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Our founder’s perspective

Our Mission

Care Oncology co-founder Dr Robin Bannister is a chemist and pharmaceutical scientist with 35 years’ experience working with licensed medicines. Close personal experience of cancer first turned his attention to the possibility of ‘repurposing’ licensed medicines to help treat the disease. Almost a decade later, Care Oncology is thriving in both the USA and the UK. Here is Robin’s story – the motivation, and the scientific drive, behind a very personal mission.

The beginnings of an idea

I am always fascinated by how little we actually know about new medicines when they are brought to market. It’s only with the passage of time and after long periods of use in humans that we really begin to understand exactly what it is that our medicines can do. Everyone of course knows the tale of aspirin derived from components of willow bark chewed by the ancient Egyptians for pain relief and even now, 2000 years later, we are starting to investigate its use in cancer.

Good science takes time – but I believe it doesn’t have to take that long.

Put simply, my passion is to understand old drugs better. My great friend and co-founder Greg Stoloff shares my belief and my frustration that potentially very useful medicines are not available to patients, and that it still takes far too long to develop a new drug.

Going back to the example of aspirin; as early as the 1950s people noticed that the way aspirin worked could potentially help in cancer. Yet here we are over 60 years later – and as far as cancer is concerned, this drug is still on the shelf. Only now are full clinical studies underway, and it will still be another few years before results of these studies are fully understood.

Greg and I talked about this conundrum for a long time. But the spark that lit the fire finally came in 2011, when my wife’s breast cancer became metastatic. And like so many who have faced that numbing reality, and felt that raw frustration, I asked myself what could I do to help? Greg was the first to listen and we realized that with our combined skills, we could do something practical – and so the Care Oncology Clinic was born.

Our guiding principles

From the very beginning we had three guiding principles:

One: We knew we wanted to work with already licensed drugs, as anything which looked promising could then be brought into the clinic very quickly. My wife did not have a lot of time.

Two: Modern medicine has such a lot to offer, and we wanted our treatment to build on that – I wanted my wife to have the best of the old and the new.  Only in this way could we build upon some of the hard-won knowledge and the gains that have been made in treatment over the years.

Three: We wanted to make a change that would not just help my wife but had the potential to help anyone with cancer. We knew that the only way to do this was to generate evidence showing that what we are doing works. We also knew that this evidence had to be of sufficient quality that it could be accepted by the entire medical community.

I wanted to realize my wife’s vision, and her wish to make a difference. She wanted to know that if cancer claimed her life, she had done something that could help make sure better treatments are available. She wanted to help people who must navigate a similar path. It’s a wish that I’m sure everyone is familiar with. We are all human.

The metabolic theory

So now we had our mission. I had the list of 6,000 or so compounds available in the Pharmacopeia of drugs and compounds as a starting point, and with this, we started to research aspects of cancer.

I was fascinated to learn about Otto Warburg’s original ground-breaking work in cell metabolism, for which he received the Nobel prize for medicine in 1931. Metabolism is the conversion of food to energy to run cellular processes and construct cellular building blocks. Warburg’s work really laid the foundations for the theory that the metabolism of cancer cells is fundamentally different to that of healthy non-cancerous cells. Since then, the science and understanding of cancer cell metabolism has of course hugely advanced, in a discipline now known as ‘metabolic oncology’.

Greg and I were convinced that manipulating the metabolic processes used by the vast majority of cancer cells represented a potentially effective way to target any cancer, regardless of type or stage. The theory goes that by using metabolically-targeted drugs to weaken the cancer cell’s ability to grow and thrive, the cell would then become much more susceptible to standard cancer therapies, such as chemotherapy, radiotherapy, and hormone or immunotherapy. With this insight, we decided to search for already licensed drugs that could target these metabolic processes.

The search

We set about researching and ranking available evidence for existing licensed drugs which have a metabolic mechanism of action. This work was painstakingly centered around a number of scientific criteria we had predetermined as being very important.

Above all, we understood that whatever treatment we developed, it must not add significantly to the burden of a patient with cancer, who obviously can be very sick. Many patients must take cancer treatments which themselves can cause a range of difficult side-effects. It was therefore important that our treatment, which was to be taken alongside these standard treatments, was to be as gentle as possible from a side-effect perspective. Safety was very important to us, and we restricted our search only to drugs that had a strong record of use in the general population, (including in cancer patients). This way, we would have some evidence of their compatibility in patients who were also taking cancer treatments.

Next, we knew we wanted to find a combination of drugs that targeted related mechanisms involved in cancer cell metabolism. In this way the activity of each drug combined could potentially produce an additive or ‘synergistic’ effect and would definitely not interfere or impede each other. We termed this approach ‘mechanistic coherence’.  

Finally, we also wanted to make sure that the drugs already had as much published evidence as possible supporting their activity and use in cancer. We took evidence from all available sources and weighed this evidence very carefully.

The COC Protocol

During the development stage we studied and discarded a huge number of drugs from the protocol. For example, drugs that did not have a good safety profile in cancer patients, or which had questionable or mixed evidence of effectiveness, or no real mechanistic reason for inclusion.

There are a huge number of drugs out there with evidence of activity against cancer, but which did not meet our strict criteria for inclusion in the protocol. We eventually arrived at an optimal regimen of four medications: metformin, atorvastatin, mebendazole, and doxycycline. We chose this combination not only because they met all our criteria very well, but also for one other very important reason. We believe this specific combination, with this particular number of drugs, gives us the best chance not only of providing patient benefit, but also for gathering sufficient evidence to start achieving our original vision, of really making a difference to all patients with cancer.

The next steps

One problem which is repeatedly encountered, and is well understood in the field of ‘drug repurposing’, is that although for many of these drugs there is a growing base of evidence supporting their use in cancer (which includes ‘test tube’ based studies, animal studies, patient tumor studies, small clinical trials, and epidemiological studies), there are no Phase III randomized placebo controlled trials. These trials are historically considered the ‘gold standard’ for evidence of effectiveness in patients. But they are also enormously expensive to run. As the drugs we work with are already licensed, and usually off-patent, there is little financial incentive for commercial pharmaceutical companies to pursue their further development.

So, we recognize that to help as many people as possible, we need to produce our own ‘gold-standard equivalent’ patient evidence. Therefore, we are very focused on our own research, to produce and publish high-quality real world data from patients attending our clinic. This is the reason why we spent an enormous amount of time and effort in designing a clinical study which the regulators would approve and endorse. In 2017, we secured approval from the MHRA (the regulator in the United Kingdom, the equivalent of the FDA) and their Research Ethics Committee (the equivalent of an IRB in the USA) to conduct an “Interventional Service Evaluation” which we have named METRICS. This was a big achievement for us as it allows us to publish our outcomes and to share our findings with the world.

We believe that our initiative is one of the only ways through which it is possible to generate the evidence we need. And we really are incredibly grateful to every patient who attends the Care Oncology Clinic, and who is helping to turn our vision of bringing benefit to all patients with cancer into reality.

COC Protocol for Early Stage and Stable Disease

Historically, patients have often presented to Care Oncology physicians with advanced disease– either they have been diagnosed with a type of cancer associated with a particularly poor prognosis or they have suffered a recurrence/disease progression and feel their conventional treatment options are becoming more limited. 

However, there are good reasons to also consider the adjunctive COC Protocol if you are a patient with either an early stage cancer diagnosis or someone who is currently well with more advanced stage 3 or 4 disease. Indeed, the likelihood of a positive outcome is greater than with late-stage presentation.

First, a significant body of research literature suggests that using anti-metabolic drugs such as metformin and statins as adjunctive therapy to standard of care can enhance overall treatment response.

Second, in a scenario where the patient is well in him/herself and/or has a lighter burden of disease, there may be an even greater likelihood of effective disease control.

Our own cohort analysis of 95 patients with Glioblastoma IV (the most common and aggressive type of primary brain tumour in adults) supports this conclusion. These patients were all prescribed the COC protocol alongside their standard of care treatment. Median overall survival of the cohort as whole is considerably better than median overall survival with standard of care alone (https://www.abta.org/tumor_types/glioblastoma-gbm/).  But, those patients who commenced the COC protocol during or soon after first line chemo-radiotherapy have a longer median overall survival than those coming to it after having suffered progression/recurrence. 

Importantly, in‘’well patients” with a good performance status, we would also expect to see better compliance with the COC protocol medicines and fewer side-effects and/or a requirement to interrupt or stop treatment as a result of abnormal blood counts or organ function. 

In addition to the work we are undertaking, a number of other studies are currently underway to explore reduced relapse in patients taking anti-metabolic medications, for example, the very large Cancer Research UK funded ADD-Aspirin trial enrolling 11,000 patients across 5 different types of cancer.

When a patient hears that they are well and perhaps ‘in remission’, they often assume that this means they are cured and are done with treatment. While the words‘remission’ and ‘no evidence of disease’ (NED) are clearly good news and can mark a major positive turning point in someone’s care and overall health,unfortunately, the true situation is often more complicated.

There is no way for doctors to know that all of the cancer cells in your body are gone, which is why many doctors don’t use the word “cured.” If cancer cells do come back, it usually happens within the 5 years following the first diagnosis and treatment. 5 year survival rates or survival statistics are available for all the different types of cancer seen in the community. These statistics are based on research from information gathered on hundreds or thousands of people with a specific cancer.

An overall survival rate includes people of all ages and health conditions who have been diagnosed with a specific cancer, including those diagnosed very early and those diagnosed very late.

Doctors are then often able to provide more detailed statistics based on the stage of cancer at diagnosis. For instance, 56% or a little more than half, of people diagnosed with early-stage lung cancer live for at least five years after diagnosis. The five-year survival rate for people diagnosed with late stage lung cancer that has spread (metastasised) to other areas of the body is 5%.

Because survival rates can’t tell you everything there is to know about your individual situation, the statistics may seem impersonal and unhelpful. But, many people feel that that knowing as much as possible about their cancer, actually helps them to reduce their anxiety, as they can then analyze the different options available to them.  

While, of course, it’s up to each individual patient to decide just how much they want to know about survival rates and overall prognosis, Care Oncology physicians believe the risk/benefit of metabolic adjunctive treatment to be in the patient’s favour if there is judged to be a significant risk of cancer progression or recurrence.

The COC protocol is:

  • Evidence-based; the weight of the available data demonstrates a significant opportunity for patient benefit. Some mechanisms which underpin the utility of the protocol drugs may be particularly helpful in a preventative setting e.g. inhibition of Cancer Stem Cells.
  • Low toxicity, generally well-tolerated and ‘easy to do’ (i.e. tablets, capsules to be taken at home).
  • An adjunctive therapy with a low drug interaction burden which can be incorporated alongside other lines of treatment
  • Almost always safe to combine with standard of care treatments (chemo-, radio-, hormone-, immuno-therapy)
  • Able to potentiate standard treatments by making cancer cells more sensitive to chemotherapy or radiotherapy than would otherwise be the case.

Click here for more information and research references

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FutureTechPodcast: Understanding and Treating Cancer: Epigenetics, Metabolic Therapy, and Repurposed Drugs

What’s the ultimate cause of cancer? Travis Christofferson is interviewed on the FutureTechPodcast.

It’s not an easy question to answer, and according to Travis Christofferson, author of Tripping Over the Truth: The Return of the Metabolic Theory of Cancer, there’s no single cause, but a series of complex interactions and events that depend at least somewhat on our environment. Christofferson explains this in terms of epigenetic responses, which result in the turning off or on of certain genes–allowing some to be expressed and blocking others from being expressed. Diet, toxins, medications, and even loneliness are just a few of the factors that could trigger epigenetic responses and ultimately contribute to the determination of whether or not someone will develop cancer.

Antioxidants and Cancer – Should I take them?

Our Care Oncology physicians often get asked their opinion on various supplement including common and uncommon antioxidants: vitamin C, vitamin E, beta-carotene, N-acetylcysteine (NAC), and glutathione to name a few. Understandably, newly-diagnosed cancer patients and their friends and family often embark on a deep search for anything that can be done to support health and immune system function. And why not antioxidants? A steady stream of media and supplement manufactures have told us for decades that antioxidants offer a panacea of health benefits. And rightfully so, a light internet search can easily lead to articles touting the virtues of antioxidants. The calculus: They may help fight my cancer, and, in the very least, they can’t hurt. Right?

Where did the idea antioxidants are good come from?

In 1972 Denham Harman, a luminary in the field of free radical biology, proposed the mitochondrial theory of ageing. It goes like this: Inside every cell mitochondria are the center of oxidative metabolism and hence the primary source of free radical generation within the body. Free radicals generated from mitochondria then precipitate a cascade of damage to surrounding mitochondria, lipids, carbohydrates and even nuclear DNA. The cell can repair most of this damage, but over time the cell slowly loses the ability to keep up with the free radical induced damage and the net damage that ensues is the proximal cause of ageing.

spoon with dietary supplements on fruits backgroundA simple and intuitively seductive assumption sprang forth from Harman’s theory: free-radical quenching antioxidants should slow ageing and prevent disease. This seemingly innocent prediction has confounded a generation of molecular biologists. In the over forty years that followed Harmon’s prediction researchers have shoved antioxidants into cell cultures, mice, rats, monkeys and humans trying to prove they slow ageing and prevent disease.

Despite their best efforts to prove otherwise, an overwhelming consensus has emerged from the decades of research on antioxidants and ageing: they just don’t work. They might correct dietary deficiencies and/or perhaps confer a slight protective effect against certain diseases, but they do nothing to prolong lifespan—worse, there is evidence to suggest they may even promote certain diseases. Yet, almost a half century of inertia and a billion-dollar supplement industry that grew out of Harmon’s prediction have managed to continue propping up the notion that antioxidants are a well-spring of health. (Don’t confuse foods containing antioxidants and antioxidant supplements. Most quality food contain high amounts of natural antioxidants and a good diet has been shown to be very beneficial.)

Studies began to challenge many assumptions about antioxidants

The blanket assumption that antioxidants slow ageing and prevent disease was first seriously challenged from a large study in 1994 that followed smokers taking massive doses of the antioxidant beta-carotene. The stunning result: The smokers taking beta-carotene had an 18% increased risk of developing lung cancer. As researchers were still scratched their heads about the confusing result a trial two years later was stopped early after it was discovered that high-dose beta carotene and retinol was shown to increase the risk of developing lung cancer by 28 percent in smokers and workers exposed to asbestos. And these early studies are not proving to be flukes: a 2011 trial involving more than 35,500 men over 50 found that large doses of vitamin E increased the risk of prostate cancer by 17 percent.

Antioxidants and cancer therapy

The above studies highlight a trend of studies suggesting that antioxidants may contribute to the incidence of certain cancers under specific conditions and may make cancer more aggressive when it occurs. However, the series of studies sparked a more immediate concern to practicing oncologists: because traditional standard of care therapies like radiation and chemotherapy kill cancer cells by the generation of free radicals perhaps patients taking antioxidants were negating or diminishing the effects of their cancer treatment. Yet, despite a flurry of studies in the early 2000’s―both observation and randomized controlled trials―no clear consensus of the effect of antioxidant on standard therapies emerged. The studies reached a wide variety of conclusions, some showing improved survival and status and others, a reduction in survival. Most likely, the common antioxidants, given at normal doses, are simply to weak to overcome the powerful effects of radiation and chemotherapy.

The smoldering debate about antioxidants and cancer was rekindled again in 2012 when Nobel Prize winner and former head of the NCI, James Watson, sounded off on the danger of antioxidants in cancer, penning a review titled Oxidants, antioxidants and the current incurability of metastatic cancers, claiming the work was “His most important work since the double helix.” His epiphany, in part, was the claim that antioxidants may be thwarting most cancer therapies if not outright causing cancer by preventing the mitochondrial driven apoptotic cascade triggered by free radicals. “For as long as I have been focused on the understanding and curing of cancer (I taught a course on Cancer at Harvard in the autumn of 1959), well-intentioned individuals have been consuming antioxidative nutritional supplements as cancer preventatives if not actual therapies. In light of the recent data strongly hinting that much of late-stage cancer’s untreatability may arise from its possession of too many antioxidants, the time has come to seriously ask whether antioxidant use much more likely causes than prevents cancer.” Watson goes on, “Free-radical-destroying antioxidative nutritional supplements may have caused more cancers than they have prevented.”

A series of studies in the years following Watson’s revelation seemed to support his claim. A 2015 study published in Science Translational Medicine, looked at melanoma because rates have been increasing and because the cancer is known to be sensitive to the effects of free radicals. They fed the antioxidant N-acetylcysteine (NAC) to mice that had been bred to be susceptible to melanoma at a dose consistent with what people typically consume in supplements. Although the treated mice did not develop more skin tumors than the control mice, they developed twice as many tumors in their lymph nodes, a hallmark of the spread of cancer. When the researchers added NAC or a form of vitamin E to cultured human melanoma cells, they again showed that the antioxidants improved the cells’ ability to migrate and invade a nearby membrane.

Additional evidence surfaced pointing to the danger of antioxidants new classes of free radical generating therapies. A study that came out immediately before Watson’s paper convincingly showed the importance of free radical induced apoptosis by the finding that the ‘first-in-class’ anti-cancer mitochondrial drug elesclomol kills cancer cells through promoting ROS generation. When these resulting free radicals were neutralized through the simultaneous administration of the antioxidant N-acetylcysteine, preferential killing of cancer cells stops. The failure of elesclomol to generate apoptosis in non-cancerous cells probably arises from the inherently lower ROS level generated by normal mitochondrial electron transport machinery.

Critically, many new therapies are being developed that lower the glutathione level in cancer cells rendering them more vulnerable—it is not clear how antioxidants will affect this new class of drugs and therapies.

The picture remains murky

Although there is no overwhelming consensus that antioxidants taken during cancer treatment will lead to worse outcomes the existing evidence throws up enough red flags to warrant caution. Not much is known about the effects of antioxidants in relation to many of the new metabolic-acting and immunotherapies. It must be considered that adjunctive therapies like the ketogenic diet, hyperbaric oxygen and the Care Oncology Protocol are also proposed to work by triggering oxidative stress in cancer cells while simultaneously reducing the cancer cells ability to manufacture internal antioxidants. It is not unreasonable to question the use of antioxidants concurrent with these therapies―especially considering they tend to generate much milder oxidative stress than tradition cancer therapies and therefore antioxidants might have the capacity to influence outcomes to a greater degree. In fact, evidence exists highlighting this tenuous relationship. It has been shown that some of the medications in the Care Oncology Protocol act by inducing oxidative stress within cancer cells. Both doxycycline and metformin are proposed to work by inducing an intolerable surge of free radicals within already oxidative-stressed cancer stem cells while simultaneously inhibiting a transcription factor called STAT3 that the cancer cell upregulates in order to manufacture internal, adaptive antioxidants—a sort of one-two punch. A 2017 study showed that the addition of the potent antioxidant N-acetylcysteine was able to cancel-out the therapeutic effect of doxycycline in a glioblastoma mouse model.

“What we’re starting to learn is that there can be bad cells from cancer that appear to benefit more from antioxidants than normal cells,” said researcher Sean Morrison from the University of Texas Southwestern Medical Center, who’s lab studies the effects of antioxidants on cancer cells. “Personally, from the results we’ve seen, I would avoid supplementing my diet with large amounts of antioxidants if I had cancer.”

Martin Bergö, Ph.D., of the University of Gothenburg in Sweden, said he was extremely concerned with the aggressive marketing of antioxidants to cancer patients. The data strongly suggest that using antioxidants “could be really dangerous in lung cancer and melanoma, and possibly other cancers,” he said. “And because there’s no strong evidence that antioxidants are beneficial, cancer patients should be encouraged to avoid supplements after they have a diagnosis.”

Care Oncology Science Advisor, Thomas Seyfried of Boston College shares Morrison’s and Bergö’s sediment. “Why would you give antioxidants to cancer patients? It runs completely counter to metabolic therapeutic interventions.”

Indeed, the general idea that oxidative stress might be one of cancer’s greatest vulnerabilities, and that antioxidants, both exogenous (taken orally or by IV) and endogenous (manufactured intracellularly), may represent a thin veil of protection that can be therapeutically targeted is also proving to hold true with the emerging class of immunotherapies. New research has shown that by reducing intracellular glutathione, the cell’s “master antioxidant”, the cell-killing effect of immunotherapies can be enhanced. The authors of the recent study state: “The inhibitory effects of cancer on T cell metabolism have been well established, but the metabolic impact of immunotherapy on tumor cells is poorly understood. Here, we developed a CD4+ T cell-based adoptive immunotherapy protocol that was curative for mice with implanted colorectal tumors. By conducting metabolic profiling on tumors, we show that adoptive immunotherapy profoundly altered tumor metabolism, resulting in glutathione depletion and accumulation of reactive oxygen species (ROS) in tumor cells.”

Well what now?

In the over forty years since Harman’s proposed free-radical driven mitochondrial theory of ageing we’ve learned that free radical biology is certainly more complex than originally appreciated. While there is no question free radicals are destructive to the cell, emerging evidence suggests mitochondrial derived free radicals may also be an important signaling system, instructing the DNA within the mitochondria to manufacture mitochondrial proteins. Free radical biology and its ultimate role in ageing is still unsettled science that has yet to be conclusively decided.

However, the relationship of antioxidants and cancer, although still murky, seems to be tilting toward a note of caution when it comes to including antioxidants as part of cancer therapy. While little if any benefit has ever been proven, the evidence pointing against their use does demand attention. A cautious approach would be to avoid high doses of antioxidants during cancer treatment. A very cautious approach would be to avoid antioxidant supplements altogether. Indeed, most dieticians agree that enough micronutrients can be obtained―and in the right ratios―from a good diet.

Some common antioxidants:

Vitamin E, selenium, zinc, N-acetylcysteine, glutathione, Vitamin C (low dose only—high doses administered by IV are oxidative), and beta-carotene

References

https://www.cancer.gov/news-events/cancer-currents-blog/2015/antioxidants-metastasis
https://www.scientificamerican.com/article/antioxidants-may-make-cancer-worse/
https://www.washingtonpost.com/news/to-your-health/wp/2015/10/14/antioxidants-may-give-a-boost-to-cancer-cells-making-them-spread-faster-study-suggests/?noredirect=on&utm_term=.1acb7963fc25
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3603456/
https://www.ncbi.nlm.nih.gov/pubmed/28842551
https://www.sciencedirect.com/science/article/pii/S155041311830319X?via%3Dihub
https://www.sciencedirect.com/science/article/pii/S1550413118301785
http://www.ascopost.com/issues/july-25-2014/avoiding-antioxidant-drug-interactions-during-cancer-treatment/
https://www.ncbi.nlm.nih.gov/pubmed/22189713

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Research shows that drugs found in the COC Protocol have an antiproliferative effect on breast cancer tumor cells, meaning that the drug inhibits the growth and spread of cancer cells.

How will the COC Protocol help treat breast cancer?

The COC protocol is a patented pharmaceutical composition of four repositioned medications. The medications have long histories treating type-2 diabetes, reducing cholesterol, parasite infection, bacterial infection and inflammation. After four years of clinical research, we know that these drugs – in combination – offer significant therapeutic value for cancer patients. Each of these drugs plays a role in weakening cancer cells and making them more susceptible to standard-of-care therapy (e.g., chemotherapy, immunotherapy).

One of the biggest problems breast cancer patients face is when their cancer becomes resistant to standard-of-care therapies. Multi-drug resistance (MDR) occurs when a patient develops resistance to one or more treatment drugs.

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Can a diabetes drug control Pancreatic Cancer?

The study — which was led by Rutgers Cancer Institute of New Jersey in New Brunswick — is to feature at the 2018 annual meeting of the American Association for Cancer Research, which will be held in Chicago, IL.

This study is not the first to suggest metformin as a potential treatment for pancreatic cancer, but it is the first to show that the underlying mechanism involves the drug’s effect on the REarranged during Transfection (RET) cell signaling pathway.

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You’ve got to believe you can beat it – Kent R. – Grade 4 Glioblastoma Patient

Glioblastoma Patient Interview – COC Treatment Protocol

Kent: Hi, my name’s Kent Rhodes and I have a Grade 4 Glioblastoma, and I was first diagnosed on the 27th of September 2016. After the initial, I suppose shock would be a good word, I visited Care Oncology on the 14th of October 2016, and met the wonderful Ndaba who told me how we were going to save my life. And the rest, as they say, is history. At the moment we are doing very well.

Ndaba: Well, thank you very much, Kent. What led you to seek additional options for treatment?0

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I am an active, 48 year old mother and wife, and I am not ready to leave my family and friends. – Glioblastoma Diagnosis

After my devastating diagnosis of Glioblastoma Multiforme, an aggressive and deadly form of brain cancer, I was told that the standard of care treatment would give me a 3% survival rate with a possibility of living for 12-15 months.

I am an active, 48 year old mother and wife, and I am not ready to leave my family and friends. I needed to find some alternative treatments because the standard medical ones were insufficient.

In my frantic and non-stop research, I repeatedly found and read about Care Oncology’s research and findings. Not until a friend in London, who happens to be in the medical field, advised me to do so, did I visit Care Oncology’s website and delve further into COC’s protocol. I was intrigued by their evidence-based approach. As I researched further, I found that the COC’s treatment was having success and garnering accolades from the research and medical community. I wanted to be part of their protocol.

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The COC Protocol – Featured in Daily Mail – Henry was given 14 months to live now his cancer is stable

We tend to associate breakthrough treatments with new — and often unaffordable — drugs.

But it seems a remarkable improvement in the survival time of patients with brain cancer has been achieved using a combination of four old drugs (a statin, a diabetes pill, an antibiotic tablet and a dewormer) that cost just £400 a year.

Results from an ongoing trial run by the private Care Oncology Clinic in London suggest that giving this new combination treatment doubled the average survival time.

Read more: http://www.dailymail.co.uk/health/article-5492485/Could-400-year-drug-cocktail-beat-one-deadliest-cancers.html#ixzz59dreUI1c
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Widely Prescribed Oral Diabetes Drug Leads to Dramatic Breakthrough Cancer Treatment

Although rare, adrenocortical carcinoma is among the most common tumors found in children with Li-Fraumeni syndrome and Li-Fraumeni-like syndrome, associated with germ-line mutations in the TP53 gene. In southern Brazil, one form of Li-Fraumeni syndrome, associated with childhood adrenocortical carcinoma, is caused by a mutation in the R337H TP53 tetramerisation domain and is attributed to a familial founder effect. Adrenocortical carcinoma is considered an aggressive neoplasm, usually of poor prognosis and is generally unresponsive to systemic chemotherapy. Optimal treatment regimens remain to be established. We report the case of a young woman with metastatic adrenocortical carcinoma, who achieved stable disease with mitotane, cisplatin, doxorubicin, and etoposide as first-line therapy, but then had an objective response to oral metformin that lasted 9 months. The presence of the R337H TP53 mutation suggests a mechanism for the observed response to metformin.

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