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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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.
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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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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Patient Testimonial – 40 year old female with breast cancer
1) When did you first visit Care Oncology Clinic and commence adjunct treatment? What led you to seek out additional treatment options?
I first visited the COC in September 2016. This was halfway through my chemotherapy treatment for breast cancer.
Despite the intended outcome of my primary cancer treatment to be curative, I was shocked by the number of women I met through support groups who had experienced a return or spread of their breast cancer in the years after completing primary treatment. I then analysed the statistics and profile of my cancer diagnosis – it suggested I also faced this risk. I simply knew I had to do more.
Here, we propose a new strategy for the treatment of early cancerous lesions and advanced metastatic disease, via the selective targeting of cancer stem cells (CSCs), a.k.a., tumor-initiating cells (TICs). We searched for a global phenotypic characteristic that was highly conserved among cancer stem cells, across multiple tumor types, to provide a mutation-independent approach to cancer therapy. This would allow us to target cancer stem cells, effectively treating cancer as a single disease of “stemness”, independently of the tumor tissue type. Using this approach, we identified a conserved phenotypic weak point – a strict dependence on mitochondrial biogenesis for the clonal expansion and survival of cancer stem cells. Interestingly, several classes of FDA-approved antibiotics inhibit mitochondrial biogenesis as a known “side-effect”, which could be harnessed instead as a “therapeutic effect”. Based on this analysis, we now show that 4-to-5 different classes of FDA-approved drugs can be used to eradicate cancer stem cells, in 12 different cancer cell lines, across 8 different tumor types (breast, DCIS, ovarian, prostate, lung, pancreatic, melanoma, and glioblastoma (brain)). These five classes of mitochondrially-targeted antibiotics include: the erythromycins, the tetracyclines, the glycylcyclines, an anti-parasitic drug, and chloramphenicol. Functional data are presented for one antibiotic in each drug class: azithromycin, doxycycline, tigecycline, pyrvinium pamoate, as well as chloramphenicol, as proof-of-concept. Importantly, many of these drugs are non-toxic for normal cells, likely reducing the side effects of anti-cancer therapy. Thus, we now propose to treat cancer like an infectious disease, by repurposing FDA-approved antibiotics for anti-cancer therapy, across multiple tumor types. These drug classes should also be considered for prevention studies, specifically focused on the prevention of tumor recurrence and distant metastasis. Finally, recent clinical trials with doxycycline and azithromycin (intended to target cancer-associated infections, but not cancer cells) have already shown positive therapeutic effects in cancer patients, although their ability to eradicate cancer stem cells was not yet appreciated.
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Massachusetts General Hospital (MGH) investigators may have uncovered a novel mechanism behind the ability of the diabetes drug metformin to inhibit the progression of pancreatic cancer. In their report that has been published in the open access journal PLOS One, the research team describes finding that metformin decreases the inflammation and fibrosis characteristic of the most common form of pancreatic cancer. Their findings in cellular and animal models and in patient tumor samples also indicate that this beneficial effect may be most prevalent in overweight and obese patients.
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