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thermograms are changing the way cancer cells are being detected

7/12/2013

mammograms are considered by some in the medical community to be so dangerous as to even promote the development of cancer, due to the heavy amounts of ionizing radiation mammograms use. A single test can expose you to the same amount of radiation as 1,000 chest X-rays—that’s nearly the equivalent of three chest X-rays per day for a year, an amount if seen from that perspective certainly gives one pause.

Indeed, according to top cancer expert Dr. Samuel Epstein, “The premenopausal breast is highly sensitive to radiation, each 1 rad exposure increasing breast cancer risk by about 1 percent, with a cumulative 10 percent increased risk for each breast over a decade’s screening.”

More importantly, mammograms an almost negligible ability to prevent cancer deaths, according to the New England Journal of Medicine. A September 2010 study found that mammograms only reduced cancer death rates by 4 deaths for every 1,000 women who received annual testing for 10 years, which means that only 1 breast cancer death was averted per 2,500 women.

What most doctors won’t tell you, however, is there’s a safer, far more accurate alternative. The technology, called thermography, does not rely on radiation, but instead scans for heat levels in the body to detect inflammation. It’s so safe in fact that it poses no risks even to pregnant and nursing women. Cancerous and pre-cancerous cells are normally characterized with inflammation first before any growth visible on by mammography, and so thermograms are able to detect cancer years earlier than any other method.

A study conducted on women who received regular thermogram screenings over a ten year period found that an abnormal thermogram scan was ten times more reliable as a risk measure for breast cancer than family medical history. In addition, it also found that thermography was the first detector of potential cancer for 60% of the women who developed it.... read more
Also see http://en.wikipedia.org/wiki/Thermography

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Scientists Cure Cancer? Yet Nothing Has Changed

12/3/2012

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Posted on 27/01/2012 by Gekko

Researchers at the University of Alberta, in Edmonton, Canada cured cancer last week, yet there is a little ripple in the news or in TV.
The cure is a simple technique using very basic drug. The method employs dichloroacetate, which is currently used to treat metabolic disorders. So, there is no concern of side effects or about their long term effects.

This drug doesn't require a patent, so anyone can employ it widely and cheaply, compared to the costly cancer drugs produced by major pharmaceutical companies today.

Canadian Scientists tested this dichloroacetate (DCA) on human’s cells; it killed lung, breast and brain cancer cells and left the healthy cells alone. It was tested on Rats inflicted with severe tumors; their cells shrank when they were fed with water supplemented with DCA. The drug is widely available and the technique is easy to use, why the major drug companies are not involved? Or the Media interested in this find?In human bodies there is a natural cancer fighting human cell, the mitochondria, but they need to be triggered to be effective. Scientists used to think that these mitochondria cellswere damaged and thus ineffective against cancer. So they used to focus on glycolysis, which is less effective in curing cancer and more wasteful. The drug manufacturers focused on this glycolysis method to fight cancer. This DCA on the other hand doesn’t rely on glycolysis instead on mitochondria; it triggers the mitochondria which in turn fights thecancer cells.

The side effect of this is it also reactivates a process called apoptosis. You see, mitochondria contain an all-too-important self-destruct button that can’t be pressed in cancer cells. Without it, tumors grow larger as cells refuse to be extinguished. Fully functioning mitochondria, thanks to DCA, can once again die.

With glycolysis turned off, the body produces less lactic acid, so the bad tissue aroundcancer cells doesn’t break down and seed new tumors.

Pharmaceutical companies are not investing in this research because DCA method cannot be patented, without a patent they can’t make money, like they are doing now with their AIDS Patent. Since the pharmaceutical companies won’t develop this, the article says otherindependent laboratories should start producing this drug and do more research to confirm all the above findings and produce drugs. All the groundwork can be done in collaboration with the Universities, who will be glad to assist in such research and can develop an effective drug for curing cancer.

You can access the original research for this cancer here.

This article wants to raise awareness for this study, hope some independent companies and small startup will pick up this idea and produce these drugs, because the big companies won’t touch it for a long time.

Andy Coghlan, New Scientist:

So, we hear news of a miraculous treatment for cancer. Disappointingly, the story is an old one which has somehow resurfaced on the blogosphere. When we originally published the story four years ago, it created a frenzy on the internet which took us by surprise. Our story reported a new type of treatment that in animal experiments showed promise of potentially being able to tackle most types of human cancer. We often report developments in cancer research, but nothing had ever attracted such a wave of interest. The drug involved, a simple molecule called dichloro-acetate, or DCA, appeared to work by blocking the unusual, sugar-gobbling mechanism called glycolysis by which most cancer cells generate their energy, and so which potentially marks them out from healthy cells. Exposed to DCA, cancer cells stopped making energy from sugar and resumed making it the way healthy cells do, in chambers called mitochondria. This stopped cancer cells from growing and multiplying, and caused them to wither and die instead. What added to the intrigue was that DCA is such a cheap, simple molecule that no-one has ever patented it. Also, it was already being used to treat rare mitochondrial diseases. Within weeks, patients were trying to get their own supplies of DCA, and some entrepreneurs set up websites to sell it, that were subsequently declared illegal and closed down by the US Food and Drug Administration. So what happened after the frenzy died down? The answer is that it was finally tested in five patients with aggressive brain cancer by Evangelos Michelakis of the University of Alberta in Edmonton, Canada, who had conducted the original experiments in animals. The results, published last year in Science Translational Medicine, revealed that it probably extended the lives of four of the patients, while one other died. Most importantly, Michelakis demonstrated from brain scans and biopsies that DCA appeared to work as he had predicted, arresting the growth of cancer cells by switching them back to normal energy production in mitochondria. The experiments also showed that beneficial effects took a few months to kick in. Importantly, Michelakis said that despite the small trial, it would be impossible to tell whether DCA works or not until it is tested in a placebo-controlled trial. As far as we know, no further trials have been conducted, so the jury is still out on whether it may do any good. We reported the new results in New Scientist and included news of other teams around the world developing treatments targeting glycolysis. Some other treatments that disrupt energy metabolism, such as the drug metformin taken by diabetics, were also showing signs of activity against cancer, for example. So for now, we are a little bit wiser about how DCA might work, but until someone does a much larger, well-organised trial, it would be unwise to assume that taking it will be safe or do any good. The more encouraging news is that other teams are now investigating the scope for targeting glycolysis, and although it could be a long haul to demonstrate whether any work, it does provide another avenue of attack against a disease which continues to push medicine to its limits. Any readers wanting to find out more about DCA may find this blog useful, posted by Cancer Research UK. There's also an excellent blog by National Geographic which goes into even more detail.

Potential cancer drug DCA tested in early trials
Posted on May 12, 2010 by Kat Arney

"Everything we wrote in the post and comments below stands – DCA is still only a ‘potential’ cancer treatment, and more research is needed to find out whether it’s safer or more effective than existing therapies " ~ Henry

The controversial drug DCA (dichloroacetate) is in the headlines again, after researchers in Canada carried out a small-scale clinical trial of the drug in five patients with advanced brain tumours.

Over the past year or two there have been several articles in the news and on the internet about DCA, which was claimed to be cheap, safe and “kill most cancers”.

Understandably this caused a great deal of interest, especially as DCA is an off-patent drug and appears to be non-toxic to humans (although it can cause significant side effects, as we’ll see later).

But before we jump to conclusions and hail DCA as a ‘wonder drug’, we need to look at the science behind the headlines.

What is DCA and how does it work?

All our cells need energy to grow and function, including cancer cells. Simply put, our cells usually generate energy by breaking down sugar (glucose). To do this, they use a process known as the Krebs cycle, which takes place in tiny structures within the cell called mitochondria (the ‘power stations’ of the cell).

But cancer cells bypass this cycle and produce energy using a simpler process, known asglycolysis, which takes place outside the mitochondria in the cell’s cytoplasm (the main part of the cell).

Mitochondria play a crucial role in cells. As well as generating energy for the cell, they can also trigger the cell to die if it is faulty – a process that helps stop cancers from forming in the first place. Because cancer cells seem to switch off their mitochondria, scientists think this is one way in which cancer cells are able to evade death and remain immortal.

DCA, or dichloroacetate, is a very simple chemical and is similar to some of the chemicals involved in the Krebs cycle. In 2007, researchers at the University of Alberta (led by Evangelos Michelakis) found that adding DCA to cancer cells grown in the lab kick-starts the Krebs cycle, turning the mitochondria back on again. This caused the cancer cells to stop multiplying and die. The team discovered that DCA didn’t affect healthy cells, because their mitochondria were functioning normally.

DCA has been tested as a treatment for children and adults with certain rare metabolic disorders. This means that, at the doses needed to treat these diseases at least, DCA has been through clinical trials aimed at assessing its safety. Based on their results, the researchers have proposed that DCA could also be useful in treating cancer.

To begin to investigate if this is indeed the case, Michelakis and his team started by carrying out experiments on cancer cells grown in the lab. The team also studied rats that had been injected with cancer cells. They found that DCA could slow the growth of the rats’ tumours, and reduce their size. This did not prove that the cancers were completely cured, or that DCA could prevent cancers from growing.

It is important to stress that DCA had not then been tested as a cancer treatment in humans, despite the implication in news headlines that it “kills most cancers”. There are many research papers produced by scientists around the world every year that reveal potential new treatments for cancer. But it is important that every discovery is carefully investigated to make sure that it is effective and safe for use in patients, and DCA is no exception.

The University of Alberta researchers received approval for a human cancer trial in September 2007, involving 50 patients. Now they have published the first results from five of those patients in the journal Science Translational Medicine.

The new trial

In this study, Michelakis and his team gave DCA to five patients with advanced glioblastoma, a type of brain tumour, in combination with surgery, radiotherapy and a drug called temozolomide. It’s important to point out that the aim of this study was not to find out whether DCA could treat glioblastoma, but to figure out the safest dose to use for cancer patients. We already know that the drug can be safely given to humans – although it can cause side effects – but this is the first time it has been tested in people with cancer.

The study shed light on the dose that could be given to patients without causing nerve problems or other serious side effects. Four patients were still alive after 18 months, and three showed some shrinkage of their tumour, but it is impossible to tell with such a small study whether this is longer than might be expected. And, given that they were also receiving other treatment, it’s hard to know if it was due to DCA at all.

As well as this small trial, the researchers also looked at the effect of DCA on tumour samples from 49 other glioblastoma patients. They found that DCA could switch mitochondria back on in the cancer cells, although – crucially – it’s still not clear exactly how it’s doing this.

Finally, the team looked at tumour samples taken from the five patients on the trial, both before and after treatment with DCA, and found that the drug was again helping to switch mitochondria on. They also discovered other differences in the cancer cells’ metabolism before and after treatment.

A key gap in this trial is that, as we’ve mentioned above, it’s not clear exactly how DCA is working. The researchers suggest that the drug may target cancer stem cells and prevent the growth of blood vessels into tumour, although they didn’t actually prove this.

Is it safe?

These results show that lower doses of DCA could, at least in theory, be given to cancer patients while avoiding some of the damaging side effects seen at higher doses. For example, a clinical trial of DCA for a childhood disease found that the drug caused significant side effects, affecting the nervous system. It is also known to be an environmental pollutant. And researchers have found that DCA can actually cause cancer in animals.

This is not necessarily a barrier to the use of DCA as a treatment for cancer – there are a number of powerful cancer drugs that are carcinogens themselves. And this is why we need to test them in clinical trials (as Michelakis and his team have begun to do here) to discover how they can be safely used to treat patients while minimising any harmful effects.

Why can’t we use it now?

It is understandable that people with cancer will want to try everything possible to help treat their disease. However, there is still no evidence – yet – to support the immediate use of DCA to treat cancer patients.

The trial in Canada is being conducted under stringent conditions both to ensure the validity of the results and to protect the participants from any unforeseen effects. Further clinical trials of DCA using more patients will help determine whether the treatment is more effective than the cancer therapies that are currently available.

There are reports that people are buying personal supplies of DCA from sources such as the internet. Cancer Research UK would strongly advise against this, as DCA still has not been shown to actually treat tumours successfully in patients. And it may be harmful when given to cancer patients without accurate dosing and medical supervision.

What will happen in the future?

It is clear that DCA is an intriguing drug – one of many currently being investigated by scientists around the world. It will be interesting to see the results of more extensive lab-based experiments and larger clinical trials of DCA. And cancer cell metabolism is certainly a productive area of research that we’re actively funding.

The fact that DCA is off-patent is no barrier to its development as a treatment for cancer. For example, Cancer Research UK has secured a licence for an off-patent drug called fenretinide, which could be used to treat rare childhood cancers. And there is certainly no “conspiracy” by pharmaceutical companies to prevent research into DCA – there is just not enough evidence at the moment to support its widespread use to treat patients.

While these results are intriguing, it is unlikely that this one compound represents “the cure” for cancer – and it is also unlikely that DCA is the “wonder drug” that the headlines portray. Cancer is a complex and multi-faceted disease, and it can be caused by a range of different faults within the cell. It is unlikely that any single drug could ever treat all forms of the disease.

There are many promising new treatments for cancer currently in development, funded by organisations across the globe – including Cancer Research UK.   If anything, these new results show why research is so important in bringing safe and effective treatments to people with cancer – they don’t provide definitive answers, but they support further investigations which may yield benefits for patients in the future.

Further reading: A more detailed analysis of the new research can be found at Respectful Insolence – DCA and cancer: Deja vu all over again

Metabolic modulation of glioblastoma with dichloroacetate.
Michelakis ED, Sutendra G, Dromparis P, Webster L, Haromy A, Niven E, Maguire C, Gammer TL, Mackey JR, Fulton D, Abdulkarim B, McMurtry MS, Petruk KC.SourceDepartment of Medicine, University of Alberta, Edmonton, Alberta, Canada. em2@ualberta.ca

Abstract Solid tumors, including the aggressive primary brain cancer glioblastoma multiforme, develop resistance to cell death, in part as a result of a switch from mitochondrial oxidative phosphorylation to cytoplasmic glycolysis. This metabolic remodeling is accompanied by mitochondrial hyperpolarization. We tested whether the small-molecule and orphan drug dichloroacetate (DCA) can reverse this cancer-specific metabolic and mitochondrial remodeling in glioblastoma. Freshly isolated glioblastomas from 49 patients showed mitochondrial hyperpolarization, which was rapidly reversed by DCA. In a separate experiment with five patients who had glioblastoma, we prospectively secured baseline and serial tumor tissue, developed patient-specific cell lines of glioblastoma and putative glioblastoma stem cells (CD133(+), nestin(+) cells), and treated each patient with oral DCA for up to 15 months. DCA depolarized mitochondria, increased mitochondrial reactive oxygen species, and induced apoptosis in GBM cells, as well as in putative GBM stem cells, both in vitro and in vivo. DCA therapy also inhibited the hypoxia-inducible factor-1alpha, promoted p53 activation, and suppressed angiogenesis both in vivo and in vitro. The dose-limiting toxicity was a dose-dependent, reversible peripheral neuropathy, and there was no hematologic, hepatic, renal, or cardiac toxicity. Indications of clinical efficacy were present at a dose that did not cause peripheral neuropathy and at serum concentrations of DCA sufficient to inhibit the target enzyme of DCA, pyruvate dehydrogenase kinase II, which was highly expressed in all glioblastomas. Metabolic modulation may be a viable therapeutic approach in the treatment of glioblastoma.
http://www.ncbi.nlm.nih.gov/pubmed/20463368

What is a Glioblastoma?

Brain tumors belong to a group of diverse tumors that affect the brain and spinal cord known ascentral nervous system neoplasms. A brain tumor is a mass of abnormal cells in the brain that have grown and multiplied in an uncontrolled fashion. Brain tumors that develop from various types of cells that make up the brain are called primary brain tumors. These types of brain tumors are usually localized (confined) to the brain itself and only rarely spread to other parts of the body. Metastatic brain tumors, also know as secondary brain tumors, originate from cancer cells in another part of the body (e.g., lung, breast) and spread to the brain through the bloodstream. The distinction between primary and secondary brain tumors is important from a clinical perspective because they are usually treated differently.

Approximately 50% of all primary brain tumors originate from specialized nerve cells in the brain called glial cells. Brain tumors that arise from glial cells are called gliomas. There are many different types of gliomas but the most common gliomas develop from glial cells called astrocytes. Primary brain tumors that develop from astrocytes are referred to as astrocytomas.

The World Health Organization (WHO) classifies astrocytomas into four distinct grades designated as Grade I, II, III, and IV (discussed in detail below) on the basis of how quickly the cells grow and spread and how the cells appear under a microscope. A glioblastoma, technically know as glioblastoma multiforme, is the fastest growing type of astrocytoma (Grade IV astrocytoma) that quickly spreads and invades nearby normal brain tissue and contains areas of dead cells (necrosis) in the center of the tumor.

Approximately 18,000 people in the United States are diagnosed each year with a malignant (cancerous) primary brain tumor. Glioblastoma multiforme (GM) is the most common type of primary malignant brain tumor in adults and accounts for about 50% to 60% of cases. Although GM can occur in all age groups, it is most commonly observed in adults 50 to 70 years in age. Less than 10% of childhood brain tumors are glioblastomas. Glioblastoma multiforme tends to occur more frequently in males than females by a ratio of about 3:2. According to the American Cancer Society, about 13,000 in the United States die each year from primary brain tumors.

http://www.glioblastoma-guidebook.com/2009/landinge.php?gid=OC009&?=a&assoc=Google&keyword=glioblastoma

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thermograms are changing the way cancer cells are being detected

Scientists Cure Cancer? Yet Nothing Has Changed

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