Alleged Cancer Cure

Texon

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Roundworms, pinworms, hookworms, Oh-My...There was a study done on Fenbendazole. It was only effective combined with Gamma Vit. E
@bzmazu @haidut Actually, the guy on the blog discusses several instances where the only medicine taken is the FZ. Plus, the original discovery was apparently by a lady who worked at Merck's animal medicine division, who used only FZ to cure her GB brain cancer. What I found really disgusting though was the email from MD Anderson, who tried to claim it was their research in 2002 that helped the guy. In fact, MDA never mentioned anything about FZ or MZ while "caring" for him.
 

Memento

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From: Repurposing Drugs in Oncology (ReDO)—mebendazole as an anti-cancer agent

While there are rare reports of reversible alopecia, urticaria, rash, gastro-intestinal upset, leukopenia, and neutropenia in some patients treated with high-dose MBZ, all adverse effects associated with other microtubule disruption agents, there do not appear to be any reports of peripheral neuropathy, which is commonly considered a classic adverse effect of microtubule disrupting agents, including the taxanes and the vinca alkaloids [27]. While this may suggest that the action of MBZ is independent of microtubule disruption, it may also be related to the fact that MBZ acts via the colchicine-binding domain, and that like colchicine, there is little effect in terms of neuropathic pain [28]. Of course, it is also possible that the anticancer activity of MBZ is mediated by additional molecular targets yet to be elucidated.

MBZ appears to be effective through p53-dependent and independent pathways
. For example, in lung cancer cell lines, it was found that MBZ treatment caused post-translational p53 stabilization and the downstream expression of p21 and MDM2 [14]. In p53-null lung cancer cells exposure to MBZ caused cytochrome c accumulation, activation of caspase-9 and caspase-8, and cleavage of PARP and procaspase-3. This independence of p53 status is also evident in the analysis of melanoma cells, where wild-type and mutant p53 cell lines were sensitive to MBZ [17].

There has been conflicting evidence regarding the effect that MBZ has on tumour neo-vascularisation
, with some reports finding evidence that it has an anti-angiogenic effect and others finding none.

In the earliest work on the anti-cancer activity of MBZ, Mukhopadhyay and colleagues reported an anti-angiogenic effect on human lung cancer xenograft models [14]. However, in vivo analysis of adrenocortical cancer models failed to detect any anti-angiogenic activity compared to controls [16]. Some support for an anti-angiogenic action comes from an in silico study, which indicated that MBZ inhibits the action of VEGFR-2 by binding to it, a finding validated in vitro using a human umbilical vein endothelial cell (HUVEC) based angiogenesis functional assay [29]. Of note, the related drug albendazole has shown anti-angiogenic properties in an ovarian cancer model and in drug-resistant cell lines [30, 31], suggesting that an anti-angiogenic action may be common across a number of benzimidazoles.

To date, the effect of MBZ or other benzimidazole on the immune response in cancer has not been investigated, though there is some evidence that albendazole synergised to stimulate the cellular immune response in mice treated for alveolar echinococcosis with the immunotherapeutic agent liposomal muramyl tripeptide phosphatidylethanolamine (L-MTP-PE) used in the treatment of osteosarcoma [32]. There is also increasing evidence that existing microtubule disrupting agents used at low or metronomic doses, including the taxanes and vinca alkaloids, exert a positive immunomodulatory action that may help to reverse the immunosuppressive effect of cancer [3336]. We can speculate, mechanistically, that some of this immunomodulatory action is related to microtubule dynamics. Therefore, there may be a similar effect with MBZ and other benzimidazoles, and this may also be a factor in the anti-cancer effects of these drugs.

So I don't think it is only about microtubule disruption. @Obi-wan
 

Obi-wan

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Repurposing Drugs in Oncology (ReDO)—mebendazole as an anti-cancer agent

"Mebendazole (MBZ) is a broad-spectrum benzimidazole anti-helminthic drug, in the same class as albendazole, flubendazole, oxfendazole, and others. It is commonly prescribed to treat a range of parasitical worm infections, including threadworm, tapeworms, roundworms, and other nematode and trematode infections in humans and domestic animals"

"The anti-parasitic action of MBZ is due to its action as a microtubule-disrupting agent acting to prevent the polymerisation of tubulin in the gut of helminths, causing the parasites to die [25]. Tubulin is vital to cell division and is therefore a cancer target for several widely used chemotherapy drugs, including paclitaxel, colchicine, and vincristine. MBZ, as with the other benzimidazoles, binds to the colchicine-binding domain of tubulin [26].The inhibition of tubulin polymerisation by MBZ has been confirmed in vitro in a glioblastoma model [19] and in a melanoma model [17]. The latter work suggested that the apoptotic response to microtubule disruption is mediated by Bcl-2 phosphorylation. Subsequent work on melanoma confirmed this result, and also showed that MBZ decreased the levels of X-linked inhibitor of apoptosis (XIAP) [18], but to date this has not been confirmed in non-melanoma cell lines."
 
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Braveheart

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@bzmazu @haidut Actually, the guy on the blog discusses several instances where the only medicine taken is the FZ. Plus, the original discovery was apparently by a lady who worked at Merck's animal medicine division, who used only FZ to cure her GB brain cancer. What I found really disgusting though was the email from MD Anderson, who tried to claim it was their research in 2002 that helped the guy. In fact, MDA never mentioned anything about FZ or MZ while "caring" for him.
Here is another dewormer...Ivermectin Antiparasitic Anticancer Wonder Drug - Jeffrey Dach MD
 
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Thanks for sharing! I think @Obi-wan might be interested too:

https://www.researchgate.net/profil...ncer_cells/links/53da4a7b0cf2a19eee88382e.pdf

Repurposing Drugs in Oncology (ReDO)—mebendazole as an anti-cancer agent

Maybe this deserves its own thread? Anti helmintics for cancer in general or something like that?

I already posted about mebendazole. Unfortunately the thread didnt get much attention. There is some additional info about how it works. And info about some other uses of MBZ in case of diabetes or stress.
Repurposing Mebendozole As An Anti-cancer Agent And Anti-diabetes Drug
 

Obi-wan

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Or your favorite Artemisinin

"Artemisinin and its derivatives have been used for the treatment of malarial and parastic worm (helminth) infections. They have the advantage over other drugs in having an ability to kill faster and kill all the life cycle stages of the parasites."


Helminthiasis[edit]
A serendipitous discovery was made in China in the early 1980s while searching for novel anthelmintics for schistosomiasis that artemisinin was effective against schistosomes,[17][18][19] the human blood flukes, which are the second-most prevalent parasitic infections, after malaria. Artemisinin and its derivatives are all potent anthelmintics.[20] Artemisinins were later found to possess a broad spectrum of activity against a wide range of trematodes, including Schistosoma japonicum, S. mansoni, S. haematobium, Clonorchis sinensis, Fasciola hepatica, and Opisthorchis viverrini. Clinical trials were also successfully conducted in Africa among patients with schistosomiasis.[21]

Cancer[edit]
Artemisinin and derivatives have been studied in many animal models. They can inhibit various molecules including catenin, adenosine monophosphate (AMP), cyclins and cyclin-dependent kinases that are involved in cancer development. They can cause cell death (apoptosis) in different cancer cells through activation of caspase-3 and caspase-9.[22] Their anticancer activity relies on their ability to produce reactive oxygen species. As of 2018, human clinical trials and other clinical research had been conducted in lung, colorectal, breast, liver, pancreas, glioma and cervical cancers, but the studies were too small to generalize from.[23]
 

Obi-wan

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Or your favorite Artemisinin

"Artemisinin and its derivatives have been used for the treatment of malarial and parastic worm (helminth) infections. They have the advantage over other drugs in having an ability to kill faster and kill all the life cycle stages of the parasites."


Helminthiasis[edit]
A serendipitous discovery was made in China in the early 1980s while searching for novel anthelmintics for schistosomiasis that artemisinin was effective against schistosomes,[17][18][19] the human blood flukes, which are the second-most prevalent parasitic infections, after malaria. Artemisinin and its derivatives are all potent anthelmintics.[20] Artemisinins were later found to possess a broad spectrum of activity against a wide range of trematodes, including Schistosoma japonicum, S. mansoni, S. haematobium, Clonorchis sinensis, Fasciola hepatica, and Opisthorchis viverrini. Clinical trials were also successfully conducted in Africa among patients with schistosomiasis.[21]

Cancer[edit]
Artemisinin and derivatives have been studied in many animal models. They can inhibit various molecules including catenin, adenosine monophosphate (AMP), cyclins and cyclin-dependent kinases that are involved in cancer development. They can cause cell death (apoptosis) in different cancer cells through activation of caspase-3 and caspase-9.[22] Their anticancer activity relies on their ability to produce reactive oxygen species. As of 2018, human clinical trials and other clinical research had been conducted in lung, colorectal, breast, liver, pancreas, glioma and cervical cancers, but the studies were too small to generalize from.[23]


Artemisinin Blocks Prostate Cancer Growth and Cell Cycle Progression by Disrupting Sp1 Interactions with the Cyclin-dependent Kinase-4 (CDK4) Promoter and Inhibiting CDK4 Gene Expression

Artemisinin Blocks Prostate Cancer Growth and Cell Cycle Progression by Disrupting Sp1 Interactions with the Cyclin-dependent Kinase-4 (CDK4) Promoter and Inhibiting CDK4 Gene Expression*

"The anti-malarial effects of artemisinin are achieved by a two-step mechanism. First, intraparasitic heme-iron catalyzes cleavage of the endoperoxide bridge. Breakage of the endoperoxide bridge then leads to formation of free hydroxyl radicals that cause extensive damage eliminating the parasites (27). Iron is an essential micronutrient for cell growth that plays an important role in energy metabolism and DNA synthesis, and iron levels are much higher in cancer cells compared with normal cells (28). This suggests that artemisinin may be more selective in its toxicity and in that it is more effective at killing cancer cells while normal cells are relatively unaffected. Although this effect may play a role in the anti-proliferative effects of artemisinin on LNCaP cells, it does not appear to be the primary mode of action. LNCaP cells treated with artemisinin in the presence of anti-oxidants ascorbic acid or dithiothreitol still displayed a strong G1 cell cycle arrest and down-regulation of CDK2 and CDK4 expression mirroring LNCaP cells treated with artemisinin alone (data not shown). This result suggests that anti-proliferative effects of artemisinin on prostate cancer cells, and likely other cancer cell types, are independent of its oxidative potential. In this regard, we observe a similar effect of artemisinin on other types of human reproductive cancer cells."

@bzmazu what is the difference between Artemisinin and Artemisia?
 
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Braveheart

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Artemisinin Blocks Prostate Cancer Growth and Cell Cycle Progression by Disrupting Sp1 Interactions with the Cyclin-dependent Kinase-4 (CDK4) Promoter and Inhibiting CDK4 Gene Expression

Artemisinin Blocks Prostate Cancer Growth and Cell Cycle Progression by Disrupting Sp1 Interactions with the Cyclin-dependent Kinase-4 (CDK4) Promoter and Inhibiting CDK4 Gene Expression*

"The anti-malarial effects of artemisinin are achieved by a two-step mechanism. First, intraparasitic heme-iron catalyzes cleavage of the endoperoxide bridge. Breakage of the endoperoxide bridge then leads to formation of free hydroxyl radicals that cause extensive damage eliminating the parasites (27). Iron is an essential micronutrient for cell growth that plays an important role in energy metabolism and DNA synthesis, and iron levels are much higher in cancer cells compared with normal cells (28). This suggests that artemisinin may be more selective in its toxicity and in that it is more effective at killing cancer cells while normal cells are relatively unaffected. Although this effect may play a role in the anti-proliferative effects of artemisinin on LNCaP cells, it does not appear to be the primary mode of action. LNCaP cells treated with artemisinin in the presence of anti-oxidants ascorbic acid or dithiothreitol still displayed a strong G1 cell cycle arrest and down-regulation of CDK2 and CDK4 expression mirroring LNCaP cells treated with artemisinin alone (data not shown). This result suggests that anti-proliferative effects of artemisinin on prostate cancer cells, and likely other cancer cell types, are independent of its oxidative potential. In this regard, we observe a similar effect of artemisinin on other types of human reproductive cancer cells."

@bzmazu what is the difference between Artemisinin and Artemisia?
Artemisinin is the pure processed form where Artemisia is the leaf extract, hence the price difference...Artemisa has abundant other plant anti cancer properties and is recently thought to actually be more effective...
Artemisia Annua, Artemisinin & 2015 Nobel Prize in Medicine - A Cancer Fighting Plant - Mihaela Catalina Stanciu Foundation for Life
 

Obi-wan

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All this talk about worms and parasites and how the med that cures them is also effective against cancer makes me wonder about this old idea Cancer as a Parasitic Disease - Jeffrey Dach MD

@bzmazu This is a very interesting

"Dr Tu Youyou ultimately isolated the active molecule in the tea, called artemisinin (figure 1 above), an effective anti-malaria drug, for which she received the 2015 Nobel prize in Medicine. Artemisinin and derivatives like artesunate are now life saving malaria drugs used by millions."

Antimalarial Drugs are Also Anti-Cancer Drugs

Dr. Das reports in a 2015 article that Artemisinin (or derivatives) are effective against 55 cancer cell lines with inhibitory effects against pancreatic cancer, osteosarcoma, lung cancer, colon, melanoma, breast, ovarian, prostate, central nervous system, lymphoma, leukemia and renal cancer cells. (1)

The molecular mechanism by which artemisinin compounds serve as effective anti-cancer agents can be found in its molecular structure, the endo-peroxide bridge which reacts with the iron molecule

Cancer cells express high levels of the transferrin receptors for internalizing iron (Fe) at a tremendous rate.(21) This is a useful difference from normal cells. The cancer cells have a voracious appetite for Iron, and contain massive quantities of iron compared to normal cells. In addition, the transport mechanism for iron in cancer cells, called transferrin receptors are massively up-regulated.(18) In fact, a correlation between expression of transferrin membrane receptor and Ki-67 (a marker of tumor proliferation) has also been reported,(19) The more aggressive the tumor, the greater number of transferring receptors. This difference in iron content and iron transport is why artemisinin compounds kill cancer cells selectively while sparing normal cells.

We believe that this perinuclear clustering of lysosomes is, in fact, an indication of autophagy induction. We observed increase of mitochondrial ROS implicating lysosomal iron as a critical mediator in ART-induced mitochondrial ROS production and cell death. It is possible that enhanced lysosomal degradation of ferritin induced by ART leads to the transient increase of cytosolic ferrous iron, which then affects the mitochondria, leading to enhanced mitochondrial ROS production.”(6)
 
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Braveheart

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@bzmazu This is a very interesting

"Dr Tu Youyou ultimately isolated the active molecule in the tea, called artemisinin (figure 1 above), an effective anti-malaria drug, for which she received the 2015 Nobel prize in Medicine. Artemisinin and derivatives like artesunate are now life saving malaria drugs used by millions."

Antimalarial Drugs are Also Anti-Cancer Drugs

Dr. Das reports in a 2015 article that Artemisinin (or derivatives) are effective against 55 cancer cell lines with inhibitory effects against pancreatic cancer, osteosarcoma, lung cancer, colon, melanoma, breast, ovarian, prostate, central nervous system, lymphoma, leukemia and renal cancer cells. (1)

The molecular mechanism by which artemisinin compounds serve as effective anti-cancer agents can be found in its molecular structure, the endo-peroxide bridge which reacts with the iron molecule

Cancer cells express high levels of the transferrin receptors for internalizing iron (Fe) at a tremendous rate.(21) This is a useful difference from normal cells. The cancer cells have a voracious appetite for Iron, and contain massive quantities of iron compared to normal cells. In addition, the transport mechanism for iron in cancer cells, called transferrin receptors are massively up-regulated.(18) In fact, a correlation between expression of transferrin membrane receptor and Ki-67 (a marker of tumor proliferation) has also been reported,(19) The more aggressive the tumor, the greater number of transferring receptors. This difference in iron content and iron transport is why artemisinin compounds kill cancer cells selectively while sparing normal cells.

We believe that this perinuclear clustering of lysosomes is, in fact, an indication of autophagy induction. We observed increase of mitochondrial ROS implicating lysosomal iron as a critical mediator in ART-induced mitochondrial ROS production and cell death. It is possible that enhanced lysosomal degradation of ferritin induced by ART leads to the transient increase of cytosolic ferrous iron, which then affects the mitochondria, leading to enhanced mitochondrial ROS production.”(6)

Enhanced mitochondrial ROS production. This is obviously really good news...for everybody's library on Artemisinin....Artemisinin our Ultimate Cancer Weapon a Gift from China - Jeffrey Dach MD
 

CLASH

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Perhaps adding medicinal mushrooms such as maitake, shiitake, enokitake, lions mane, reishi, chaga and/ or turkey tail would synergize with the herbal targeting of the cancer cells by simultaneously enhancing the immune system to attack the cancer as well; a two pronged approach.

Conjoin this with a sound diet to stop the inflammation that lead to the cancer and pro-metbolic substances to change the context with which the cancer exists and you have a multi-pronged approach hitting the pathology from different angles:

1) enhancement of immune attack on the canced by medicinal mushrooms

2) direct attack of the cancer by herbal compounds

3) stopping of the inflammation by adjusting the diet

4) changing of the physiologic context of the body with which the cancer exists by using pro-metabolic substances



*A bit tangential but theres often talk on the forum of cancer cells requiring/ addicted to fatty acids. What if the cells are addicted to the fatty acids so that they can restore themselves to a proper energetic state i.e. what if someone with cancer ate a diet high in beef tallow, coconut oil, cocoa butter with the above approach? Would the fats help to stabilize the cancer cells energy metabolism such that they differentiate back into normal cells/ undergo apoptosis (this doesnt imply low carb, carbs can still be kept to adequate levels with adequate protein)?
 

Texon

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This is an amazing testimonial!
For sure. As usual though the hard part is getting the news out to as many people as possible....and the white coat syndrome that elevates MD's to godlike status. Did you like the part where MD Anderson emailed the guy to say they were so happy he had gotten benefits from their research?
 

Obi-wan

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For sure. As usual though the hard part is getting the news out to as many people as possible....and the white coat syndrome that elevates MD's to godlike status. Did you like the part where MD Anderson emailed the guy to say they were so happy he had gotten benefits from their research?


Fenbendazole acts as a moderate microtubule destabilizing agent and causes cancer cell death by modulating multiple cellular pathways

Fenbendazole acts as a moderate microtubule destabilizing agent and causes cancer cell death by modulating multiple cellular pathways


"Altogether, our findings show microtubule disruption, p53 stabilization and interference with glucose metabolism as collective underlying mechanisms of FZ induced preferential elimination of cancer cells both in vitro and in vivo."

This is better than the chemo drug that I am currently on (Taxotere)

8ad6b7_1ceb511a6012468eb56a6149977493f1~mv2_d_3024_4032_s_4_2.jpg
 

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