Cancer Therapy Based On Metabolism Dysfunction

SeamusR

Member
Joined
Feb 26, 2018
Messages
23
Hi All,

I've been studying metabolic theory in relation to Cancer Therapy for some years now & would like to discuss this actively with a larger group.

The goal is to come up with a viable therapy (metabolic systems level, low cost, low toxicity), centered on metabolic paths (no gene mutation theorists please).

I'd specifically like to hear from anyone with a technical background that can refine/enhance what I have come up with.

Areas of special interest would be cell membrane transport, tumor micro environment & nano materials.
Anyone interested ?.

Let me know if you are interested in joining the initiative ?.

regards,

Shay.
 

bawild

Member
Joined
Jan 1, 2016
Messages
33
I'm interested. I've got a friend with adenocarcinoma with unknown primary, metastatic to retroperotineal lymph. Not a good outlook with standard of care therapy, FOLFIRINOX + Herceptin since it's Her2+. I've been scouring PubMed for the metabolic flexibility/plasticity articles. The metabolic flexibility of cancer is formidable. Studies suggest adaptation to OXPHOS if glycolysis/FAO/FAS, glutamine and autophagy are inhibited. Studies also suggest cancer stem cells tend to use OXPHOS and tend to grow and divide more like typical cells.

Have you reviewed Jane McLellands work? She seems to cover many of the pathways to induce apoptosis and sensitize the cancer to low dose chemo. She uses compounds like metformin and statins in certain cases to inhibit cancers or CSCs using primarily OXPHOS. When is OXPHOS inhibition a good strategy? Can the metabolic preferences of a cancer be determined? PANC-1 cells seem to use OXPHOS to proliferate. Pancreatic Physiology/Pathophysiology: Roles of autophagy and metabolism in pancreatic cancer cell adaptation to environmental challenges

Based on what I've read and @haidut posts, it seems like some or all of these may be worth addressing with food, lifestyle, supps and safe drugs.

- Inhibit glycolysis and lactate production (B1, B3, coffee, red light, doxy, mildronate, pyrucet, baking soda, OJ w/MB, thyroid)
- Inhibit lipolysis, FAO, FAS, acyl (niacinamide, aspirin, mildronate)
- Inhibit the glutamine pathway/deplete arginine (glycine, EGCG?, L-NAME (is this available and safe?))
- Inhibit autophagy/mitophagy (EGCG?, PCG-1a inhibitors?)

- Increase NAD/NADH ratio (B3,
- Increase OXPHOS (B1, B2, B3, B6, p5p, biotin, K, Mg, pyrucet, sweet fruit/juices).
- Reduce GSH/increase ROS (OJ + MB (DHAA)+sucrose+K)
- Reduce hypoxia/increase intracellular CO2 (bag breathing, baking soda, acetazolamide, B1)
- Reduce inflammation, histamine & NO (E, aspirin, no PUFA, stearic acid, MB, red light, lapodin, cinnamon, cyproheptadine, agmatine)
- Reduce TLR4 signaling/endotoxin/increase bile acids (raw carrot, charcoal, coconut oil, bamboo shoot, mushroom soup, ketotifen, taurine)
- Reduce extracellular acidosis (baking soda,

- Promote ECT steps (mb, Cu foods, red light, )
- Boost NK cell count/T cell/immune responsiveness. ICIs? (D, forest bathing, baking soda, ? )
- Reduce catabolic stress hormones (estrogen, cortisol, serotonin, adrenalin) - A, E, D, K, contrition, P4, P5, salt, sugar, theanine, famotidine)
- Boost anabolic youth hormones GABA, T/DHT, P4, P5, dopamine
- Increase Ca/Phos ratio. (dairy, gelatin, less muscle meat)

Would love to get more forum input on this and any experience people have implementing metabolic strategies.

https://metabolicpathways.stanford.edu/resources/FullSubwayMap221.pdf
 

LeeLemonoil

Member
Joined
Sep 24, 2016
Messages
2,454
Senescence, Autophagy and Apoptosis are intertwined and cancerous cells are very varied.

Increasing NAD/NADH-ratio is also problematic as a whaolesale approach when cancer already is present. Some cancerous cells thrive on that too.
 

bawild

Member
Joined
Jan 1, 2016
Messages
33
Isn't autophagy a good thing? Why inhibit it?
Here's one study that discusses autophagy

...Basal, but not stress-induced, autophagy is necessary for PaCa cell proliferation, and AA supply is even more critical to maintain PaCa cell growth. To gain insight into the underlying mechanisms, we analyzed the effects of autophagy inhibition and AA depletion on PaCa cell metabolism. PaCa cells display mixed oxidative/glycolytic metabolism, with oxidative phosphorylation (OXPHOS) predominant. Both autophagy inhibition and AA depletion dramatically decreased OXPHOS; furthermore, pharmacologic inhibitors of OXPHOS suppressed PaCa cell proliferation. Roles of autophagy and metabolism in pancreatic cancer cell adaptation to environmental challenges - PubMed

As LeeLemonoil mentions this may be unique to only a few cancers but at least pancreatic seems to use autophagy to get nutrients.
 
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