by Sayer Ji
A Failed War On Cancer
Ever since Richard Nixon officially declared a war on cancer in 1971 through the signing of the National Cancer Act,[i] over a hundred billion dollars of taxpayer money has been spent on research and drug development in an attempt to eradicate the disease, with trillions more spent by the cancer patients themselves, but with disappointing results.
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Even after four decades of waging full-scale “conventional” (surgery and chemo) and “nuclear” (radiotherapy) war against cancer, one in every four Americans will be diagnosed with the disease within their lifetimes – and this number is projected to grow – unabated — not unlike the process of cancer itself.
Could this colossal failure reflect how profoundly misunderstood the condition is, and misguided are our attempts to prevent and treat it?
The Question That Must Be Answered Anew: What Is Cancer?
Perhaps we need to return back to the fundamental question of ‘What Is Cancer’? After all, until we find an accurate answer to this question, all attempts to ‘prevent’ and ‘treat’ a disease we do not understand are doomed to fail.
For the past half century, the “Mutational Theory” has provided the prevailing explanation for the cause of cancer, where, as the story goes, accumulated mutations within our cells lead a few susceptible ones to “go berserk,” their “insane” and “violent” behavior a result of multiple destructive events to the intelligent code within the cell (DNA) that normally keep them acting in a ‘civilized’ manner relative to the larger multicellular community as a whole (i.e. the body). In this view, these rogue cells replicate incessantly and form a tumor which spreads outward in a cancerous manner (cancer = Greek for “crab”), in many ways simulating the characteristics of an infectious process within the host, until the growths obstruct vital processes, resulting in morbidity and death.
According to this theory, which was heavily influenced by the Darwinian theory of evolution and is sometimes called “Internal Darwinism,” what drives the evolution of the healthy cells into cancerous ones is a process very similar to natural selection, i.e. random mutations beneficial to the survival and reproduction of cancerous cells in a tumor are naturally selected for and conserved, driving them towards malignancy. Damage to the DNA can occur either through inheriting defective DNA sequences (“bad genes” in the family) or exposures to DNA-damaging chemicals (e.g. tobacco) or radiation.
While this view has some explanative value, it can also be quite misleading. For instance, a fundamental tenet of evolution is that random mutations are almost always harmful, resulting in immediate cell death. Cancer cells, however, seem to get quite ‘lucky’ because they appear to thrive on them. Rather than dying like normal cells when faced with random mutations, they exhibit the exact opposite response: they become immortalized, incapable of undergoing the programmed cell death required of healthy cells.
Is randomness and chaos, then, really at the root of the transformation of healthy cells into cancer?
Tumors, after all, express highly organized behaviors, seemingly impossible to induce through strictly random forces such as mutation…
A collection of cancer cells (tumors), for instance, are capable of building their own blood supply (angiogenesis), are able to defend themselves by silencing cancer-suppression genes and activating tumor-promoter genes, secreting corrosive enzymes to move freely throughout the body, alter their metabolism to live in low oxygen, high sugar and acidic environments, and know how to remove their own surface-receptor proteins to escape detection by white blood cells. Could these complex behaviors really be a result of random mutations? And is it possible that random mutations could result in the formation of the same “lucky” set of genetic properties, each and every time a new cancer forms in a human?
Random mutations, no doubt, play a major role in the initiation and promotion of cancer, but are not alone sufficient for a complete explanation. One group of scientists, in fact, have offered a much more compelling explanation. They view multiple mutations causing an unmasking of an ancient survival program within the cell….
tree of life
Cancer as An Ancient Survival Program Unmasked
A brilliant new theory, introduced by Arizona State University scientist, Paul Davies, and Australian National University scientist, Charles Lineweaver, sheds much needed light on the true nature of cancer. According to Davies:
“Cancer is not a random bunch of selfish rogue cells behaving badly, but a highly-efficient pre-programmed response to stress, honed by a long period of evolution.”
In their seminal paper, titled “Cancer tumors as Metazoa 1.0: tapping genes of ancient ancestors,” Davies and Lineweaver propose that cancer is an evolutionary throw-back, drawing from a genetic ‘tool-kit’ at least a billion years old, and which still lies buried – normally dormant – deep within the genome of our cells. Davies calls this subterranean genetic layer Metazoa 1.0, and it contains pathways and programs that were once indispensable for our ancient cellular predecessors and their early proto-communities to survive in a radically different environment.
Without the highly differentiated cells and specialized organs of higher multicellular/animal life (Metazoa 2.0), cells with the genetics of Metazoa 1.0 would have favored traits that enabled them to survive direct contact with what was a much different and harsher (to us) environment.
For example, 1 billion years ago atmospheric oxygen was exceptionally low, since photosynthesis has not yet evolved to produce an abundant supply. This means that cellular life at that time would have had to learn to thrive in a low or no oxygen environment, which is exactly what cancer cells do, using aerobic glycolysis for energy instead of oxidative phosphorylation.
Davies and Lineweaver summarize their view as follows
“The genes of cellular cooperation that evolved with multicellularity [animal life] about a billion years ago are the same genes that malfunction to cause cancer. We hypothesize that cancer is an atavistic condition that occurs when genetic or epigenetic malfunction unlocks an ancient ‘toolkit’ of pre-existing adaptations, re-establishing the dominance of an earlier layer of genes that controlled loose-knit colonies of only partially differentiated cells, similar to tumors. The existence of such a toolkit implies that the progress of the neoplasm [cancer] in the host organism differs distinctively from normal Darwinian evolution.”
Instead of viewing the hallmark trait of cancer, namely, incessant proliferation, as a newly evolved trait spurned by random mutations, it would be considered the default state of the cell, having been developed a billion years ago when ‘not dying’ would be the first priority. Remember, this ancestral assemblage of cells would not have had the differentiation of cell type and specialization of tissue associated with higher animals, i.e. skin, hair, claws, etc., with which to protect themselves against the environment.