January 10, 2013
Legendary DNA Discoverer James Watson Criticizes Current Cancer Research And Suggests A Novel New Direction
Jedidiah Becker for redOrbit.com — Your Universe Online
Just one day after a comprehensive national report was released essentially stating that the U.S. is dragging its feet in the fight against cancer, one of the twentieth century´s most renowned scientists has launched a scathing critique against the status quo in current cancer research.
In a paper published Tuesday in the prestigious journal Open Biology, Professor James Watson — the American scientist who in 1953 co-discovered the double-helix structure of DNA that revolutionized the study of biology — criticized what he sees as the misguided and exorbitantly expensive search for cancer cures in the form of antioxidants and cancer-specific genetic mutations.
Though inconspicuously titled “Oxidants, antioxidants and the current incurability of metastatic cancers,” Watson has called his iconoclastic new paper “among my most important work since the double helix.” The report is the culmination of several months of work and over a half century of cancer research. Shortly before receiving the Nobel Prize in medicine for his role in uncovering the structure of DNA, Watson began teaching courses in cancer at Harvard University, an experience that sparked a career-altering interest in the relationship between genetics and cancer.
The 84-year-old researcher´s strong words have ruffled the feathers of the 'cancer research establishment', and with good reason. For instance, the intrepid researcher stated that a $100 million federally sponsored project that went looking for specific genetic changes behind nine types of cancer is "not likely to produce the truly breakthrough drugs that we now so desperately need." And of the current craze for antioxidants in everything from ordinary nuts to exotic berries, he says that "the time has come to seriously ask whether antioxidant use much more likely causes than prevents cancer."
Although no doubt unwelcomed in many quarters of the research community, Watson´s report comes at a time when even the most ardent devotees of the cancer research establishments are growing increasingly disheartened over the meager progress being made by current approaches to cancer treatment. As other scientists have pointed out, even the modest decline in cancer rates in recent years are due mostly to the fact that fewer people are smoking in the U.S. rather than any major advances in cancer treatment.
A number of Watson´s disgruntled colleagues have already begun to rally behind him in recognition of the disappointing results of the past several decades of cancer research. And the problem, they believe, has been the narrow focus on finding individual genetic signatures for each individual type of cancer and then attempting to base cures on these.
"The great hope of the modern targeted approach was that with DNA sequencing we would be able to find what specific genes, when mutated, caused each cancer," molecular biologist Mark Ptashne of Memorial Sloan-Kettering Cancer Center in New York told Reuters.
After they found these specific mutated genes, researchers believed that they simply had to create a drug that would block their activity and thus hinder the development of cancer cells. However, they found that this simple solution didn´t work quite as well as they had expected.
As Watson explained, the effects of most of these new therapies only lasted a few months. That´s because cancer cells are clever. If a drug blocks one of their biochemical pathways for growth and proliferation, they simply activate a different pathway that works just as well, leading to a virtually endless cat-and-mouse game of ever new drugs that lead to ever new pathways.
And for this reason, Watson has proposed that cancer researchers should start to consider a broader, more unified approach to treatment by focusing on characteristics that all cancer cells have in common.
ANTIOXIDANTS OR ANTI-ANTIOXIDANTS?
One of those features common to different types of cancer is oxygen radicals, those deviant little oxygen molecules that are so destructive of vital cellular components like DNA. In fact, this is exactly why antioxidants have been almost universally accepted as anti-cancer agents, since the help cells to remove those vicious, cancer-causing oxygen radicals.
But Watson and others suspect that this schemata gets considerably more complicated once someone already has active cancer cells in their body. For instance, since cancer treatments like radiation and chemotherapy actually use oxygen radicals to destroy cancer cells, a cancer patient who is consuming high levels of antioxidants may actually be counteracting the intended effects of their therapy.
"Everyone thought antioxidants were great," Watson told Reuters in a rare interview. "But I'm saying they can prevent us from killing cancer cells." He added that this theory would help to explain "why cancers that become resistant to chemotherapeutic control become equally resistant to radiotherapy." The logical feature that they have in common would thus be their reliance on a cell-killing mechanism based on oxygen radicals.
And there is already much existing research that corroborates this view. Several studies have already demonstrated that taking antioxidants like vitamin E can actually increase the risk of developing cancer, while pharmaceuticals and foods that block antioxidants — or "anti-antioxidants" — could potentially enhance the effects of existing cancer medications.
Another little understood yet promising target for future cancer research is a protein known as Myc, says Watson. The Myc protein regulates the activity of over a thousand other biomolecules, many of which are known to be involved in the growth of cancer cells. Some existing research indicates that shutting down the genes that code for Myc could induce apoptosis — or self destruction — in cancer cells.
"The notion that targeting Myc will cure cancer has been around for a long time," cancer researcher Hans-Guido Wendel explained. "Blocking production of Myc is an interesting line of investigation. I think there's promise in that."
Unfortunately, little research and few funds have been devoted to the study of Myc and, as such, its role in cancer activity remains largely a mystery. The reason, Watson explained, is that the majority of research resources in recent years have been poured into those specific, cancer-causing mutations that have proven to be a dead-end.
In short, Watson wrote, the greatest challenge to finding a cure for cancer right now may be what he describes as "the inherently conservative nature of today's cancer research establishments." And unless this changes, "curing cancer will always be 10 or 20 years away."