Obi-wan
Member
- Joined
- Mar 16, 2017
- Messages
- 1,120
-
By using this site you agree to the terms, rules, and privacy policy.
-
Charlie's Restoration Giveaway #2 (Entire Home EMF Mitigation & Protection Along With Personal Protection) - Click Here To Enter
-
Dear Carnivore Dieters, A Muscle Meat Only Diet is Extremely Healing Because it is a Low "vitamin A" Diet. This is Why it Works so Well...
Rest the rest of this post by clicking here
-
The Forum is transitioning to a subscription-based membership model - Click Here To Read
Click Here if you want to upgrade your account
If you were able to post but cannot do so now, send an email to admin at raypeatforum dot com and include your username and we will fix that right up for you.
GAF
Member
I am glad to hear about immune system boosting qualities of these products. I am going to keep some handy and at the first inkling of any kind of toxin attack, I will super boost my immune response.
Obi-wan
Member
- Joined
- Mar 16, 2017
- Messages
- 1,120
"Feverfew appears to deplete glutathione in the cancer cells and causes cell death while leaving healthy cells unaffected."
Obi-wan
Member
- Joined
- Mar 16, 2017
- Messages
- 1,120
"SASP-induced cystine/cysteine starvation leading to glutathione depletion may be useful for therapy of prostate cancers dependent on extracellular cystine."
''Interfering with one of the two reactions furnishing energy to tumour cells is not enough to kill them,'' noted Dr. Warburg and colleagues from the Kaiser Wilhelm Institute for Biology back in 1927. ''It is necessary to stop both respiration and fermentation, if the cells are to be killed for want of energy.'' THE METABOLISM OF TUMORS IN THE BODY
Texon
Member
- Joined
- Nov 28, 2016
- Messages
- 671
@haidut @Regina @bzmazu @burtlancast Here is probably my favorite excerpt from the cancer patient's blog,
"After he very excitedly told me the continued good news of being "all clear" for a second consecutive quarter, I asked him a "very loaded" question. I asked, "Doc, what is really going on here? Can you disclose to me how I am doing versus all of the other patients on the clinical trial with the exact same condition"?
His answer was what I already suspected. He said, "Joe we can't explain it, but you are kind of a sole data outlier right now." Meaning with hundreds of like kind patients, I was the only one with a cure. I knew then my other alternative regimen was largely responsible, but I decided to come clean anyway.
I said, "Doc, I'm glad you told me that about my results within the trial, because I have something to share with you". I proceeded to tell him all about the canine dewormer as I watched his jaw drop :)
His next words I'll never forget (and remember for context he and I had become good friends by this time). He said, "You little s###, I knew there was something up with you.....and....I've had some weird days here at MD Anderson, but this one probably tops them all."
His next sentence almost floored me. He said, "You know, we've known for decades that these anthelmintic class of drugs (meaning to destroy parasites in the intestines) could have possible efficacy against cancer, and in fact in the 80's and 90's there was a drug called Levamisole that was used on colon cancer and it is an anthelmintic drug."
I said, "Doc, if you have known for decades why hasn't more work been done on it?" His answer was honest. He said, "Probably because of money...all of these drugs are far off-patent and nobody is going to spend a gazillion dollars to repurpose them for cancer.....only to have generic competition the next day."
I knew he was right.
And he knew I was onto something incredible for me and my story.
As I said, levamisole is the one that started it all but all *soles *zoles likely have the same effects.
Obi-wan
Member
- Joined
- Mar 16, 2017
- Messages
- 1,120
Found these two studies of interest:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC124244/pdf/pq1102007408.pdf
"VES, an esterified vitamin E analog, has little antioxidant activity"
VES is Vit E Succinate
https://www.researchgate.net/publication/260343692_Effects_of_fenbendazole_and_vitamin_E_succinate_on_the_growth_and_survival_of_prostate_cancer_cells
"Vitamin E succinate (VES), the most potent derivative of vitamin E for anti-
tumor activity"
"Fenbendazole is a benzimidazole drug commonly used
for treating pinworm outbreaks in laboratory rodents"
See A Pinworm Medication Is Being Tested As A Potential Anti-Cancer Drug
"Some of the lab animals got infected with pinworms, the same parasite my son had. The veterinarian at Johns Hopkins treated the whole colony of mice with an animal version of mebendazole.
The drug staved off the parasite, but it also did something surprising. Before the mice were treated for pinworms, Riggins and his team had implanted cancer cells into the animals' brains.
But after the mice got the pinworm drug, the cancers never developed. "Our medulloblastoma stopped growing,"
Per https://www.researchgate.net/public..._growth_and_survival_of_prostate_cancer_cells
"FBZ+VES significantly inhibited growth of PCa cells
and induced apoptosis in vitro. To our knowledge, this is
the first time these drugs have been tested together in
PCa cell lines. In a previous study, a concentration of 50
µg/ml of VES was shown to be effective on PC-3 cells
(Malafa et al., 2006). For FBZ, we tested a range of
concentrations based on a dosage used for Mebendazole
treatment of melanoma cells in culture (Doudican et al.,
2008). A dosage of 25 µg/ml of VES and 14 ng/ml of FBZ
was optimal for the treatment of prostate cancer cell lines
we tested. Higher concentrations of FBZ produced a
rapid rate of cell death during the initial 48 h period and
lower concentrations did not cause any change in cell
growth compared to controls. The agents were combined
at the specified dosages because alone neither produced
results that were as striking as when they were together.
This synergistic ability of inhibition is very interesting,
although the mechanisms involved is unclear. One
hypothesis is that vitamin E activates multiple pro-
apoptotic pathways such as targeting NF-κΒ (Ni and Yeh,
2007), and caspase-4 (Malafa et al., 2006), and if used
with an agent that inhibits cell division such as one of the
benzimidazoles, can be antagonistic to tumor growth.
These agents are worth further exploration since they are
both relatively safe and easy to administer."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC124244/pdf/pq1102007408.pdf
"VES, an esterified vitamin E analog, has little antioxidant activity"
VES is Vit E Succinate
https://www.researchgate.net/publication/260343692_Effects_of_fenbendazole_and_vitamin_E_succinate_on_the_growth_and_survival_of_prostate_cancer_cells
"Vitamin E succinate (VES), the most potent derivative of vitamin E for anti-
tumor activity"
"Fenbendazole is a benzimidazole drug commonly used
for treating pinworm outbreaks in laboratory rodents"
See A Pinworm Medication Is Being Tested As A Potential Anti-Cancer Drug
"Some of the lab animals got infected with pinworms, the same parasite my son had. The veterinarian at Johns Hopkins treated the whole colony of mice with an animal version of mebendazole.
The drug staved off the parasite, but it also did something surprising. Before the mice were treated for pinworms, Riggins and his team had implanted cancer cells into the animals' brains.
But after the mice got the pinworm drug, the cancers never developed. "Our medulloblastoma stopped growing,"
Per https://www.researchgate.net/public..._growth_and_survival_of_prostate_cancer_cells
"FBZ+VES significantly inhibited growth of PCa cells
and induced apoptosis in vitro. To our knowledge, this is
the first time these drugs have been tested together in
PCa cell lines. In a previous study, a concentration of 50
µg/ml of VES was shown to be effective on PC-3 cells
(Malafa et al., 2006). For FBZ, we tested a range of
concentrations based on a dosage used for Mebendazole
treatment of melanoma cells in culture (Doudican et al.,
2008). A dosage of 25 µg/ml of VES and 14 ng/ml of FBZ
was optimal for the treatment of prostate cancer cell lines
we tested. Higher concentrations of FBZ produced a
rapid rate of cell death during the initial 48 h period and
lower concentrations did not cause any change in cell
growth compared to controls. The agents were combined
at the specified dosages because alone neither produced
results that were as striking as when they were together.
This synergistic ability of inhibition is very interesting,
although the mechanisms involved is unclear. One
hypothesis is that vitamin E activates multiple pro-
apoptotic pathways such as targeting NF-κΒ (Ni and Yeh,
2007), and caspase-4 (Malafa et al., 2006), and if used
with an agent that inhibits cell division such as one of the
benzimidazoles, can be antagonistic to tumor growth.
These agents are worth further exploration since they are
both relatively safe and easy to administer."
Last edited:
Obi-wan
Member
- Joined
- Mar 16, 2017
- Messages
- 1,120
This study was sponsored by the U.S. Army Medical Research and Materiel Command, Fort Detrick, Maryland 21702-5012
https://apps.dtic.mil/dtic/tr/fulltext/u2/a545657.pdf
CONCLUSIONS:
Benzimidazoles were identified from a screen that selectively target highly metastatic prostate cancer cells but not toxic to normal cells. We determined that the preferential antitumor activity of these agents was mediated partly through cell cycle arrest and induction of apoptosis, both in vitro and in vivo. We further demonstrate that benzimidazole treatment prolongs the survival of mice bearing prostate cancer lung metastases and inhibit the growth of prostate cancer cells growing in the bone microenvironment. More strikingly, these anti-tumor effects remain active against prostate cancer cells that are resistant to paclitaxel, the standard chemotherapy for men with advanced prostate cancer, both in vitro as well as in vivo. Our study further supports the use of benzimidazoles as potential anti-cancer therapy for men with metastatic prostate cancer.
https://apps.dtic.mil/dtic/tr/fulltext/u2/a545657.pdf
CONCLUSIONS:
Benzimidazoles were identified from a screen that selectively target highly metastatic prostate cancer cells but not toxic to normal cells. We determined that the preferential antitumor activity of these agents was mediated partly through cell cycle arrest and induction of apoptosis, both in vitro and in vivo. We further demonstrate that benzimidazole treatment prolongs the survival of mice bearing prostate cancer lung metastases and inhibit the growth of prostate cancer cells growing in the bone microenvironment. More strikingly, these anti-tumor effects remain active against prostate cancer cells that are resistant to paclitaxel, the standard chemotherapy for men with advanced prostate cancer, both in vitro as well as in vivo. Our study further supports the use of benzimidazoles as potential anti-cancer therapy for men with metastatic prostate cancer.
B
Braveheart
Guest
Of possible interest?....Panning for proteins identifies a malaria drug’s cancer target
Fractality
Member
- Joined
- Jan 23, 2016
- Messages
- 772
RP said that isn't safe, do you know why?
Obi-wan
Member
- Joined
- Mar 16, 2017
- Messages
- 1,120
Another great study on Fenbendazole at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3436308/
"In recent years, there has been a great deal of interest in proteasome inhibitors as a novel class of anticancer drugs. We report that fenbendazole (FZ) (methyl N-(6-phenylsulfanyl-1H-benzimidazol-2-yl)carbamate) exhibits a potent growth-inhibitory activity against cancer cell lines but not normal cells"
"We then compared the antiproliferative ability of FZ with other established anticancer drugs. The results of a time-dependent growth assay clearly indicated FZ to be a more effective cytotoxic agent as compared with cisplatin and taxol"
"Altogether, our results indicate that FZ induces cytotoxicity in cancer cells via impairment of proteasome function and induction of unfolded protein response."
"Therefore, we propose FZ as a novel drug candidate that targets the ubiquitin-proteasome pathway and effectively kills cancer cells."
"In recent years, there has been a great deal of interest in proteasome inhibitors as a novel class of anticancer drugs. We report that fenbendazole (FZ) (methyl N-(6-phenylsulfanyl-1H-benzimidazol-2-yl)carbamate) exhibits a potent growth-inhibitory activity against cancer cell lines but not normal cells"
"We then compared the antiproliferative ability of FZ with other established anticancer drugs. The results of a time-dependent growth assay clearly indicated FZ to be a more effective cytotoxic agent as compared with cisplatin and taxol"
"Altogether, our results indicate that FZ induces cytotoxicity in cancer cells via impairment of proteasome function and induction of unfolded protein response."
"Therefore, we propose FZ as a novel drug candidate that targets the ubiquitin-proteasome pathway and effectively kills cancer cells."
Last edited:
B
Braveheart
Guest
Obi, I know your emphasis/expertise is on killing the cancer...for someone trying to avoid cancer, what have you learned?...what are your recommendations?....
Makrosky
Member
- Joined
- Oct 5, 2014
- Messages
- 3,982
About the *zoles... all I can say...
#jawdropped
#jawdropped
Obi-wan
Member
- Joined
- Mar 16, 2017
- Messages
- 1,120
That's a big question depending how cancer really gets started. Is it a microbial issue? a hormonal issue? a stress issue? a environmental issue? There are people that will be taking Fenbendazole and or Artemsinim the rest of their lives. I will probably be one of them.
Reading Cancer as a Parasitic Disease - Jeffrey Dach MD
"Conclusion: The link between cancer and parasitic disease is intriguing. Animal models in which invading parasites transform normal cells into cancer cells has shed light on this connection. The sheer fact that a wide array of anti-parasitic drugs serve as potent anti-cancer agents tends to support the hypothesis that cancer is a form of parasitic disease."
Last edited:
B
Braveheart
Guest
Artemisinin for the rest of mine...I think for me it was stress...
Obi-wan
Member
- Joined
- Mar 16, 2017
- Messages
- 1,120
Cancer prevention at Dietary phytochemicals and cancer prevention: Nrf2 signaling, epigenetics, and cell death mechanisms in blocking cancer initiation and progression
" Recently, dietary chemopreventive phytochemicals, including curcumin, EGCG, resveratrol, SFN, and PEITC have all been shown to alter epigenetic processes, which appear to facilitate the inhibition of tumor growth"
SFN sulforaphane
PEITC phenethyl isothiocyanate
EGCG (−)-epigallocatechin-3-gallate
9. Conclusions and perspectives
As discussed above, compelling data demonstrating the anti-cancer effects of phytochemicals have been accumulating. Throughout this review, we introduced the great potential of dietary phytochemicals: (1) blocking the initiation of carcinogenesis via the induction of detoxifying/antioxidant enzymes; (2) inhibiting the progression of carcinogenesis via the activation of the apoptotic pathway and cell cycle arrest; (3) the restoration of aberrant epigenetic alterations as an anti-cancer mechanism; and (4) the removal of the self-renewal potential of CSCs. Table 1 describes various phytochemicals that have demonstrated anti-cancer effects using in vitro and in vivo approaches involving these mechanisms. Daily exposure to various toxicants, such as environmental pollutants, carcinogens, dietary mutagens, and solar radiation, is inevitable. Oxidative stress and inflammatory damages caused by these toxins result in the dysregulation of oncogenes and tumor suppressor genes, aberrant epigenetic alterations, and the initiation of CSCs. These stresses and reactive metabolites of carcinogens are strong driving forces behind carcinogenesis. Thus, integrating the Nrf2-Keap1 signaling system in chemoprevention using relatively non-toxic dietary phytochemicals would be a logical approach to block the initiation of carcinogenesis through the inhibition of the oxidative stress/inflammation/reactive metabolites of carcinogens. In addition, at the later stage of carcinogenesis, induction of apoptosis and cell cycle arrest in pre-cancerous cells and carcinoma cells can also be an appealing biological target of dietary phytochemicals to block the progression of these tumor cells. Furthermore, epigenetic modifications and the CSC model are emerging key players in carcinogenesis due to their critical roles in cellular evolution and regulation. A greater understanding of the global pattern of these epigenetic modifications by dietary phytochemicals can yield improved insights into chemopreventive strategies and the potential of dietary phytochemicals to inhibit CSC development.Fig. 6 summarizes our thoughts on the potential cancer chemopreventive strategies discussed above.
Cancer chemoprevention strategy using dietary phytochemicals and non-toxic therapeutic drugs. Oxidative stress, inflammation and reactive intermediates of carcinogens can cause genetic mutations and epigenetic alterations. Through the promotion/progression stages, initiated cells become advanced/metastatic tumor cells. Applying dietary phytochemicals at the early stage of carcinogenesis may block further development of carcinogenesis. Treatment with dietary phytochemicals and/or relatively non-toxic therapeutic drugs on cancer cells may induce positive results, including autophagy, cell cycle arrest, apoptosis, and differentiation, and may block tumor development.
Although significant progress has been achieved for current cancer imaging and diagnostic tools, the detection of tumorigenesis in its early stages is still not promising because cancers are often asymptomatic, with long latencies, and they continue to threaten human health. Thus, cancer preventative strategies to inhibit the initiation of carcinogenesis using naturally occurring dietary phytochemicals consumed daily are key players in chemoprevention.
" Recently, dietary chemopreventive phytochemicals, including curcumin, EGCG, resveratrol, SFN, and PEITC have all been shown to alter epigenetic processes, which appear to facilitate the inhibition of tumor growth"
SFN sulforaphane
PEITC phenethyl isothiocyanate
EGCG (−)-epigallocatechin-3-gallate
9. Conclusions and perspectives
As discussed above, compelling data demonstrating the anti-cancer effects of phytochemicals have been accumulating. Throughout this review, we introduced the great potential of dietary phytochemicals: (1) blocking the initiation of carcinogenesis via the induction of detoxifying/antioxidant enzymes; (2) inhibiting the progression of carcinogenesis via the activation of the apoptotic pathway and cell cycle arrest; (3) the restoration of aberrant epigenetic alterations as an anti-cancer mechanism; and (4) the removal of the self-renewal potential of CSCs. Table 1 describes various phytochemicals that have demonstrated anti-cancer effects using in vitro and in vivo approaches involving these mechanisms. Daily exposure to various toxicants, such as environmental pollutants, carcinogens, dietary mutagens, and solar radiation, is inevitable. Oxidative stress and inflammatory damages caused by these toxins result in the dysregulation of oncogenes and tumor suppressor genes, aberrant epigenetic alterations, and the initiation of CSCs. These stresses and reactive metabolites of carcinogens are strong driving forces behind carcinogenesis. Thus, integrating the Nrf2-Keap1 signaling system in chemoprevention using relatively non-toxic dietary phytochemicals would be a logical approach to block the initiation of carcinogenesis through the inhibition of the oxidative stress/inflammation/reactive metabolites of carcinogens. In addition, at the later stage of carcinogenesis, induction of apoptosis and cell cycle arrest in pre-cancerous cells and carcinoma cells can also be an appealing biological target of dietary phytochemicals to block the progression of these tumor cells. Furthermore, epigenetic modifications and the CSC model are emerging key players in carcinogenesis due to their critical roles in cellular evolution and regulation. A greater understanding of the global pattern of these epigenetic modifications by dietary phytochemicals can yield improved insights into chemopreventive strategies and the potential of dietary phytochemicals to inhibit CSC development.Fig. 6 summarizes our thoughts on the potential cancer chemopreventive strategies discussed above.
Cancer chemoprevention strategy using dietary phytochemicals and non-toxic therapeutic drugs. Oxidative stress, inflammation and reactive intermediates of carcinogens can cause genetic mutations and epigenetic alterations. Through the promotion/progression stages, initiated cells become advanced/metastatic tumor cells. Applying dietary phytochemicals at the early stage of carcinogenesis may block further development of carcinogenesis. Treatment with dietary phytochemicals and/or relatively non-toxic therapeutic drugs on cancer cells may induce positive results, including autophagy, cell cycle arrest, apoptosis, and differentiation, and may block tumor development.
Although significant progress has been achieved for current cancer imaging and diagnostic tools, the detection of tumorigenesis in its early stages is still not promising because cancers are often asymptomatic, with long latencies, and they continue to threaten human health. Thus, cancer preventative strategies to inhibit the initiation of carcinogenesis using naturally occurring dietary phytochemicals consumed daily are key players in chemoprevention.
Last edited:
Obi-wan
Member
- Joined
- Mar 16, 2017
- Messages
- 1,120
Mostly Cruciferous vegetables. Broccoli is a big one!
B
Braveheart
Guest
From the ROS thread...
Learn to pay attention to possible warning signs for cancer... early warning signs are often neglected...this could be critical...
10 Ways To Detect Cancer In Its Earliest Stage - HealthPrep
plus I have my puppers watching out for me....
https://www.dogsnaturallymagazine.com/can-dogs-sniff-out-cancer/
Learn to pay attention to possible warning signs for cancer... early warning signs are often neglected...this could be critical...
10 Ways To Detect Cancer In Its Earliest Stage - HealthPrep
plus I have my puppers watching out for me....
https://www.dogsnaturallymagazine.com/can-dogs-sniff-out-cancer/
I think he said that about all *zoles / *soles, not just levamisole. I think in some cases it can cause agranulocytosis, and I suspect this is what makes him cautious about it.
Agranulocytosis - Wikipedia
EMF Mitigation - Flush Niacin - Big 5 Minerals
Similar threads
