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Folks, I cannot find any evidence of a conspiracy to prevent development of 3-bromopyruvate as a cancer treatment. Pogofrog brings up many recent papers about ongoing research. It's in the pre-clinical phases now. It will take a while for it to get to human testing.
Clinical trials requires commitment from one of a handful of well established pharma companies.
Has anyone read the current issue of Time magazine? The cover story is "How to Cure Cancer." The article discusses the need for a more collaborative approach to cancer treatment.
"As if the non-small-cell lung cancer that had defied conventional therapies had not been enough, the tumors in and around Tom Stanback's lungs grew so large that he was having difficulty swallowing and breathing. Unwilling to go quietly, Stanback actively sought out clinical trials (surprisingly, most patients don't) in search of anything that might extend his life. One of them, at Johns Hopkins in Baltimore, is focused on studying the enzymatic on/off switches that sit atop the underlying genome and regulate whether and how loudly those genes will be expressed. This includes the mutated genes that crank out cancer cells. While science can't do much to change the genome, epigenetic functions are manipulated all the time--sometimes inadvertently, by exposure to environmental chemicals, say; other times cleverly, by drugs. Stanback, a 62-year-old, 40-year former smoker, was involved in a trial to see if a new epigenetic drug could shrink his tumors.
In his case, the answer was no, not quite. But the leaders of the cross-disciplinary, cross-institutional research team behind the work (one of nine, soon to be 10, main teams backed by SU2C) weren't finished. They postulated that even if the epigenetic manipulation alone didn't knock out the cancer, it had a priming effect, improving the likelihood that other treatments administered later would work. That's exactly what happened when Stanback returned home for a round of radiation therapy at Memorial Sloan-Kettering Cancer Center in New York City and joined a second clinical trial. His tumors have shrunk markedly in the past year and a half and were not visible on a recent CT scan. "The drug nudges the T cells to being alive and active," he says. "I'm alive. I'm healthier than I've ever been." Even better, a few other patients in the study have enjoyed what appears to be complete remission. The team behind these victories is led by Dr. Stephen Baylin, an oncologist at Johns Hopkins, and Dr. Peter Jones, a biochemist and molecular biologist at the University of Southern California. They ride herd on a diverse group of experts--geneticists, pathologists, biostatisticians, biochemists, informaticists, oncologists, surgeons, nurses, technicians and specialists who normally wouldn't have been working as an ensemble. The team was awarded its grant in May 2009 and within the year was able to extend the epigenetic clinical trial that enrolled Stanback and launch new ones. That is light speed in modern research--the lab to clinic cycle in cancer is typically a decade.
This kind of institutional transformation is not easy, but it's the only way to take advantage of the dazzling scientific and technological advances that have taken place in just the past three years--advances in bioengineering, nanotechnology, drug compounds and data gathering, including protein data, splicing data and mutation data, all of which is being hoisted into view by ever cheaper computational muscle. Sequencing the first human genome took more than a decade and $2.7 billion. Today sequencing can be done for a few thousand bucks in a few hours." The Conspiracy To End Cancer - TIME
There is no conspiracy theory for hiding cancer therapies. Could you find a specific grain of sand in an entire sandbox? No? Well that's what trying to detect and find cancer is like. Not only is it incredible difficult to detect very early, you have to specifically target a cancer cell without harming all of the normal cells. That's only the beginning. Let's say you have a population of cancer cells within your body and you give a chemo drug to kill them. Many times there are some cancer cells left over that are resistant to the therapy. Cancer simply comes back in a chemo resistant fashion because you selectively chose a resistant population--in essence it is like speeding up evolution, just like you do to create antibiotic resistant bacteria. Thirdly, it's not that scientists are trying to hide cures for cancer, it's simply the fact that much of pharmaceutical science and biology is done wrongly. Pharmaceutical sciences and medicinal chemistry effort evolved from phenotype approaches toward developing a new drug, to more targeted based approaches. The idea sounds very plausible--study a specific target with a known effect, manipulate that target with drug X, then there should be the observed effect. This approach to drug development has proven however to be a colossal failure IMO. Targeted based science has its uses, but in the grand scheme of things, it is almost never true. The cell is a beautiful and insanely complex piece of machinery, often times targeted based approaches to drug development fail to understand that even if you manipulate a target Y, the cell has all sorts of other pathways to compensate for knocking out target Y's metabolic or signaling pathways or all sorts of feedback mechanisms to shut down signaling further downstream if Y is being turned on with drug X. Targeted based science has led to high profile failure one after the other because humans simply aren't smart enough yet to understand the complexities of the cell. Targeted based approaches for drug development get all the attention because it sounds plausible and academic. Chemists or biochemists can easily design a drug or biologic against a single target through rational design and molecular biologists can easy study the target. That's not the way life works however. Ever since target based pharmaceutical science took over, the success rate of the pharmaceutical industry has declined. There used to be a higher rate of success for less money when new drugs (and there are plenty of them) were discovered using a phenotypic approach. The idea behind a phenotypic approach is simple--throw a whole slew of potential new chemical entities into a batch of cells and look for an observed effect. If you see something happening that you want, take the compound and develop it. You don't have to explain how it works, all that matters is that it works. People are surprised to learn that the FDA does NOT require an explanation for mechanism of action for a new drug. All a drug has to do is do what you say it does, that's it. This approach used to be wildly successful, why did we abandon it? Many drugs often work because later on it is discovered that they affect multiple different pathways and mechanisms---and that's exactly what is required to treat cancer. Chemists are resistant to the phenotypic approach because how do they design a molecule against an unknown target or targets? Biologists get up in arms over this approach because they absolutely feel the need to explain a mechanism of action to justify their jobs. The phenotypic approach, however, realizes that nature and life is much more powerful than our crappy models that show a few signaling cascades with some arrows pointing around to downstream targets. A much more holistic approach with drug design and development is needed to developing new cancer drugs. Drug science needs a sweeping change in culture and a return to methodologies that were used back in the old days that were also very successful.
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