March 31, 2013
Debunking the Cancer Drug Conspiracy Myth by Craig Dees
There is a widespread belief in a conspiracy to hide cancer cures, or prevent them from being discovered. Anyone who works in the field knows this is not true.
I often hear theories about why there is currently no cure for cancer. These well-meaning but occasionally off-the-wall hypotheses come from people in all walks of life, from the manager of a billion dollar fund to a nuclear physicist, not to mention the plumber and the mailman. Once someone learns that I work in the field of cancer research, they feel the need to test their beliefs on someone they perceive to be a cancer “expert.”
My favorite theory came from a nuclear physicist, who called me one evening shortly after midnight to share his insights. While sleepily listening to his convoluted explanation of cancer involving strong and weak intranuclear forces at the atomic level, I began laughing. “Cancer isn’t all that mysterious,” I said. “It’s just a difficult problem to solve for a number of reasons. The causes of cancer at the molecular level do not need obtuse quantum mechanical explanations.”
The physicist seemed genuinely surprised by my assertion that cancer isn’t so inexplicable and listened to my standard lecture on the known causes of cancer and why this group of diseases proves so difficult to treat. I was amused to find myself educating such a bright individual – a “hard science” type – about the complexity of biology and biochemistry, what we call life. It is debatable whether the physicist’s epiphany was worth the loss of sleep, but to change people’s misperceptions on this subject is generally worthwhile.
However, the most common cancer “theory” involves some sort of conspiracy, which goes something like this: large companies, doctors, hospitals, and the entire healthcare industry, including our academic institutions, are colluding to prevent a cancer cure from reaching the public, mostly to protect profits from current treatments.
This theory is based on the common knowledge that today’s cancer treatments are, for the most part, highly toxic, minimally if at all effective, and generally very expensive. Many cancer conspiracy theorists are convinced the “cure” has already been found but has been hidden, which makes the alleged conspirators all the more evil. The cancer conspiracy theory, in all its many forms, helps mythologize this disease and takes people’s minds off the facts.
Why It Took So Long to Find the Anti-Cancer Antibiotic
In debunking the cancer conspiracy theory, I begin with practical considerations before launching into the “hard science.” A cancer cure would be impossible to keep secret, or secure for that matter. A secret that big, that earth-shattering, would tempt the most dedicated employee over leaking it, and not a few others to steal it if that were possible.
When I left my postdoctoral fellowship and joined a mid-sized pharmaceutical and biologics company as research director, it did not take long for me to learn who knew all the secrets in the company (hint: it was not me, or anyone at my management level).
Moreover, it would be difficult for any individual to give up the lasting fame and adulation of being the “discoverer” of a cancer cure, not to mention the potential financial gain. It is hard to conceive of an individual with so selfless an ego.
Finally, the possessor of a cancer cure would make more money commercializing it than they could ever conceive of earning through their current cancer treatment portfolio. A genuine cure for cancer would command the highest price of any medical treatment, and have a potential market of tens of millions of stricken individuals in the developing world.
So the conspiracy theory of cancer can be debunked summarily based on the foibles of human nature and the profit motive.
Why Cancer is so Difficult to Cure
Cancer is not one disease, but many diseases with multiple causes. Every type of overt cancer, such as breast cancer, is in reality different diseases. Cancer occurs in many different tissue types with differing biochemistry, under the control of different genes, and in multiple different organs with their own unique physiology. The anatomical locations of tumors compound the problem of addressing the multiplicity of “diseases” that are lumped together under the description of “cancer.”
Secondly, cancer has many different etiologies that may include infection by oncogenic viruses, exposure to toxic materials or radiation, normal aging, failure of anticancer defenses, and inborn errors in our genetic blueprint. It is obvious that combining etiology with anatomy and genetics adds up to a perplexing, almost insurmountable set of factors to consider with respect to treatment.
An alien invader like bacteria or viruses entering the body doesn’t cause cancer. For the most part cancer arises from within, albeit sometimes under the influence of exogenous factors. That is to say that tumors arise from the patient’s own tissue, so killing the diseased cells without affecting normal tissues becomes close to impossible. An analogy might be asking a major league baseball player to kill a mosquito that has landed on your face by taking a full swing with his bat. He’d kill the mosquito (perhaps), but you would wind up with a pretty serious headache. The same sort of problem occurs with cancer biochemistry, which seeks to find unique targets on cancer cells to attack. The targets are almost never unique to cancer cells however, so pounding them with chemotherapy will likely kill healthy cells as well. In rare situations where the targets are unique, or thought to be, finding a drug that only acts on that target is one of the most difficult tasks in molecular medicine.
It is for these reasons that medical science has not uncovered a broad-spectrum “antibiotic-like” treatment for cancer. Unique biochemical pathways in bacteria, for example for folate, do not exist in humans. Antibiotics have side effects, some quite severe, but those are incidental to their activity, not built-in by virtue of cross-reactivity with healthy human cells.
So to date, most cancer treatments are horribly toxic to normal cells, and some cause cancer themselves. It has been estimated that the majority of current cancer drugs and radiation are on the order of 1.1-1.2 times more toxic to cancer cells than to normal, healthy cells. Therefore, the poor long-term efficacy of chemotherapy and radiation, and their plethora of side effects, should come as no surprise. An almost universal side effect of cancer treatments is an increased likelihood for developing new cancers later in life, if one survives the initial treatment.
The other hurdle presented in developing an antibiotic-like, broad-spectrum cancer treatment is that its target should be present in at least significant groups of cancers, if not all tumors. Not only must the target be unique to cancer cells, it has to be an “Achilles heel.”
The Cancer “Antibiotic”
Emerging cancer treatments are based on narrow specificity to cancer targets. Since the “attack” on cancer cells is more specific, safety improves, as should efficacy. One of these targeted therapies is Reolysin™, a modified reovirus with very high specificity for cancer cells. Also under development are specific inhibitors of protein kinases elevated in cancer cells. However, since kinase inhibitors tend to target very narrow classes of proteins, they are unlikely to perform as an “antibiotic” against cancer.
Recently it has been shown that cancer cells appear to have a common weakness which when attacked can cause the destruction of cancer cells while sparing normal tissues. The Achilles heel of cancer cells is the subcellular structures called lysosomes. Lysosomes can be visualized as little bags of degradative enzymes that can destroy large molecules that living cells are constructed of and use as “food” and building materials. Within the lysosomes are a wide variety of these enzymes that function under acidic conditions (e.g. acid hydrolases). Cancer cells that grow at an abnormal rate and require large amounts of “fuel” are highly dependent on acid hydolases within the lysosomes. Therefore, attack on these “bags” of enzymes is the downfall of cancer cells. When the lysosomes are damaged or ruptured, the enzymes are released into the interior of the cell and kill the cell by “digesting” the cancer cell components.
Recently, a common red dye, PV-10, was shown under the right conditions to localize specifically within tumor tissue. Once inside, PV-10 partitions into the diseased cellular membranes while staying out of normal cells. When PV-10 encounters the acid environment of the lysosome, it causes this organelle to leak or rupture, which releases the acidic degradative enzymes into the interior of the cancer cells. PV-10 functionally causes the cancer cell to destroy itself.
PV-10 attacks cancer cells not only through highly specific targeting, it hits them in a critical spot that results in their immediate self-destruction. Further, this critical spot appears common to all cancer cells. Table 1 [no table available] shows that PV-10 kills every cancer cell tested to date including cancer cells (e.g., lung cancer cells) that have strong resistance to chemotherapy agents. Clinical trials now in Phase II testing have also shown that PV-10 can resolve melanomas that were refractory to radiation or chemotherapy treatment.
Fortuitously, PV-10 overcomes the barriers at the anatomical, physiologic, and molecular levels that inhibited the finding of an “antibiotic” for cancer. It specifically attacks a critical target seemingly common to all cancer cells while leaving normal cells intact. Early stage clinical trials testing for efficacy and safety in human breast cancer and melanoma support this assertion. As more types of cancers are treated, judgment that this is the closest the medical community has come to an antibiotic for cancer will be confirmed.