we became multicellular organisms and a more rudimentary type of cooperation between cells existed (i.e. tumor) which enabled them to survive in a dramatically different, and perhaps far harsher environment.

Cancer cells are, in fact, surprisingly well-coordinated for cells that are supposed to be the result of strictly random mutation. They are capable of building their own blood supply (angiogenesis), are able to defend themselves by silencing cancer-suppression genes, secreting corrosive enzymes to move freely throughout the body, alter their metabolism to live in low oxygen and acidic environments, and know how to remove their own surface-receptor proteins to escape detection by white blood cells. These complex behaviors, which involve the type of cooperation between cells which is the very definition of Metazoan behavior (multicellularity, i.e. animal life), call into question the view that mutation within ‘rogue cells’ is the primary cause of cancer. What if cancer was the unmasking of a more ancient survival program within the cell, activated as a last ditch effort to survive an increasingly hostile bodily environment, saturated through with carcinogenic and immunotoxic agents?

This new view may shed light on why chemotherapy and radiotherapy have such dismal track records. Tumors often contain a mixture of both highly malignant and benign cell populations. The treatment may destroy the benign cells, releasing the “chemoresistant” and “radioresistant” populations to wreak havoc on the body of the patient. Often treatment failure is attributed to the “treatment resistant” nature of the cancer, when it is a direct result of the inherent toxicity and lack of effectiveness of the therapy being used. In the same way that antibiotics like methicilin have spawned “super germs” like MRSA (Methicillin-Resistant Staphylococcus Aureus), conventional cancer treatment is often responsible for generating greater resistance and subsequent malignancy within certain tumor populations.