Three years before James Watson, 84, shared the Nobel Prize in medicine for his role in discovering the double helix, he taught a course on cancer at Harvard University. Currently he is the Oliver Grace Professor of Cancer Research at Cold Spring Harbor Laboratory, New York. One would imagine the man might know a thing or two about the disease.

Yet, the New England Journal of Medicine refused the Nobel laureate's recent paper, which represents the culmination of decades of thinking about the subject, saying "we only publish facts not ideas."

Are James Watson's ideas (not facts) ahead of his time or simply unsubstantiated?

One day after an exhaustive national report on cancer describes slow progress against the disease, Watson's paper appeared in the journal Open Biology. Cancer mortality, despite decades of research, has remained stubbornly high with the exception of blood cancers and he is asking one simple question: "Why?"

"The public is constantly being fed 'we are making all these advances' but we are not getting very far," said Watson.

In his paper, he argues that chemotherapy kills cancer cells by causing reactive oxygen to form but its effect diminishes. The tumor cells fight back by releasing antioxidants to block the damage. "If you are going to cure it then you are going to have to get rid of the antioxidants," he said.

He pointed out that exercise triggers the release of reactive oxygen. Yet we know that regular exercise has been shown to reduce the risk of diabetes and can improve memory in Alzheimer's patients. Regular exercise has also been associated with reduced cancer risk. "What it means to me, oxygen species are doing something necessary where if you don't have them you get diabetes," he said.

Further, Watson suggests that taking antioxidants may therefore be working against these disease-blocking processes. Meanwhile, the US spends up to $40 billion a year on antioxidant products.

Almost none of the new drugs, 'personalized' to target genetic anomalies and based on DNA sequencing, cure cancer. "These new therapies work for just a few months," Watson told Reuters. Yet these drugs consistently fail because, if a drug blocks one biochemical pathway to growth and proliferation, the cancer cells activate a different, equally effective pathway. And this is the reason Watson seeks to target features that all cancer cells have in common.

His favored target is a protein in cells called Myc, which controls more than 1,000 other molecules inside cells, including many involved in cancer. Although studies suggests that cancer cells might self-destruct if Myc is turned off, there is no real money funding such ideas. Many more research dollars are invested in "personalized medicine" that targets a patient's specific cancer-causing mutation.