treatment protocol gliosarcoma
I have kept in touch with Daniel for months and my friend Marcos. My lack of time has prevented me from participating in the forum.
My mother is having new growth of glioblastoma (diagnosed in 2015)
We are using the same 2DG metronomic protocol as Marcos. Currently it seems that everything is stable.
I will share our treatment line. Any suggestions will be appreciated:
- Nanothermia 2 times a week at 120w
- 2DG Metronomic once a week at 3grs. (3ml / h.) Combined one day with nanothermia
- 80mg temozolamide combined the two days of 2DG
- 600 mg of ribavirin every day
- 200 mg celecoxib every day
-1700 mg metformin every day
- 10 ml empty liposomes all days (20ml in nanothermia days)
- 100mg canagliflozin combined 1 day with nanothermia
(distanced 48 hours from 2DG)
I am studying taurolidine .... and a peptide vaccine directed to the PTEN mutation
Daniel suggested me:
- Besentabs but they can also help reduce the acidity around the tumor and that may be good for glyoblastoma that are highly acidic. Just that we need to clarify the impact on the absorption of temozolamide.
- Add another cycle of metronomic 2dg in the week
-Add another mitochondria inhibitor next to Metformin like Atovaquone
-Add an MCT1-MCT4 inhibitor like Ibuprofen if possible, to reduce the lactic acid export that may result following the use of Metformin
-Use other glycolysis inhibitors during the days my mom is not on 2DG. One that is accessible is Vitamin C in high dose, but you can try to search for other glycolysis inhibitors.
If not, maybe you extended the use of canagliflozin to a time closer to 2DG admin but not overlapping that ............................. ..........
I hope to participate in the forum!
Best regards to all
Thank you so much for taking the time to write this comment. I understand how difficult it is as you have so much to take care of, including taking care of your dear mom and working full time as the same time. So please use your time for that instead of spending time discussing on this website. What i only ask from you and others with whom I communicate by e-mail is that when there are general questions (not personal), please ask them on this website from time to time so that others can benefit from the related discussion. This is because lately I spend most of my time answering e-mails and calls, and as a result I have no more time to reflect the learnings here on the website so that others benefit.
I would also like to add again that all the ideas and knowledge I share with you or others (including that going through private communications) goes with the Disclaimer on this website. Everyone has to use that as input only while discussing with their medical doctor the best approach in line with patient’s status, and should not replace the medical advice.
Beyond that, I am happy to hear about the fact that your mom is doing better and she is now in a stable situation since you implemented approaches to support chemo, which as I understood was not anymore effective prior to that. I very much think 2DG metronomic plays a major role in that outcome.
Indeed, I think Taurolidine is a treatment approach that is relevant for glioblastoma, but it requires an intensive treatment.
Increasing slightly the frequency of 2DG metro may be an easier approach that could help.
The priority for me would be to build a coherent strategy. So that even if there are drugs that may be very relevant, if we really need to take out some in order to add more along the strategy, I would take out those that are not part of the specific strategy.
In my view, one of the essential strategy in GMB is related to the fact that GMB is known to be very glycolitic. This is why I would build the strategy such that will address that aspect as good as possible. Having this in mind, here is how I think:
– Metfomin – has high priority as a part of the metabolic approach and pH approach (even if it is increasing glycolisisi it will decrease blood glucose levels and will address the cancer cells relying on respiration – using Metformin, means we also need to make sure we add glyco inhibitors)
– QUETIAPINE is a good one but we can remove if we need to make place for another better drug – therefore, this drug has medium priority
– Ezitimibe – medium priority as it is part of the cholesterol approach (which is good but this is another strategy)
– Statin – medium to high priority as it is part of the metabolic, pH and cholesterol approach
– NAPROXEN or CELEBREX – high priority due to anti inflammation action that is important specifically for brain c patients
– Mebendazole/Fenbendazole – high priority but would use only one of them instead of two at the same time (e.g. one week one and the other week another one) to make space for more drugs
– SODIUM PHENYLBUTIRATE – high priority due to relevance to brain c patients (is may act like DCA)
– Thalidomide – medium priority (although good for anti angiogenesis effect)
– Tamoxifen – high priority (multiple actions)
– Aspirin low dose – high priority (anti inflamation)
– CANAGLIFLOZIN – high priority (anti glycolisis)
– Supplements you use are very good in my view
Therefore, based on the list above you could remove QUETIAPINE, Ezitimibe, Thalidomide. That doesn’t mean they are not good, it’s just making choices given the limitations. We could always start them again at a latter point.
By removing those, I would make space to introduce:
– Acetozolamoide or TOPIRAMATE to address CA IX (pH strategy)
– Stiripentol which is a LDH inhibitor (metabolic strategy) https://www.cancertreatmentsresearch.com/a-list-of-mitochondria-inhibitors/#comment-7986
– Syrosingopine would be great to inhibit MCTs but this is difficult to find https://www.ncbi.nlm.nih.gov/pubmed/30540938
Of course, if we feel that things are going right as used now, I would not change anything.
But it’s important that we keep in mind the profile of GMB as highly glycolitic and the fact that we now know and have tools to influence that. I like cholesterol strategy a lot but I think its important to be stronger on the metabolic line, that is why some of the drugs from the list above and part of the cholesterol strategy have lower priority – it’s all about the context and limitation of nr of drugs we can use.
From a metabolic point of view, the drugs in the list above are doing the following:
– Metformin (mito activity lowering and blood glucose lowering),
– Statin (MCT lowering).
– Aspirin (MCT lowering),
– Mebendazole/Fenbendazole (GLUT1 lowering)
– Sodium Phenylbutyrate (activate mito if not the case)
– Tamoxifen (fibroblast lowering if any in brain c – they are suppliers for fuel)
– Canaglifozin (glucose transport lowering)
– Omega 3 may lower Na/H exchange
If glycolisis is still active, Acetozolamoide will help to acidify the cell when using glyco so it can be killed. https://www.cancertreatmentsresearch.com/ph-cancer-a-top-treatment-strategy/
And Stiripentol will try to stop glycolisis somewhere at a downstream level.
Tranilast, I like it a lot but maybe Tamoxifen is enough to address fibroblast (in brain c the existence of fibroblasts is a little debate, in literature).
Manuel, I hope the above helps!