Case Report Stage IV Sarcoma: Good News from JG

Dear Friends, 

This post is related to a man from Europe, JG, with whom I am in contact since May 2018, and his successful treatment of an aggressive form of Stage IV sarcoma.

A week ago, JG contacted me to share some very good news, as he is now at a point where there is no more evidence of disease. He specifically asked me to share his story but also keep his identity confidential, which is what I am going to do here. He would like to share his story in order “to give hope and help to other people suffering from this disease”.

Here is JG’s short report received during December 2018:

“I am JG, I am 26 years old and I had a sarcoma, grade III, stage IV in mediastinum (several tumors). I followed a surgery and several complementary treatments such us:

  • 2 DG metronomic 
  • Low carb diet 
  • Meditation 
  • Oncothermia & radiation
  • Suplements: melatonin, Vit D3, probiotics, prebiotics, honokiol, HCA 
  • Drugs: cimetidine, celecoxib, ciclofosfamide, mebendazol, lovastatin. These have been changed over the time, but I write the most important here. I don’t know if it a good idea because I assumed several interactions in order to try to kill microscopic disease, other people should be aware of this interactions. 

The results from the last MRI showed no evidence of disease although the surgical resection was not complete.

It may be relevant to mention here that JG has a medical doctor training, which helped him to easier navigate through various treatment options. While I cannot share more details here, the only point I can make is that the past and present of JG is very impressive. That can be summarized in a few words: A challenging life turned into success for himself and others. And JG is only 26 years old. I am sure those results will continue, and it’s great to meet such people.

I do realize that the report above may be a little too short. Therefore, in order for the reader to have a more clear understanding of the context for the results mentioned above, I will also share with you small parts of our (extensive) e-mail conversation. However, at the same time I will keep confidential any personal data from JG.
.

May 2018,
JG contacted me via e-mail, writing the following:

“Hello, My name is JG and I have been following your website since I was diagnosed a very rare and aggressive type of sarcoma. It was controlled but recently it has losed all control and it has metastasized to the chest wall. I know you cannot give precise advice etc, but your opinion is too important for me. I have been managing my own treatment and I will continue doing the same. I will expose briefly what I think could be a good strategy to start as quick as possible, and i would be really grated if you can give me your opinion. 

– Ketogenic Diet – 2DG and vit C infusions 
– Ozone / Hiperbaric oxigen 
– ECCT   
– Oncothermia or Nanothermia applied to the lessions 
– Cocktail: Cimetidine, Heparin, Mebendazole, Ciclophosfamide, Metformin, DCA, Lovastatin, Doxyciclin, Hydroxycloroquine, Tranilast

….”

June 2018,
after several e-mails exchanged between the two of us, JG writes:

“… After talking with the Surgeon I have decided to operate the main tumors ( 3 ), located in the chest wall. It seems they could be removed completely, and with that surgery they would remain  2 little nodules of 1 cm approx in the thorax ( which are not going to be removed ). So now it is really important for me designing a strong anti recurrence protocol in order to avoid recurrence after the surgery. The measures and drugs i have planned using are:

pre operation: Heparin, cimetidine, MCP, Celecoxib, Diclofenac, Propranolol, Hydroxichloroquine, Viscum album, PSK, Silimarine, Curcumine, Garlic, Cruciferous extract, Lactoferrin, EGCG, AHCC, Fish oil, Filgrastim/neupogenmaybe ? (not sure about this). Of course I will cut off all the drugs that cannot be used pre surgery some days before the surgery, such us heparin.

peri operation: ketorolac (following the videoinstructions)

post operation: Same drugs and supplements used pre operation ; Vit C IV( 3 times / week); 2 DG protocol; Metronomic chemotherapy: ciclophosphamide, etoposide ; Local Hiperthermia in the places where the tumors were growing and in the two nodules that are not going to be removed surgically.

…”

July 2018,
following a question from JG on approaches to reduce the chance for recurrence after surgery (besides addressing inflammation in general) here is a part of my response which I share as it may inspire other people, and/or trigger discussions: 

“… Regarding ways to support radiotherapy/chemotherapy while reducing chance for recurrence, I think there are several major lines that should be addressed:

1. Increase immune system effectiveness and reduce pro-growth tumor environment. 
It is known that radiotherapy/chemo may trigger necrosis of tumor cells that in turn may trigger immune reactions. Sometimes the immune reactions following radiotheraphy/chemo can be so large that would lead to an abscopal effect, where tumors in other parts of the body can also be wiped out after radiotheraphy to a single spot. In order to increase the chance for such reactions and reduce chance for reccurence, we need to maximize the effectiveness of the immune system to the best of our knowledge.

For this, I would consider some of the following:

a. Reducing T-regs, M2, and MDSC

– low dose Cyclophosmamide to reduce T- regulatory cells https://www.ncbi.nlm.nih.gov/pubmed/22761338

– Cimetidine may also reduce T-regs https://ecancer.org/journal/8/full/485-repurposing-drugs-in-oncology-redo-cimetidine-as-an-anti-cancer-agent.php

– M1 macrophages, protect against infection and can work to destroy tumours, and M2 macrophages promote wound-healing and have been linked to tumour growth and spread. So we want to target and block the accumulation of M2 cells in tumours after radiotheraphy. Doxycicline is an inhibitor of the M2 https://www.ncbi.nlm.nih.gov/pubmed/24505138  Cyclooxygenase-2 Inhibition also Blocks M2 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3646746/ this is why Aspirin or Celecoxib may help here but also in general to reduce the chance of metastasis. There is one more drug here very good, but difficult to get as it is very expensive (Plerixaforhttps://www.cancertreatmentsresearch.com/plerixafor-mozobil/

– MDSC also need to be inhibited. Retinoic acid and Vitamin D3 could help on this line https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019895/ Cimetidine will also help here https://www.cancertreatmentsresearch.com/antihistamine/ Tadalafil can also reduce MDSC https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4329916/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5931815/
Phosphodiesterase-5 inhibition reduces postoperative metastatic disease by targeting surgery-induced myeloid derived suppressor cell-dependent inhibition of Natural Killer cell cytotoxicity https://www.societederecherchesurlecancer.ca/en/news/drug-repurposing-viagra-and-agriflu-help-to-fight-cancer Pharmacological inhibition of COX-2 blocks ARG-1 expression in MDSC and prevents the local and systemic expansion of MDSCs, leading to a lymphocyte-mediated antitumor response (Ref.). Therefore, Celecoxib could be a good option here.

– Histamine inhibition by Cimetidine and Cetirizine https://www.cancertreatmentsresearch.com/antihistamine/

b. Increasing the activity of T-cells via supplements such as Coriolus

c. Increasing the chance of effectiveness of T-cells by re-balancing the PH around the tumors with alkalizing approaches such as Basentabs or proton pump inhibitors (should not be used with weak-acidic chemotherapy – only with those weak-basic)

d. Reduceing fibroblasts using  anti-fibrotic agents (nonsteroidal anti-inflammatory drugs [NSAIDs] or tranilast) that should also reduce the infiltration of tumors with immunosuppressive cells (regulatory T cells and myeloid-derived suppressor cells) https://onlinelibrary.wiley.com/doi/abs/10.1111/cas.12584

2. Reduce HA with 4-MUhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369655/ in order to reduce inflammation and create a tumor micro-environment that is easily addressable by drugs such as chemo therapies. I would use this only in combination with major treatments such as chemo, etc. If no major treatments are used, could be better not to use 4-MU as HA may create a temporarily slower tumor growth https://www.cancertreatmentsresearch.com/the-hyaluronic-acid-cage-to-open-or-not-to-open/

3. Increase Tumor oxygenation via e.g. – local hyperthermia prior to and after radiotheraphy https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3357106/– using Niacin supplement prior to radiation and drinking some coffee prior to radiation. The above reference discuses in entire strategy focused on “Targeting Tumor Perfusion and Oxygenation to Improve the Outcome of Anticancer Therapy”

4. Decrease intracellular PH in cancer cells via proton pump inhibitors and hyperthermia
The above would be a strategy to support major therapies and/or to reduce chance for recurrence. “Major treatments” are a different discussion that we touched in some e-mail exchange we already had. By major treatments, I am thinking of treatments that directly and strongly attack cancer cells. Those include, chemo, radio, new treatments (such as 2DG, 3BP, Salinomycin, Diflunisal, etc). 

…”

Disclaimer:

This site is not designed to and does not provide medical advice, professional diagnosis, opinion, treatment or services to you or to any other individual. Through this site and linkages to other sites, I provide general information for educational purposes only. The information provided in this site, or through linkages to other sites, is not a substitute for medical or professional care, and you should not use the information in place of a visit, call consultation or the advice of your physician or other healthcare provider. I am not liable or responsible for any advice, course of treatment, diagnosis or any other information, services or product you obtain through this site. This is just my own personal opinion regarding what we have learned on this road.

Please read an extended version of the Disclaimer here: https://www.cancertreatmentsresearch.com/?page_id=1794

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18 thoughts on “Case Report Stage IV Sarcoma: Good News from JG

  1. D, this is great!
    We seem to have finally hit a point of traction with these patient success stories.

    One thing that we might consider now is to include those interested into a prospective study. The problem with reporting patient that do well is that those who did not do well are often not reported. What perhaps you could now do is ask those who first contact you if they would be willing to have their anonymized patient reports posted to this forum after they had received treatment for some time. We would have a prospective information! Others following these reports would then have greater confidence that there was no cherry picking: They would have a much better idea of what they could reasonably expect from different treatments.

    I find it very frustrating that cancer clinics typically only report the patients that had a good outcome. This makes it so difficult to know how truly effective a treatment is!

    1. Hi J, your point is very important indeed!

      I very much agree with you, yet the reality in the field is so that it is so challenging to collect feedback as most of the patients and clinics do not keep track of everything they are doing. And that is normal as they have to move fast and when dealing with advanced cancers often therapies have to be changed. Even for myself who I like to write down everything we did in terms of treatments, it was very challenging to write everything. As a patient or caregiver you need to take care of so many things, like researching what you need, communicating with doctors and other patients, ordering products, thinking about what’s next, taking care of financials, food, all things around the house, job, etc …. On the other hand as a clinic, your have so many patients and so many other challenges …

      This is why, in reality we can only expect structured and consolidated data when the patient is treated in a hospital where the patient is under observation and there are people paid to write down the details about treatments and results … such as in the clinical trials. But off course, the clinical trials and data reported have own bias and weak points …

      The most annoying part for me is that it is difficult to demonstrate clearly when the patient benefited or not from specific choices, compared to either using conventional treatments alone or just not doing anything at all. In clinical trials they have the different arms to compare and perform statistics. Yet, I do not like that approach since by design some patients will have more chances than others. So you see, everything is debatable.

      But finally I realized we have to work with what we have, and try to improve that step by step. We can at least draw a clear conclusion when there are results showing complete or partial remission in cases where we would not expect that. Or when people survived much longer than they were expected to survive and in much better conditions. We can also identify patterns when looking at multiple patients while knowing most of the treatments they used, and how were used. That is also very valuable in order to identify relevant directions.

      Everything clear up when we understand that humanity is still in the exploratory phase in terms of finding a solution to cancer. This phase is a more creative, chaotic and divergent phase. In this phase the search for value is less structure and we need to understand and accept that (that is what I am telling to myself too). Only when we identify value, we need to stop, focus on that and create a framework to further uncover that value – this is a more advanced phase where we now like to see 2DG metronomic moving to.

      Coming back to the case report discussed here, in my view, the relevance of case reports such as the one presented here is
      – on one hand to see that it is possible – Even Stage IV aggressive cancers can be controlled and in some cases eliminated when improved treatment strategies are employed
      – on the other hand to expose valuable approaches – and the fact that they are unbiased reports is unique and extremely valuable – and this is possible as our goal here is to see the truth (typically, a lot of the info coming to us regardless if it comes from pharma industry, academia, private clinics, hospitals, it is biased due to various reasons).

      We here can share info and judge results here, as we often know personally the people involved (who also often become friends) and the science related to the drugs they are using. It’s not perfect but I think we are on the right track as we saw lately more and more positive results. Our understanding is evolving fast and I expect we will see more and more good results.

      Finally, it’s interesting to see that those stage IV patients who see positive results they are related to patients/clinics who
      – made the step into re-purposed drugs
      – combined conventional treatments with new treatments (including new intravenous treatments)
      – the patient or caregiver acted pro actively in understanding treatments and taking decisions related to this
      – and a medical trained person was involved to support, at least from time to time

      One of the major points I came to realize lately is that not only the cancer cells but also the micro environment must be addressed in order to increase the chance for positive outcome, and continuity of that. That is even more important in Stage IV. And the nice thing is that we have tools to address that + we have friends and contributors like you searching every day for new and effective “tools” and sharing their finding here. Thank you for that!

  2. Jcancom raises a great point, and I think we’re here to try and produce alternative treatment options that outperform the current standards, because we believe that’s possible, right?

    What better way to try and achieve this by focussing on those cancers with the worst prognosis, like glioblastoma and pancreas cancer? It would be so much easier to establish the value of experimental complementary treatments when only dealing with the most difficult to treat cancers. With that type of cancers ANY patient success story offers valuable information! Because frankly, what we have today for those tumors is total failure. And it’s expensive, by now you’d expect they’d offer their rx and chemo for free!

  3. @johan: the problem is not the lack of better performing treatments, but that such treatments have to be validated by the medical establishment before reaching the patients, and this takes a very long time.
    For instance, in Glioblastoma (and brain metastases from other cancers), the addition of Macitentan to therapy greatly improves outcomes in mice, but since 2015 nothing new was published regarding human trials. Also nothing new about the synergy between Aprepitant and Ritonavir against GMB.
    In PDAC, there are many new discoveries that could greatly improve outcomes, but translation into clinical practice will take years. Last year I updated my article “Pancreatic cancer: Towards increasing treatment effectiveness”, and got just a “Thanks!” from Daniel, no one else bothered to comment on the new info. 🙁

  4. Hi Ovidiu, it’s good to hear from you!

    The problem I have with oncologists is that they often discourage people to be proactive about their disease, even when they have very little to offer outside surgery in cancers such a GBM. They get all excited about drugs like Avastin, but when you look closer that’s just another drug with little benefit. Of course it’s expensive, and sales so far have been great: US$ 50 billion. My sister-in-law has stage4 Ovarian cancer, and is taking Avastin, she has to do 22 cycles. Her insurance refused to pay for 2 cycles so far and she had to get a lawyer. Luckily she won the case if not she’s had to pay us$25.000 for those 2 cycles. Imagine the stress of dealing with that on top of dealing with life with advanced cancer. In a clinical study Avastin improved OS in patients with ovarian cancer with 3 months. That’s an expensive drug for a gain of just 3 months, and with the risk of many serious side effects.

    Most oncologists will say you can eat whatever you feel like, yet *we* know that’s false. Here’s a new study:
    High-fructose corn syrup boosts intestinal tumour growth in mice
    https://ecancer.org/news/15650-high-fructose-corn-syrup-boosts-intestinal-tumour-growth-in-mice.php

    A well designed anticancer diet could add many more months, if not years, to most cancer patients life, much more then Avastin, and at little or no extra cost. Yet you’re almost ridiculed for bringing up the subject of diet in order to slow down cancer/tumor growth.

    About macitentan I read this: “Despite encouraging preclinical data, results from the Phase I/Ib open-label studies in patients with recurring glioblastoma and newly diagnosed glioblastoma disappointingly do not support further investigation in this indication. Dose escalation had reached 300 mg per day, without any significant tolerability issues, before the decision was made to stop the investigation.”

    I hadn’t read your article on novel treatments for pancreatic cancer, I don’t think I was on this forum at that time. It’s extremely valuable. One thing Daniel could do is add the updates to the original article, as that would make it easier to read.

    Regards

    1. Thank you for the info on the failed trial of Macitentan. I tried to figure out possible reasons, and probably it’s because Macitentan has poor brain penetration. While I found no actual data on brain penetration, I found that it’s over 99% protein bound, and this is usually associated with poor brain penetration. Other data, it has about 74% oral absorption rate, and about 17 hours elimination half-life.
      While I am reluctant to give personal advice, you may want to keep and eye on Disulfiram nanoformulations against GBM, and Macitentan and Nintedanib against ovarian cancer.
      Brain- and brain tumor-penetrating disulfiram nanoparticles: Sequence of cytotoxic events and efficacy in human glioma cell
      lines and intracranial xenografts. PMID: 29423059
      Macitentan blocks endothelin-1 receptor activation required for chemoresistant ovarian cancer cell plasticity and metastasis. PMID: 26776834
      Standard first-line chemotherapy with or without nintedanib for advanced ovarian cancer (AGO-OVAR 12): a randomised, double-blind, placebo-controlled phase 3 trial. PMID: 26590673

    1. This may be useful against ovarian cancer: Bevacizumab combined with tocotrienol results in a rate of disease stabilization of 70%, with very low toxicity. Also Abraxane (unfortunately expensive) may be useful, together with GM-CSF, if MDSCs are kept low (could use Lansoprazole for synergy with Abraxane, and Cimetidine to lower MDSCs).
      Delta tocotrienol in recurrent ovarian cancer. A phase II trial. PMID: 30639384
      Phase II trial of albumin-bound paclitaxel and granulocyte macrophage colony-stimulating factor as an immune modulator in recurrent platinum resistant ovarian cancer. PMID: 28089377

  5. That looks really useful indeed. I especially like the delta tocotrienol supplementation(3x300mg/day) because of the safety profile, looks really promising.
    Many thanks!!

    1. No need to thank me, but if this suggestion will really help, that good news will be my reward.
      Now about Tocotrienols, it’s not so simple… Their bioavailability is low and variable, especially if mixed with Tocopherols (they compete for absorption). In the article they used Traptol, which is an obscure brand, from Denmark (same as the authors). But they mentioned it was produced by American River Nutrition (you should search their website to confirm info), so it must be DeltaGold, which can be found in other brands too. On their website ARN mention a study that wasn’t available on Pubmed (and I missed it, until today), Pharmacokinetics and bioavailability of annatto δ-tocotrienol in healthy fed subjects. From that study I would say that the AUC of delta-tocotrienol is much greater with 500 mg doses than with 250 mg doses (more than twice). So if someone could tolerate 3 x 500 mg every 8h, with food (improves bioavailability), that should result in more consistent anti-cancer activity.
      I also found an article: Effects of antibiotics on degradation and bioavailability of different vitamin E forms in mice. PMID: 30694588. I’m not sure how to interpret it, generally it’s not a good idea to mix antibiotics with anti-cancer drugs, and probiotics do help against cancer.

    2. @johan: I tried to find previous information that you may have posted on the ovarian cancer case, but couldn’t find any.
      Just “stage4 ovarian cancer, currently on Avastin” is not enough info to provide advice, hopefully there are more details available.

      1. Hi ovidiu,
        I agree with at least trying the higher 500mg doses, thanks for noticing that.

        I hadn’t mentioned it before. She has Epithelial ovarian cancer, with liver metastases. Dx October 2016. She’s only 40 so she has that going for her I think. She has had clear scans since she finished chemo, and has been on Avastin since, first every 3 weeks but now every month (for insurance purposes). She has a PET scan scheduled for saturday as she’s feeling more pain again.

        Regards

        1. I understand that the chemo resulted in a complete radiological response, it would be nice to know which chemo, since it may still work, especially in combination with some chemosensitizer.
          Also, it seems you don’t know which mutations drive that cancer (as a result of testing on a biopsy sample), I suggest to find out such info, since best treatment options may be quite different, depending on found mutations.
          If Abraxane (nab paclitaxel) is covered by insurance, it may be an option. If not covered, it may cost about 2000 euros for 400 mg.
          A phase I trial of azacitidine and nanoparticle albumin bound paclitaxel in patients with advanced or metastatic solid tumors. PMID: 28881739
          I saw your post about PARP inhibitors in the forum. PARP inhibitors can also be useful against ovarian cancer, in combinations delivering synthetic lethality. But such combinations can be very expensive.

            1. OK, good news, so there’s no point to ask about the mutations, and hopefully never will be. 🙂
              About the bursitis, I looked into adverse effects of Avastin, and it may be related, but it would be wise to rule out infection, before treating with anti-inflammatory.

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