Studies showing cancer reversal / shrinking

cs3000

@Mauritio its an aldehyde so doesnt sound like a healthy compound / pro metabolic outside of specific use nah (probably best not to take generally outside of cancer) so its one of those things that has an outweighing effect on cancer cells, the anti-cancer dose didnt show toxicity though so i guess healthy cells can deal with that amount well enough but probably some extra burden

apparently low amounts can stimulate cancer growth but higher amounts triggers the apoptosis process (thats normally lacking because of damage making it inefficient, and pH change, needs to be more acidic inside the tissue for apoptosis to happen optimally, cancers are acidic nearby but higher end pH inside - maybe methylglyoxal accumulation makes the tumor more acidic?)

Also it has two carbonyl groups , koch and reinstorff back in the day thought these can be used to take out things with strong bonds that are sticking around blocking mitochondria respiration and enable healthy processes again. maybe @dapose has more to to say on that

Following Glo1 inhibition, cancer cells switch from glycolysis to tricarboxylic acid (TCA) cycle to avoid apoptosis induced by MGO accumulation.

for some reason cancer cells are more sensitive to MGO overload than normal ones even though they have higher glutathione (which sounds to me like the effect is less about damage and more about re-enabling apoptosis unless for some reason they accumulate extreme amounts) https://www.science.org/doi/10.1126/science.160.3832.1140.a

Mauritio

@cs3000 ok thanks.

Mauritio

I feel like oleocanthal and oleurupin deserve more attention.

Check this out. 97% reduction in cancer growth in-vivo!
Mostly by inhibiting estrogen.
But it's also been shown to be effective in other cancers.

"Treatment with 5 mg/kg or 10 mg/kg (−)-oleocanthal resulted in 97% inhibition of tumor growth in orthotopic athymic mice bearing BT-474 tumor xenografts compared to vehicle-treated animals. (−)-Oleocanthal treatment reduced total levels of estrogen receptors in BT-474 cells both in vitro and in vivo. "

"Anticancer activity of (−)-oleocanthal has been demonstrated in different tumor types including breast carcinoma, prostate carcinoma, hepatocellular carcinoma, colon cancer, melanoma, and multiple myeloma (Akl et al., 2014; Elnagar et al., 2011; Fini et al., 2008; Fogli et al., 2016; Pei et al., 2016; Scotece et al., 2013)"

https://pmc.ncbi.nlm.nih.gov/articles/PMC5542686/

the_black_jew

farcarinol (from carrots and related plants like ginseng) and related compounds for colon cancer

also knows as panaxynol or carotatoxin

interestingly-- the nrf2 stimulating activity is apparently higher in relevant dietary doses from carrots than it is from cruciferous vegetable. another contradiction in the peater world

Mauritio

https://bioenergetic.forum/post/40427

cs3000

1 haidut posted before:

BRAF + MEK inhibition therapy {inhibiting MAPK through selective paths} + the doxycylcine antiobiotic = regression in a person who had metastasised melanoma into liver & bile duct
https://pmc.ncbi.nlm.nih.gov/articles/PMC4699264/
https://rupress.org/jem/article/218/9/e20210571/212494/Activation-of-the-integrated-stress-response

alone didnt do much , but helped delay the eventual resistance seen in the yellow line

In the person it gave full remission as doxycycline + the mapk inhibitors

To assess the relevance of our in vitro and preclinical findings, we followed the clinical course of one 73-yr-old female patient at our clinic. The patient was diagnosed with stage III melanoma in 2011 and with a relapse of her disease in 2016 after an episode of jaundice, which was related to a tumor mass in her gallbladder and bile duct.
the presence of brown pigment associated with these cells was highly suggestive for a melanoma metastasis.
Subsequently BRAF-MEK inhibitor therapy was initiated. Response assessment after four cycles showed that while the liver metastasis had responded to the treatment, the gallbladder did not.
Due to a skin infection (an acne-like rash) the patient received doxycycline during her fifth BRAF-MEK inhibitor cycle for a total of 12 d.
Strikingly, the gallbladder metastasis started to regress after six cycles, as measured by CT scan, and the PET-CT scan after eight cycles showed a complete response. The patient was under BRAF-MEK inhibitor therapy and had a persistent response for >36 mo (Fig. 6 C). This particular case study highlights the potential clinical benefit of using tetracyclines to sensitize intrinsically resistant lesions to MAPK inhibitors.

*Lipoic acid is a mapk inhibitor, and showed decent effects slowing tumors alone i posted in the first post.
https://onlinelibrary.wiley.com/doi/10.1155/2022/1894379

ALA inhibited a variety of mitogen-activated protein kinase (MAPK) signaling pathways in the epithelial cells

So i wonder if a combo of lipoic acid + doxycycline could be good for giving regression of melanoma / metastasised melanoma to other areas
50 - 150uM is too high to hit in vivo probably, its like 20ug/ml blood i think
so maybe for topical applied to melanoma as the combo. lipoic acid can penetrate if absorbs in right thing, propylene glycol or heated mct oil. not sure about doxycycline . But short half life on lipoic so would have to get a lot in
https://pmc.ncbi.nlm.nih.gov/articles/PMC3648887/ here they got 14ug/cm2 to pass through normal skin
but melanoma = melanocytes so i guess easier to penetrate as doesnt have the outer SC layer?
maybe theres something else for systemic use

extra: (not showing remission but metastasis effect)
B-Glucan (particulate) melanoma matastasis prevention
https://www.researchgate.net/publication/327193765_Beta-glucan-induced_inflammatory_monocytes_mediate_antitumor_efficacy_in_the_murine_lung

oat b-gluten best effect at 200kda size
https://www.researchgate.net/publication/320392541_Systemic_Administration_of_bglucan_of_200_kDa_Modulates_Melanoma_Microenvironment_and_Suppresses_Metastatic_Cancer

turkey tail glucan is 100kda https://pmc.ncbi.nlm.nih.gov/articles/PMC10000499/

Feeding inhibition effect (but is anti androgen)
https://pubmed.ncbi.nlm.nih.gov/26408688/

cs3000

Another showing regression of existing tumors
human squamous cell carcinoma

Feeding high amounts of silymarin
(note silymarin / milk thistle inhibits thyroid hormone transport, not suitable for general use)

Shrank the pre existing tumors

doi.org/10.1093/carcin/23.3.499

melanoma, 500mg/kg ~ 3g human only using 1 dose every 2weeks slowed
but didnt regress (maybe lower dose more often could have too)
10.1002/mc.22208

200mg/kg 5days a week for 5 weeks , didnt show kidney or liver toxicity 10.1177/1010428318776170
stalled growth in an oral tumor until the end, but didnt get to regression

Can penetrate skin in Propylene glycol and stays in skin cells for long while https://www.sciencedirect.com/science/article/abs/pii/S0378517322009863

glycerol / glycerine increases growth of some tumors so probably not appopriate as to use for entry
https://pmc.ncbi.nlm.nih.gov/articles/PMC8908677/

Propylene glycol is different. maybe some connection but is used as penetration enhancer in anti tumor studies with effect still so
https://pubmed.ncbi.nlm.nih.gov/23186833/

Mct oil might be good if it dissolves well, warmed in a saucepan

cs3000

@cs3000
450mg daily created regression in this persons liver tumor, to half its size. but the effects stalled and it re-grew after around a year
https://pmc.ncbi.nlm.nih.gov/articles/PMC2769275/

Ultrasonography in our outpatient department revealed a large tumour with central necrosis, measuring about 11 cm in diameter,
CT scan of the liver was performed again and revealed HCC regression, with tumour size reduced to about 4.6 cm in diameter, and portal vein thrombosis (Figure 3).
Silymarin 450 mg daily was the only regularly prescribed medicine during HCC reduction.
The tumour size did not contract persistently as shown by abdominal echo. CT scan of the liver was performed prior to the surgery, revealing an HCC size similar to the previous readings and portal vein thrombosis.

@cs3000 said in Studies showing cancer reversal / shrinking:

Another showing regression of existing tumors
human squamous cell carcinoma
Feeding high amounts of silymarin
( note silymarin / milk thistle inhibits thyroid hormone transport, not suitable for general use)
Shrank the pre existing tumors

cs3000

Natural compound Physachenolide C (but not commercially available yet) gave complete remission in melanoma. in 1/3 of the mice it stayed regressed. (in the other 2/3, maybe doxycycline could have brought back the effect)
its a highly potent BET inhibitor

https://pmc.ncbi.nlm.nih.gov/articles/PMC8571524/#sec0011

enhanced immunotherapy for regression (enhance with b-glucan?)
https://pmc.ncbi.nlm.nih.gov/articles/PMC8802328/#S19

cs3000

interesting find - if u target a main 2% subset of melanoma cells the tumor goes in most cases without destroying the other part. if some are left theres potential for the regression to return
(does doxycyline help these ones get destroyed when combined with inhibitors?)

https://www.pnas.org/doi/10.1073/pnas.1009069108

we revealed that established tumor lesions can be efficiently eradicated by targeted elimination of the less than 2% subset of melanoma cells with the CD20+ high molecular weight melanoma-associated antigen (HMW-MAA)+ phenotype without targeting the tumor cell mass, whereas targeted elimination of any minor subset is less effective.
These data provide a strategy for improving the biological therapy of melanomas and, moreover, for redesigning current drug development paradigms used in the treatment of cancer.

HMW-MAA+ cells gave rise to melanomas upon transplantation, whereas sorted HMW-MAA− cells from the same melanoma did not.
indicating that these cells exhibit melanoma-initiating capacities.
T cells with redirected specificity for CD20 eradicated established melanoma lesions in four out of five melanoma biopsies, although the targeted cells represented less than 2% of melanoma cells.
It is noteworthy that transplanted tumors of patient 5, in which no CD20+ melanoma cells were detected, could not be eradicated by a CD20-redirected T-cell attack.

Where tumors were eradicated, no tumor relapse occurred during the observation period of >36 wk.
Because no tumor relapse was observed in any case during the >36 wk observation period, such melanoma eradication is obviously long lasting
We conclude that CD20 is not functionally crucial but marks a specific cell population. The unexpected observation, however, is that targeting the minor CD20+ melanoma cell population is as effective as targeting the majority of tumor cells. A caveat for a broad therapeutic application is that obviously some melanomas, in our cohort one out of five patients, do not harbor CD20+ melanoma cells

The observation that the specific elimination of a minor subset of tumor cells results in eradication of established melanoma lesions is crucial for the understanding of the biology of melanoma. Continuous melanoma growth obviously requires the presence of a minor population of cells, which displays the CD20+ HMW-MAA+ phenotype;Elimination of these cells is obviously required to eradicate the melanoma irrespective of the bulk of tumor cells

cs3000

@cs3000 WIlliam Koch the chemistry of natural immunity, cases at the bottom pages showing amazing recoveries

https://ia801601.us.archive.org/2/items/TheChemistryOfNaturalImmunityWilliamKoch/The chemistry of natural immunity William Koch.pdf

@cs3000 said in Studies showing cancer reversal / shrinking:

Human trial with methylglyoxal {aka pyruvaldehyde} (william Koch compound)
https://web.archive.org/web/20161017113947/http://www.cancer-therapy.org/CT/v4/B/HTML/17. Talukdar et al, 205-222.html

Long term in a variety of cancers, ~80% of the people had remission or stability
,