Prostate Cancer

This post is intended to be a part of the “Cancer Type” category, and represents a list of info including drugs and supplements that may be relevant when fighting prostate cancer. Note that these drugs and supplements must not represent the replacement of conventional therapies. Instead, they may be used in agreement with the medical doctor to increase the chance of success of current therapies or represent additional options when conventional treatments are not available anymore. Based on the references below, here are the drugs and supplements I would consider:

  1. Metformin (typical dose: 1000mg to 2000mg/day)
  2. Atorvastatin (typical dose: see drug info)
  3. Aspirin (or Celecoxib) (typical dose: 100mg/day)
  4. Vitamin D3 (typically taken at about 5000ui to 10.000ui/day by cancer patients) D3 blood level needs to be monitored from time to time. Here is an example of a home test kit to do that http://www.vitamindtest.org.uk/
  5. Zinc + Chloroquine or Disulfiram
  6. Xanthohumol
  7. Pyrvinium pamoate (typical dose: see  previous post)
  8. Vitamin C and Vitamin K3 and Vitamin E
  9. Lycopene
  10. HCA+ALA (see below why and read more about this route here)
  11. Baicalein
  12. Low dose Perhexiline
  13. Artemisinin (see below why and read more about this route here)

Also see the following article published in 2018: Drug Repositioning for Effective Prostate Cancer Treatment

Although not intended, some of the above are also part of the Anti cholesterol strategy I put together sometime ago: https://www.cancertreatmentsresearch.com/reduce-cholesterol-in-cancer-cells-to-fight-cancer/ Due to the hormonal connection of prostate cancer, and since cholesterol represents the fuel for hormone production, I believe the anti cholesterol strategy is very relevant in prostate cancer.

Update on 27 Sept 2017: Supporting my expectation stated above, recently, a prostate cancer patient reported on this website response to HCA+Alpha Lipoic Acid (lasting for about 2 years) (Ref.). HCA is indeed an important elements in the Anti-cholesterol strategy, that I expect to be relevant to prostate cancer.

Update on 24 June 2019: in early stage, energy production via fermentation (glycolisis or Warburg effect) is less relevant in prostate cancer (Ref.). Instead, the cancer cells are relying much more on energy production via the mitochondria. This is why, in early phase or prevention phase of prostate cancer, mitochondria inhibitors such as Metformin should represent a core part of the treatment strategy. Here is a list of mithocondria inhibitors (Ref.).

List of info including drugs and supplements that may be relevant when fighting prostate cancer:

This list will further updated during the coming days/weeks/months/years.

Metformin

Metformin is widely accessible at pharmacies around the world, is cheap and it is typical used at a dose of 500mg to 2000mg/kg. In general, I would go for 1000mg to 1500mg/day. I would start with 500mg/day and increase the daily dose each week with 250mg towards the target dose.

Molecular pathways and targets in prostate cancer https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202120/  “A recent population study performed in Toronto showed that increasing duration of metformin use among diabetic men after a diagnosis of prostate cancer was associated with decreased prostate cancer–specific and all-cause mortality [347]. The findings were significant irrespective of what treatments the subjects were receiving for their PCa. Metformin is a widely used drug to treat type II diabetes, and is currently explored in numerous types of cancer, including PCa, in about 10 trials. In particular, addition of metformin to various forms of ADT is explored based on the rationale that ADT is associated with the metabolic syndrome, hyperinsulinemia and insulin resistance. Hyperinsulinemia was reported to stimulate tumor growth and development of CRPC via activation of IGFR. Metformin through its activation of the AMPK-LKBI pathway reduces liver gluconeogenesis secondarily decreasing insulin levels, which might explain the effects on tumor growth. Other effects of metformin on cellular metabolic processes could contribute to its anti-cancer properties, such as indirect effects on mTOR and SIRT1. Metformin acts directly on mitochondrial complex I reducing respiration rates, and this activity is probably relevant to the recently demonstrated improvement of prostate tumors oxygenation and radiotherapy response in vivo [348]. Metformin use was associated with significant decrease in biochemical relapse in patients [348].” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202120/

Metformin sensitizes prostate cancer cells to radiation through EGFR/p-DNA-PKCS in vitro and in vivo. https://www.ncbi.nlm.nih.gov/pubmed/24844651  Our results indicate that metformin enhances prostate cancer cell radiosensitivity in vitro and in vivo. Exposure to metformin before radiation therapy could be a beneficial option for the treatment of prostate cancer.

Metformin and Prostate Cancer: a New Role for an Old Drug https://www.ncbi.nlm.nih.gov/pubmed/28444639  Overall available data support the potential dual benefit of metformin on ADT-induced metabolic syndrome and in its antineoplastic activity in prostate cancer, justifying the need for ongoing clinical trials to confirm these effects as the evidence currently available for standard practice is lacking.

A prospective, randomized pilot study evaluating the effects of metformin and lifestyle intervention on patients with prostate cancer receiving androgen deprivation therapy. https://www.ncbi.nlm.nih.gov/pubmed/21933330 The present study shows the potential benefits of metformin and lifestyle changes in ADT-treated men. Further studies will aim to determine which intervention is most important, and may show that overall survival can be improved.

Mechanistic Study of Inhibitory Effects of Metformin and Atorvastatin in Combination on Prostate Cancer Cells in Vitro and in Vivo. https://www.ncbi.nlm.nih.gov/pubmed/28769006 Results of the present study indicate the combination of metforminand atorvastatin may be an effective strategy for inhibiting the growth of prostate cancer and should be evaluated clinically.

Atorvastatin (and other statins)

Combined effects of atorvastatin and aspirin on growth and apoptosis in human prostate cancercells. https://www.ncbi.nlm.nih.gov/pubmed/28075470 The findings provide a strong rationale for clinical evaluation of the combination of atorvastatin and aspirin in patients with prostate cancer.

Mechanistic Study of Inhibitory Effects of Metformin and Atorvastatin in Combination on Prostate Cancer Cells in Vitro and in Vivohttps://www.ncbi.nlm.nih.gov/pubmed/28769006 Results of the present study indicate the combination of metforminand atorvastatin may be an effective strategy for inhibiting the growth of prostate cancer and should be evaluated clinically.

A phase II study of atorvastatin and celecoxib in patients with rising PSA following local therapy for prostate cancer (PC)https://www.ncbi.nlm.nih.gov/pubmed/28143349 In this ongoing phase II trial, the combination of low dose atorvastatin and celecoxib has been well tolerated and demonstrates a tendency of increasing PSA doubling time. Enrollment continues with analysis of IL-6, CRP, and PGE-2 to be correlated to individual clinical results.

The differential effects of statins on the metastatic behaviour of prostate cancer. https://www.ncbi.nlm.nih.gov/pubmed/22531631 Lipophilic statins reduce the migration and colony formation of PC-3 cells in human BMS by inhibiting GGPP production, reducing the formation and the spread of metastatic prostate colonies.

Statins, especially atorvastatin, may improve survival following brachytherapy for clinically localized prostate cancer. https://www.ncbi.nlm.nih.gov/pubmed/16939047 The patients taking statin medications had significantly lower prostate-specific antigen values, percent positive biopsies, and prostate volume than those patients not taking statin medications. Statin usage resulted in a nonstatistical improvement in all survival parameters with the results most pronounced for atorvastatin.

Statin Use in Prostate Cancer: An Update https://www.ncbi.nlm.nih.gov/pubmed/27441003 Although still premature, accumulating clinical evidence suggests that statin use may be beneficial in the prevention and/or treatment of prostate cancer.

Aspirin and Celecobix

Regular Aspirin Use and the Risk of Lethal Prostate Cancer in the Physicians’ Health Study. https://www.ncbi.nlm.nih.gov/pubmed/28189429 Current regular aspirin use was associated with a lower risk of lethal PC among all participants. Current postdiagnostic use was associated with improved survival after diagnosis, consistent with a potential inhibitory effect of aspirin on PC progression. A randomized trial is warranted to confirm or refute these findings.

Aspirin Use Reduces the Risk of Aggressive Prostate Cancer and Disease Recurrence in African-American Men. https://www.ncbi.nlm.nih.gov/pubmed/28292923 Regular aspirin use before and after a prostate cancer diagnosis may prevent the development of aggressive disease in AA men who are at risk of a lethal malignancy

Prostate Cancer and Aspirin Use: Synopsis of the Proposed Molecular Mechanisms. https://www.ncbi.nlm.nih.gov/pubmed/28377721 Aspirin, a non-steroidal anti-inflammatory drug (NSAID), affects the proliferation, apoptosis, resistance and metastasis of PCa cell lines, through both COX-dependent and COX-independent mechanisms. It also lowers levels of the PCa diagnostic marker prostatespecific antigen (PSA)

Do Aspirin and Other NSAIDs Confer a Survival Benefit in Men Diagnosed with Prostate Cancer? A Pooled Analysis of NIH-AARP and PLCO Cohorts. https://www.ncbi.nlm.nih.gov/pubmed/28507039 However, aspirin use both before and after prostate cancer diagnosis was associated with longer overall survival, highlighting the importance of comorbidity prevention among prostate cancer survivors.

Aspirin may help men with prostate cancer live longer, study suggests http://www.sciencedaily.com/releases/2012/08/120828170725.htm

Celecoxib versus placebo for men with prostate cancer and a rising serum prostate-specific antigen after radical prostatectomy and/or radiation therapy https://www.ncbi.nlm.nih.gov/pubmed/16782912

Vitamin D3

Vitamin D Receptor Protein Expression in Tumor Tissue and Prostate Cancer Progression https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3107752/ High VDR expression in prostate tumors is associated with a reduced risk of lethal cancer, suggesting a role of the vitamin D pathway in prostate cancer progression.

Associations of Circulating 25-hydroxyvitamin D with prostate cancer diagnosis, stage and grade https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3378478/ Our study provides evidence that lower 25(OH)D concentrations were associated with more aggressive cancers

Vitamin D Deficiency Predicts Prostate Biopsy Outcomes https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104275/ In AA men, vitamin D deficiency was associated with increased odds of PCa diagnosis on biopsy. In both EA and AA men, severe deficiency was positively associated with higher Gleason grade and tumor stage.

Molecular pathways mediating the anti-inflammatory effects of calcitriol: implications for prostate cancer chemoprevention and treatment. https://www.ncbi.nlm.nih.gov/pubmed/19926709 Calcitriol or its analogs may have utility as chemopreventive agents and should be evaluated in clinical trials in PCa patients with early or precancerous disease.

Mechanisms of vitamin D-mediated growth inhibition in prostate cancer cells: inhibition of the prostaglandin pathway. https://www.ncbi.nlm.nih.gov/pubmed/16886660 We postulate that the regulation of the PG pathway contributes to the growth inhibitory actions of calcitriol. We also propose that calcitriol can be combined with non-steroidal anti-inflammatory drugs (NSAIDs) that inhibit COX enzyme activity, as a potential therapeutic strategy in PCa.

Zinc & Zinc Ionophores

Role of zinc in the pathogenesis and treatment of prostate cancer: critical issues to resolve http://www.nature.com/pcan/journal/v7/n2/full/4500712a.html?foxtrotcallback=true  Prostate malignancy involves the metabolic transformation of normal zinc-accumulating citrate-producing cells to citrate-oxidizing malignant cells that have lost the ability to accumulate zinc. Malignant cells in PCa virtually never contain high zinc levels. The lost ability to accumulate zinc is an essential metabolic transformation that is required for the manifestation of the malignant activities of the neoplastic malignant prostate cell. Downregulation of ZIP (zinc uptake) transporter gene expression might be responsible for the lost ability to accumulate zinc; and, therefore, could be a significant genetic factor in PCa.

According to the article above we need to find a way to enhance the zinc uptake into the cells.

Here there is a paper indicating that Chloroquine drug (previously discussed on this website) acts as a Zinc ionophore and has the potential to increase the cellular Zink uptake:

Chloroquine Is a Zinc Ionophore http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109180 Chloroquine enhanced zinc uptake by A2780 cells in a concentration-dependent manner, as assayed using a fluorescent zinc probe.

According to the article above Clioquinol drug (available at the pharmacy) seems to also be able to do a similar job, i.e. transport Zinc inside the cell. Here is their previous article demonstrating that https://www.ncbi.nlm.nih.gov/pubmed/15833873

Yet another approach may be to combine Disulfiram with Zinc, as Disulfiram seems to be a Zn ionophore as well. The drawback is that the patient will not be able to drink any amount of alcohol when using Disulfiram (an antialcohol drug). The dosage for  Disulfiram and Zn can be found in the following patent: https://www.google.com/patents/WO2008068746A2?cl=en

Here is a recent PhD thesis discussing the combination of Disulfiram and Zn in breast cancer as an anticancer approach: Investigation into the effects of zinc on the anti-breast cancer properties of disulfiram https://orca.cf.ac.uk/87744/1/2016WigginsHPhD.pdf also stating the following: “The low concentrations of either copper and zinc required to increase disulfiram potency, suggest that increasing the availability of either metal ion could be achievable in vivo with oral supplements to enhance the cytotoxic effects of the drug.”

Therefore this trick may be relevant to other cancers. Indeed, it is well known that some tumors (like breast cancer) accumulate higher level of Zinc compared to normal cells. Even more, the higher the Zinc level in those tumors the more aggressive they are. However, the PhD thesis above demonstrates that these tumors have their own way to balance that high level of Zinc, and when that is disrupted and more Zinc is pushed into the cell (using Zinc inophores such as Disulfiram) they will be killed.

Note that Chloroquine is a base (from a chemical point of view) and it may not cross the acidity area around some tumors. This means that “alkalizing” the tumor environment during the Zinc + Chloroquine usage may help. “Alkalizing” may be done with e.g. proton pump inhibitors like Omeprazole (an over the counter drug) or possibly with Sodium Bicarbonate (I would prefer the first approach).

Xanthohumol 

Xanthohumol, a natural extract that can be found online as a supplement (e.g. here), prevents the receptor from translocating to the cell nucleus, thus inhibiting its potential to stimulate the secretion of PSA and other hormone-dependent effects (Ref.)

Why beer is the latest hope in fight against cancer (Ref.) Researchers at the German Cancer Research Centre in Heidelberg have discovered that beer contains a powerful molecule that helps protect against breast and prostate cancers.

Xanthohumol impairs human prostate cancer cell growth and invasion and diminishes the incidence and progression of advanced tumors in TRAMP mice. https://www.ncbi.nlm.nih.gov/pubmed/22952060 The ability of XN to inhibit prostate cancer in vitro and in vivo suggests that XN may be a novel agent for the management of prostate cancer.

Growth Inhibitory and Apoptosis-inducing Effects of Xanthohumol, a Prenylated Chalcone Present in Hops, in Human Prostate Cancer Cells https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3846352/ Induction of apoptosis by XN was associated with the inhibition of prosurvival Akt, NF-κB and mTOR signaling proteins and NF-κB-regulated anti-apoptotic Bcl-2 and survivin. These studies provide a rationale for clinical evaluation of XN for the treatment of hormone-refractory metastatic prostate cancer.

Pyrvinium pamoate

I already discussed this drug in details here https://www.cancertreatmentsresearch.com/pyrvinium-pamoate/

New medication treats drug-resistant prostate cancer in the laboratory https://www.eurekalert.org/pub_releases/2013-06/tes-nmt061713.php

The novel role of pyrvinium in cancer therapy. https://www.ncbi.nlm.nih.gov/pubmed/28500633 The overwhelming insights into the mechanism of anticancer properties of PP can help establishing novel and future anti-tumor treatment strategies.

New medication treats drug-resistant prostate cancer in the laboratory https://www.sciencedaily.com/releases/2013/06/130617160730.htm

Non-competitive androgen receptor inhibition in vitro and in vivo http://www.pnas.org/content/106/17/7233.full Pyrvinium inhibits AR-dependent gene expression in the prostate gland in vivo, and induces prostate atrophy. These results highlight new therapeutic strategies to inhibit AR activity.

3BP

So far I was in direct contact with two prostate cancer patients who responded to 3BP treatment (one using the oral version and the other using injection). The substance and application approaches are described in this post https://www.cancertreatmentsresearch.com/3-bromopyruvate/

4-methylumbelliferone (4-MU)

This element has been often cited as a potential oral chemopreventive, and therapeutic agent that targets PCa development, growth, and metastasis by abrogating HA signaling (Ref.) Sold in Europe under the name Cantabiline (e.g. here). I already discussed 4-MU in this post: https://www.cancertreatmentsresearch.com/the-hyaluronic-acid-cage-to-open-or-not-to-open/

Here are some articles on this subject:

Can a Simple Dietary Supplement Cure Prostate Cancer? http://sperlingprostatecenter.com/can-simple-dietary-supplement-cure-prostate-cancer/

Antitumor activity of hyaluronic acid synthesis inhibitor 4-methylumbelliferone in prostate cancer cells. https://www.ncbi.nlm.nih.gov/pubmed/20332231 Therefore, the anticancer effects of 4-MU, an orally bioavailable and relatively nontoxic agent, are primarily mediated by inhibition of HA signaling.

Targeting hyaluronidase for cancer therapy: antitumor activity of sulfated hyaluronic acid in prostate cancer cells. https://www.ncbi.nlm.nih.gov/pubmed/21555367  Taken together, our findings offer mechanistic insights into the tumor-associated HA-HAase system and a preclinical proof-of-concept of the safety and efficacy of sHA to control prostate cancer growth and progression.

Tranilast

Izumi et al. [61] have reported that the treatment with oral TN (300 mg/day) promoted a reduction of prostate-specific antigen (PSA) levels in 4 out of 16 patients with advanced castration-resistant prostate cancer (CRPC). Accordingly, in the subsequent follow-up pilot study, oral treatment with TN (300 mg/day) for a median period of five months documented a continuous PSA inhibition in 3 out of 21 patients with advanced CRPC. Overall survival rates at 12 and 24 months were 74.5% and 61.5%, respectively [167]. As a whole, these results suggest that TN could be used to improve the prognosis of patients with advanced CRPC. However, the two clinical investigations had some limitations: (1) open-label studies with one arm; (2) short follow-up period; (3) small sample size; (4) all patients were Japanese. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4177740/  http://www.ncbi.nlm.nih.gov/pubmed/20683058/

Tranilast is a very interesting drug highly relevant against cancers. It is one of a few available to address the specific anti cancer mechanisms that is targeting. However, its accessibility is not the best as it is only available in Japan.

Taurolidine

See my post https://www.cancertreatmentsresearch.com/taurolidine/ and the references related to prostate cancer.

Bisphosphonates 

See my post https://www.cancertreatmentsresearch.com/bisphosphonates/ and the references related to prostate cancer.

Debatable but I think I should mention it: Testosterone

If the cancer is castration-resistant prostate cancer, you may want to discuss the comments at the end of this post https://www.cancertreatmentsresearch.com/androgen/#comment-1648 and consider this approach http://www.sciencemag.org/news/2015/01/cancer-paradox-testosterone-injections-combat-lethal-prostate-tumors This treatment should be essay to access

Ranolazine

In case we use hormonal treatment, this may be relevant: The drug ranolazine is a fat oxidation inhibitor that earned FDA approval in 2006 to treat angina. When scientists experimented with fat burning inhibitors and anti-androgens in cancer cell lines, they found that the addition of ranolazine to anti-androgen therapy made tumors more sensitivity to the anti-androgen drug enzalutamide. https://www.sciencedaily.com/releases/2017/05/170515125937.htm

Perhexiline

An even better alternative to Ranolazine may be Perhexiline. Low dose Perhexiline added to anti-androgens can stop prostate tumor growth:

“Proliferating cancer cells have increased need for lipids []. Interestingly, here we observed that inhibition of ECI2 expression and perhexiline treatment led to prominent accumulation of lipids into cells, which did not promote cancer cell proliferation. Normal prostate cells have an incomplete TCA cycle and therefore cannot rely on typical energy producing pathways []. This metabolic adaptation has been shown to sensitize prostate cancer cells to compounds inhibiting mitochondrial activity, and specifically sensitize the cancer cells to other treatments []. Here we propose that this metabolic adaptation forces prostate cancer cells to derive a significant fraction of their energy through alternative pathways, such as lipid degradation. In agreement with this model, inhibition of lipid degradation decreased glucose utilization and led to accumulation of starvation /autophagy markers (Figure (Figure3D3D and Figure Figure5C)5C) []. Instead of successful, cell-survival promoting autophagy, inhibition of lipid degradation led to the activation of the cell death response in prostate cancer cells … We are the first to show that perhexiline has prominent anti-tumor activity once combined with second-generation anti-androgens, Abiraterone and Enzalutamide” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5503531/

Vitamin C and Vitamin K3 and Vitamin E

A 12 Week, Open Label, Phase I/IIa Study Using Apatone® for the Treatment of Prostate Cancer Patients Who Have Failed Standard Therapy http://www.medsci.org/v05p0062.htm Seventeen patients with 2 successive rises in PSA after failure of standard local therapy were treated with (5,000 mg of VC and 50 mg of VK3 each day) for a period of 12 weeks. Prostate Specific Antigen (PSA) levels, PSA velocity (PSAV) and PSA doubling times (PSADT) were calculated before and during treatment at 6 week intervals. Following the initial 12 week trial, 15 of 17 patients opted to continue treatment for an additional period ranging from 6 to 24 months. PSA values were followed for these patients. At the conclusion of the 12 week treatment period, PSAV decreased and PSADT increased in 13 of 17 patients (p ≤ 0.05). There were no dose-limiting adverse effects. Of the 15 patients who continued on Apatone after 12 weeks, only 1 death occurred after 14 months of treatment. Conclusion: Apatone showed promise in delaying biochemical progression in this group of end stage prostate cancer patients.

α-Tocopheryl succinate promotes selective cell death induced by vitamin K3 in combination with ascorbathttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856000/ These finding support the emerging idea that synergistic combinations of some agents can overcome toxicity and other side-effects associated with high doses of single drugs creating the opportunity for therapeutically relevant selectivity.

Alpha-Tocopheryl Succinate Inhibits Autophagic Survival of Prostate Cancer Cells Induced by Vitamin K3 and Ascorbate to Trigger Cell Death https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3525640/ α-TOS, a mitochondria-targeting apoptotic agent, switches at sub-apoptotic doses from autophagy-dependent survival of cancer cells to their demise by promoting the induction of apoptosis. Given the grim prognosis for cancer patients, this finding is of potential clinical relevance.

Baicalein

This is a plant extract coming from Traditional Chinese Medicine. It is one of my favorites natural anti cancer extracts and  it has been suggested to act against prostate cancer:

Downregulation of ZFX is associated with inhibition of prostate cancer progression by baicalein http://tcr.amegroups.com/article/view/16170 Our study provides evidence that baicalein plays important roles in PCa therapy probably by downregulating ZFX expression, which was demonstrated to be involved in PCa progression, and thus may be developed as a novel and efficient candidate agent for PCa therapy

Baicalein inhibits prostate cancer cell growth and metastasis via the caveolin-1/AKT/mTOR pathway https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4502300/ In conclusion, these findings suggested that baicalein can induce apoptosis and inhibit metastasis of androgen-independent PCa cells through inhibition of the caveolin-1/AKT/mTOR pathway, which implies that baicalein may be a potential therapeutic agent for the treatment of androgen-independent prostate cancer patients.

Baicalein can be found in whole plant supplements made of Scutellaria baicalensis, or as a pure extract to be ordered on Alibaba website.

Artemisinin

Artemisinin is an extract from the plant Artemisia Annua that I previously discussed in this (Ref.) post.

Preliminary Case Series of Artemisinin for Prostate Cancer in a Naturopathic Practice 
Objective: To determine if oral artemisinin is safe and has a short-term effect on prostate specific antigen (PSA) kinetics in patients with prostate cancer (CaP).
Design: Retrospective case series.
Setting: A private naturopathic urology clinic in Seattle, WA. Patients: All artemisinin-treated CaP patients were identified retrospectively between 2005 and 2008. A total of 15 patients were identified who had taken artemisinin and included in the study, comprising 5 patients who had previously undergone radical prostatectomy (RP) and were having biochemical recurrences as well as 10 patients with no prior conventional therapy for CaP. Interventions: High-dose, pulsed oral artemisinin 300–400 mg three times a day every other week for 3–24 months (median 9.5 months, IQR 5–12 months). All patients were treated with an array of other naturopathic therapies.
Outcome measures: The primary outcomes were the PSA doubling time and
velocity; secondary outcome measures were signs and symptoms of metastasis and survival.
Results: Of those patients who have previously undergone RP, 2/5 (40%) had improved PSA kinetics after artemisinin therapy. Of those with no prior RP, 5/10 (50%) had improved PSA kinetics. No patient developed signs of metastasis and no patients died. There were no reported adverse effects.
Conclusions: This pilot study provides preliminary evidence to suggest that highdose, pulsed oral artemisinin therapy may have activity in patients with CaP. A larger controlled trial is warranted to confirm these preliminary beneficial effects.

Cabergoline (dopamine agonist)

Treatment, which decreased the plasma prolactin as a potential treatment against androgen-independent prostate cancer. Here is a recent successful case report https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6578577/

Other relevant references:

Molecular pathways and targets in prostate cancer https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202120/

Human chorionic gonadotropin (hCG) interacts with lovastatin and ionizing radiation to modulate prostate cancer cell viability in vivo. http://www.ncbi.nlm.nih.gov/pubmed/18379195

Suppression of human prostate cancer cell growth by ciprofloxacin is associated with cell cycle arrest and apoptosis http://www.ncbi.nlm.nih.gov/pubmed/12632069

A glycolytic phenotype is associated with prostate cancer progression and aggressiveness: a role for monocarboxylate transporters as metabolic targets for therapy. http://www.ncbi.nlm.nih.gov/pubmed/25875424

Combining the typical hormonal treatment with abiraterone (also used for prostate cancer) seems to lead to improved outcome https://www.theguardian.com/society/2017/jun/03/prostate-cancer-therapy-study-abiraterone

A supplement that may very much help specifically for prostate cancer is Boron.

PhD thesis 2016: The role of estrogen receptors in prostate cancer development and their contributions in new treatment opportunities

Disclaimer:

This site is not designed to and does not provide medical advice, professional diagnosis, opinion, treatment or services to you or to any other individual. Through this site and linkages to other sites, I provide general information for educational purposes only. The information provided in this site, or through linkages to other sites, is not a substitute for medical or professional care, and you should not use the information in place of a visit, call consultation or the advice of your physician or other healthcare provider. I am not liable or responsible for any advice, course of treatment, diagnosis or any other information, services or product you obtain through this site. This is just my own personal opinion regarding what we have learned on this road.

Please read an extended version of the Disclaimer here: https://www.cancertreatmentsresearch.com/?page_id=1794

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78 thoughts on “Prostate Cancer

      1. D, the radiotherapies in prostate seem to be moving quickly in clinical trials.
        Sometimes high quality cancer treatments can linger for decades without any forward progress,
        yet Lu-177 appears too good to stop.

        https://clinicaltrials.gov/ct2/show/NCT03042312?term=Lu177-PSMA-617&rank=1

        Oops! Missed the mention of C+ K3 +E.
        What do you think of this one?
        https://www.ncbi.nlm.nih.gov/pubmed/22584645

        This one seems much better than K3, though they do not even have a mouse study.
        This is another off the shelf compound with a bromine substituted in.
        Yet, after all of these years it is still not clear whether it could be helpful or very dangerous.

        1. Hi J, this is interesting but not accessible. In general, I am looking at what is both interesting/potentially relevant and accessible. However, we should keep in mind those with high potential and not accessible for the moment when we can also support somehow financially thee advancement of research and testing. Maybe I should start up a post where all of us could do a brainstorming on ways to develop a successful framework that can attract world wide financial support, to identify and support development/testing of those treatment techniques with high potential but not financially interesting for the industry. I think this world already has enough knowledge, technology and capable people to find a solution to cancer. Just that the current framework intended to address that is wrong. When I look at what happens to the cryptocurrencies, I realize the world is ready to change to new frameworks. We just need to find the right one for the medical world. What do you think?

          1. Yes, D, after all of these years it is still as frustrating as ever that a true revolution in cancer treatment from the grassroots as not happened. It does not make sense! 20,000 people per day die of cancer. I was thinking recently that if people were to simply take a dose of 3-BP just before cancer claimed them, then it would be immediately clear that 3-BP is helpful for some patients. How has 3-BP been allowed to be endlessly delayed for the people who medicine has disowned? Why has euthanasia been allowed to be seen as a more palatable choice than actually trying things such as 3-BP? Cancer treatment now would be greatly more effective if people at imminent risk of cancer mortality were given the opportunity to more fully choose their treatment.

            For some reason, those people who have advanced very bad logic to oppose 3-BP have won.
            The idea that 3-BP is too dangerous a drug to treat someone is at imminent risk of death from cancer is not rational.
            3-BP is not more dangerous than the risk posed from the last moments of terminal cancer.

            In the new age of the internet and leveraging of people power, why haven’t good ideas won?
            It does not take that much research to realize that effective cancer are now clearly approaching.
            Metastatic cancer was cured over 30 years ago in lab models.
            How much longer for people?

            It is also a good point to try and stay with treatments that can be of use to people right now.
            One thing that we could do on the forum is to give 30 day treatment suggestions.
            For example, with vitamin C treatment: one could cycle through a range of combos for a week or two
            to see which one might be of especial usefulness. As it is people now probably stick with one
            treatment protocol even if it is not particularly effective. By rotating through say, Vitamin K3,
            alpha lipoic acid, phenylascorbate, doxycycline, etc. one could look for the weak point.

            1. dear Jcancom,

              i totally agree. I think it is not just because of the way companies work – it is also because of the way people think. About authority. Most people believe 100% of what they hear from their doctors. And these doctors are not always open minded (the doc of Ergin’s mother is not the norm but the exception).

              I can assure you that most oncologists in Central Europe have not even heard about 3-bp, metabolic treatment or even about re-purposed drugs. Or if they did they simply dont care as those are not part of the paradigm.

              And cancer patients dont question their authority.

              Of course this is rooted in the fact that many people are selling false hope with lies and senseless methods.

            2. Hi J,

              I think the answer to most of your points is: wrong focus or fragmented focus.

              Wrong focus: most of the pharma companies, full of well intended people, can search for cancer solutions as long as there is someone who is investing his money in that. Those investing money (btw many of which are former, current or future cancer patients) need more money back – otherwise they will better keep them in a bank or invest them is e.g. construction, consumer goods or whatever. The pharma needs to deliver back to the investor while doing their best to help people. But that fundamentally limits their search and potential outcome. The search and approval of the outcome is extremely expensive so the result is an expensive solution with limited effectiveness. The point is that almost everyone in pharma industry has the best intentions but because of the framework, the results are of very small benefit for humans.

              Fragmented focus: there are a lot of grassroots and foundations trying to do something good. But they do not work together. Everyone has own little goal with own little investment. In other words CHAOS. A lot of positive energy defocused. Imagine what you could do with all this energy if you could focus it on the right subjects. What is wright we may not know, but if we would focus on some high priority subject we may quickly come to great results.

              The world is full of people who would like to do something good in oncology and contribute. But the KEY questions is what kind of framework we can put in place to capture all this energy and focus? That would be like collecting the light from many bulbs and build a laser out of it.

              I feel that a block chain like project may be the answer here. I am trying to understand that technology better and how we could use that to achieve the above.

              This project I recently came across may help us to get some ideas: https://bowheadhealth.com/
              What do you think? (this is a question for all the friends reading this, off course)

              Kind regards,
              Daniel

    1. Thanks Carl. I will have a look at Clorgyline. As the summer ends I will restart my research activities.

      These days I am specifically triggered by the role of viruses in triggering and maintaining cancer. I see too many cases in which someone next to a cancer patient (genetically related) may relatively soon develop cancer as well. I know this may also be related to mind (e.g. new germanic medicine) but I suspect that is related to a combination of virus + genetic profile.

      What is interesting is to see that most of the anticancer drugs we are discussing have also known anti viral action.

      Kind regards,
      Daniel

      1. Hell Daniel,

        I think it is also related to grief. it makes the immune system weaker. Of course, this does not mean that the virus connection is false. As you surely know about HPV…. By the way – you could look at the cancer incidence among people with AIDS as part of your research.

        1. Hi W,
          Thanks. I find it a strange coincidence to see that (based on the limited information I have) it happens more often to the family members with the same genetic line. I totally agree that grief plays a role. It also well known that some cancers have a virus as trigger. But my point is that it may be bigger than just some cancers. It may be most. What if the genetic profile makes you more vulnerable to some known and/or unknown viruses. And when the grief and/or life is reducing the immune system effectiveness and changing other balances in the body could just support the initiations of what we call tumors. It is like planting a seed (virus) in the right ground (weak body due to grief etc.). I know it sounds simple, but if this is the case, there may be huge value in focusing the treatments on well knwon mechanisms in viruses. And that is interesting because for example virus activity strong depends on pH and proton pump inhibitors may strongly influence that (as we know same happens in cancer cells). Same with ion dynamic which is extremely important for viruses (and as we know for tumor cells). And so on.
          I am not saying that this is it. I am saying that this may be a perspective that could go deep towards the origin of cancer. That in turn may lead to more effective treatment strategies. Anyway, I will do a deep dive on this perspective asap.

          I hope you are doing well W.

          Kind regards,
          Daniel

  1. Hi Daniel,
    Thank your for writing a new post about prostate cancer. Yesterday I was at a psychology course about healing and there I spoke with a man who had prostate cancer stage 4 grade 4, who is now cured, even though it is considered at this grade incurable. He based his healing on the faith in God and some energy that God gives you. He goes to the monastery regularly and brings people there, does a lot of good deeds, is helping people and he changed his lifestyle.
    I wish everyone coming here on the site health and to remember that the psychological and spiritual transformation is also important when trying to heal.
    Kind regards,
    Anca

    1. HI Anca,

      Thank you for sharing. I very much believe that. Humanity understands very little about how human body works and actually how everything works, while doing its best to evolve that. Unfortunately, in the quest of learning and evolving, we are doing to little at understanding the spiritually and focus most of our efforts on understanding physical mechanism. I think the ultimate healing, and evolution, can come from the spiritual path. But that takes time for many of us as it requires changes of own paradigms. And when fighting cancer time is essential. This is why I believe that a short term focus on drugs and supplements to gain time, and a long term focus on spirituality is best combination for a cancer patient, while working on both at the same time.

      Kind regards,
      Daniel

      1. Hey Daniel.
        It’s great to see you keeping busy.
        I must say i admire your energy.
        Our warm thoughts go with you and our friends and family here.
        Always thankful.
        Please take care,

        Alex

  2. Hi Daniel,

    Very interesting piece!
    I have reviewed the role of metformine also recently. The evidence for metformine as anti cancer agent is really strong! But thus far only tested found in diabetics, so there is a caveat.
    A doctor is now looking into K3 and cancer for me, as our product is up for review. I keep you updated.

    Regards,
    Joris

      1. Well, nothing you didn’t discover already for prostate cancer. There is also evidence for buccal cancers (Krisnamurthi S et al;Radiology 1971 May; 99(2):409-15; PMID 55535581), where K3 improves the effectiveness of radiotherapy, and for liver cancer (High dose vitamin K3 infusion in advanced hepatocellular carcinoma. Sarin SK, Kumar M, Garg S, Hissar S, Pandey C, Sharma BC. J Gastroenterol Hepatol. 2006 Sep;21(9):1478-82.). In both cases they applied high doses K3 monotherapy.

        Kind regards,
        Joris

  3. Hi Daniel,

    I know from you that Metformin is really good in most cancers, but now my mother has such a bad taste in the mouth when taking any drugs (except minerals and vitamins and Melatonin and plants extract) and she says she feels something very chemical in her mouth after taking Metformin. What is your opinion on that? Should she take it, no matter what she feels afterwards? This is the effect of the chemotherapy, and especially Caelyx destroyed her, she could not eat or drink water after Caelyx first session, then she did another one even though Virgil said we should stop it, now my mother regrets doing the second dose of caelyx. Thanks to you we go at the clinic where we do Vitamin C and Vitamin B17 and Magnesium IV, and my mother can eat something and drink. She stopped chemotherapy a month and a half ago, and she also stopped all animal food then, she is eating wheat germs, and other germs with olive oil, rice , lentil and apricots or plums. That is all she can eat. She has diarrhea a lot, unfortunately because of the anxiety, we didn’t manage to eliminate all panic attacks or claustrofobia. One panic attack (from claustrofobia if she leaves the house to a darker and small place) has a harmful effect for a week. So the mental well-being is very important.
    I guess I am lucky that my mother is still alive, I see her walk in the garden and enjoying the fresh air. Faith is very important and staying outside the house. We will go to the oncholgyst Luca on 14th September, but we try to avoid all the harming things and the toxic stuff, because Caelyx was too much to handle and now a simple drug like Metformin is unbearable for my mother.
    May God help anyone with pancreatic and other types of cancer coming on the page!
    Thank you for writing everytthing so well documented, Daniel.

    Kind regards,
    Anca

    1. Dear Anca,

      Thank you for your comment. Metformin is expected to slow down the activity. I think that if your mother feels/thinks that does’t help her and makes her feel less good, you may want to let her decide if she wants to stop. If that happens, I would consider replacing that with Berberine. This is a natural extract that is expect to have similar action as Metformin – btw, Metformin is also made of a natural extract (Ref.). Also, as a reminder, if the oncologist decides to start with a new round of chemo, is best to stop Metformin or any drug that slows down the tumors several days prior to chemo and restart those during the same day with chemo.
      I hope your mom will be better and better.

      All the best,
      Daniel

      1. Dear Daniel,
        Thank you for your reply :). My mother will be happy to hear Metformin is made of a natural extract, and that there is also a similar drug (Berberine). I don’t think my mother trusts chemo any more, because she spoke with a lady from Targu-Jiu who has ovarian cancer, was very weak, she lost 20-30 kilos, and chemotherapy made her feel so bad, that is why the woman interrupted it 6 months ago, and she is better and stable now, only with vitamin C IV and Magnesium IV and Vitamin B17 IV and Potassium IV and a supplement form plants Hyper-Tum, that we find in Romania (it is antitumoral and it it stimulates the immune system, it contains more than 10 plants). That woman used Vitamin B17 every day for one month, then 3 times a week and now only one time a week (all these are costing her a lot of money, she pays 65 euro for one dose of Vitamin C and vitamin B17 IV, twice the money my mother pays for them, in Targu-Jiu these things are very expensive). The woman gained 6 kilos back, is feeling good, so my mother has hope now from that person (who was as bad as my mother, with diarrhea every day). It is always good to speak with people who went through this to give you hope.
        Thank you Daniel. I put you and your wife at the acatist in the monastery. I hope the workers did a great job for your wife’s funeral stone.

        Kind regards,
        Anca

  4. Dear Daniel,
    Have you heard about a substance called equol? From the wikipedia article:
    Equol (4′,7-isoflavandiol) is an isoflavandiol metabolized from daidzein, a type of isoflavone found in soybeans and other plant sources, by bacterial flora in the intestines. While endogenous estrogenic hormones such as estradiol are steroids, equol is a nonsteroidal estrogen. However, only about 30% of people in the West have intestinal bacteria that make equol (file:///C:/Users/Ethan/Downloads/metabolites-05-00056-v2.pdf). Equol preferentially binds estrogen receptor beta.
    By binding to the estrogen receptor, equol may inhibit prostate cancer progression in tumors that have the ERG+ phenotype.
    Another aspect of its anti-cancer activity is its ability to bind to DHT. Equol may be one reason why men in China and Japan are said to have less prostate cancer. In these countries there is a large consumption of soy products. Also, a higher percentage of people in these countries have the gut flora to convert daidzein to equol.
    There is a simple urine test for equol production from soy (file:///C:/Users/Ethan/Downloads/metabolites-05-00056-v2.pdf). Unfortunately not literature is available about the role of equol in prostate cancer. It would be valuable to conduct a clinical trial to measure its effectiveness.

    1. Dear Hasapiko,

      We had some intensive discussions here and almost missed your comment … thanks a lot for sharing that. I haven’t heard of Equol. I will check it asap as it sounds very interesting. I will let you know if I find anything else interesting about it. Please note that the links you shared are actually not web links but from your local computer. So they cannot be accessed. Whenever you find other interesting substances/treatments please let me know.

      Kind regards,
      Daniel

        1. Yes, they do look very good and long lasting!
          The big drawback is that it seems that only 1% of patients have the mutations.

          D, there is some very impressive cancer treatments coming online lately.
          It is surprising how good Loxo is and yet it is still flying under the radar.

          Look at page 15 from the pdf for LOXO.
          Almost all the patients had ongoing responses if they first achieved a response withint the first 2 months.

          The company even has a second generation TRK, to help those like with Gleevec who progressed, though they have not needed to use to it because most patients respond so well.

          Also exciting that there are patients with a wide range of tumor types that are responders melanoma, breast …

          The company is ready to file a NDA over the next few months, so perhaps it will be available to patients soonish.
          Might be one to test for now, the company might allow expanded access.

  5. D, the numbers for Loxo look extremely impressive!
    There is an entirely new generation of very effective cancer treatments that are now emerging.
    We talked about the strategy of throwing a bunch of darts at the dart board until you hit a bullseye.

    Loxo101 is one dart.
    Cancer patients might have a 1% chance of having a TRK fusion, though if they did then LOXO could be such a blessing.
    If they did not have a TRK fusion, then time for another dart.

    Loxo is also developing LOXO-292 for RET rearrangements, LOXO-195 second generation TRK, LOXO-305 …

    LOXO-292 is early stage, yet it could be another dart.
    These fusion proteins seem like such a great point of attack against cancer.
    Why hadn’t they be targeted before? They are so abnormal that they make a perfect target.
    I checked the liver patient. He had a DNAJB1-PRKACA fusion. Wonder if anyone is in the process of developing something for them?

    “RET fusions have been identified in approximately 2% of non-small cell lung cancer, approximately 10-20% of papillary thyroid cancer, and a subset of colon and other cancers. RET point mutations account for approximately 60% of medullary thyroid cancer.

    RET gene fusions, much like TRK gene fusions, occur when the RET gene abnormally fuses to another gene. The hybrid gene that is created as a result drives tumor growth.

    Both RET fusion and select RET mutated cancers are primarily dependent on this single activated kinase for their proliferation and survival. This dependency, often referred to as “oncogene addiction,” renders such tumors highly susceptible to small molecule inhibitors targeting RET. LOXO-292 was designed to inhibit native RET signaling as well as anticipated acquired resistance mechanisms that could otherwise limit the activity of this therapeutic approach. LOXO-292 is currently being studied in a Phase 1 trial.”
    https://www.loxooncology.com/docs/presentations/2016_EORTC_LOXO-292_POSTER.pdf

    “Policy for Access to Investigational Agents

    Loxo Oncology is committed to helping patients who have not responded to available therapies and may benefit from its investigational therapies. Loxo Oncology’s Policy for Access to Investigational Agents describes the principles that the company will follow when considering a request, ”

    https://www.loxooncology.com/pipeline

    For LOXO101 consider the Duration of Response Figure on page 15.
    https://www.loxooncology.com/docs/presentations/Hyman_Larotrectinib_ASCO_2017_FINAL.PDF
    93% of responding patients remained on treatment.

    There were only a few non-responders ( for example, the patient eight from the top with the green band.
    In fact many of those who had not yet responded were still fairly early in the treatment course.
    (From what I read, patients who had very serious illness were included in the trial who traditionally would not
    be, because they wanted to treat all comers. At the bottom of the Figure, there are 6 patients who did not develop a response and went off-treatment after only 1 month. These probably are some of those seriously ill patients.

    The next page has median duration of response. The number of patients is small though the responses seem to stretch out for years. The Figure after shows 63% of the patients were progression free at two years. They did not even mention survival, though it must be very encouraging.

    If more patients had these TRK fusions, then we would have heard more about this treatment before. The NDA will be sent to the FDA within a few months. They moved this product through trials in only 2 years! When there is something this good the FDA will not stand in its way.

    1. Hi J,

      Yes, I specifically enjoyed seeing slide 15. And indeed, it seems that after 1.8 months the patient knows if he/she is responding or not. The drawback is the 1% only respondents but the advantage is that those can be tests prior to the therapy for TRK fusion status that may be present regardless of cancer type.

      Here is a list of tests types and testing centers they suggest:

      • FoundationOne (Foundation Medicine)
      – 315 genes included + 28 genes for fusions
      • FoundationOne Heme (Foundation Medicine)
      – 405 genes included + 265 genes for fusions
      – Can be ordered for solid tumors, not just hematologic malignancies
      • MI Profile (Caris Life Sciences)
      – 592 genes included
      – Make sure that the Fusion Analysis is included
      • Solid Tumor FOCUS::ONCOMINE NGS Panel (Cancer Genetics)
      – Indicate on the order form to include fusions
      • Oncomine™ Focus Assay (Sirona Dx)
      – 52 genes, including 23 genes for fusions
      • SmartGenomics NGS Solid Tumor (PathGroup)
      – 62 genes, including fusions
      • Universal Fusion/Expression Profile (Neogenomics)
      – 1,385 genes, including fusions
      • GeneTrails Solid Tumor Fusion Gene Panel (Knight Diagnostic Laboratories)
      – 20 genes for fusions
      • OmniSeq Comprehensive (OmniSeq)
      – 144 genes, including fusions
      http://www.trktesting.com/HowToTest.pdf

      Kind regards,
      Daniel

  6. Exactly D!

    This is so critically important from the patient perspective.
    Knowing that you will probably respond within a 2 month window is very important information.
    If you have not responded in that window, then you could plan from there.
    Yet, even several of those who did not respond early, did respond later.
    It might be very difficult for cancer to work around an anti- fusion treatment

    Notice that most of the patients had yellow dots after at 2 months. Nearly all of those with a yellow dot
    than had these prolonged ongoing responses that stretch out to 2 years with this preliminary data.
    Only 3 of the patients with a yellow dot stopped responding, though this data is still early.

    So many cancer drugs give a response though it can many months to know if the patient is in the responder
    class and then the response itself might only be for a few months or even weeks.

    LOXO-101 apprears to be a true breakthrough product.
    The responses are early, and they typically are long lasting– into years.

    You are right about 1% being a disappointment, though there are these other fusions.
    For example, the liver patient and Fibrolamellar hepatocellular carcinoma.

    “A recent study showed the presence of the DNAJB1-PRKACA chimeric transcript (resulting from a 400kb somatic deletion on chromosome 19) in 100% of the FHCCs examined (15/15)[2] This gene fusion has been confirmed in a second study.” wiki

    From above, RET fusions appear in 2% of NSCLC and others.
    Fusions look like such a great target.
    You can attack the fusion, few side effects and the cancer finds it difficult to mutate around.

    Possibly the genetic approach really will work out.
    All you need to do is find all the escape routes that cancer has available and then close them off.

  7. D, fusion proteins are a very exciting avenue of cancer research!

    I do not believe people have been fully aware of how important a concept this is.
    Consider that an onco-fusion protein is highly abnormal; it combines two separate proteins there should be a way
    to specifically attack it while leaving other cells alone.

    The anti-fusion drugs have already been successful (Gleevec — BCR-ABL fusion protein in leukemia).
    The liver patient had a fusion and this might have involved the BSG gene which is of high relevance to 3-BP effectiveness.
    The TRK patients and the liver patients exhibited ongoing responses to monotherapy.
    This suggests that the fusion cancers are locked into their addictions without an easy resistance escape route.

    This article notes that up to 20% of cancer morbidity is associated with fusion proteins and in fact 50% of prostate cancer has the TMPRSS2-ERG fusion. Do they have any drugs in development for this?

    “The total number of gene fusions is now estimated to be 10 000, with over 90% of these being identified in the past 5 years due to advances in deep-sequencing and fusion detection algorithms (12). The prevalence of gene fusions varies widely between cancer types (10): at one extreme, gene fusions occur in (and frequently drive) 90% of all lymphomas, over half of leukemias (13), and one third of soft tissue tumors (14). In prostate cancer, one specific fusion (TMPRSS2-ERG) is the most common genetic alteration, being found in over 50% of patients (15). However, many recurrent gene fusions occur at low frequencies, such as the KIF5B-RET fusion, which is present in 1–2% of lung adenocarcinomas”
    {Strangely they do not mention TRK above.}

    https://academic.oup.com/nar/article/44/10/4487/2516680/Discovering-and-understanding-oncogenic-gene

  8. Here’s a list of fusions from COSMIC.
    Really wonder if there might be some more good targets.
    http://cancer.sanger.ac.uk/cosmic/fusion

    Would love to know how patients respond to different treatments conditioned on Fusion status.
    Fusion Samples Mutations Papers

    BCR-ABL1 8638 5412 233 xxx Gleevec
    TMPRSS2-ERG 6264 2623 114 xxx 50% of prostate patients
    EWSR1-FLI1 2132 1332 164
    EML4-ALK 11213 701 508
    KIAA1549-BRAF 1383 612 79 xxx BRAF
    CCDC6-RET 6833 593 162
    SS18-SSX1 1313 577 135
    PML-RARA 545 544 36
    PAX3-FOXO1 1163 382 72
    NCOA4_ENST00000452682-RET 4431 358 136
    ETV6-RUNX1 2277 357 42
    FUS-DDIT3 627 351 47
    SS18-SSX2 1314 348 136
    NPM1-ALK 1344 319 86
    KMT2A-AFF1 2465 308 74
    TCF3-PBX1 3645 301 53
    STIL-TAL1 1771 284 29
    COL1A1-PDGFB 399 262 51
    CRTC1-MAML2 632 253 36
    NAB2-STAT6 295 246 12
    EWSR1-ATF1 357 179 45
    ETV6-NTRK3 1059 144 47 xxx LOXO-101
    EWSR1-ERG 1639 122 90
    EWSR1-WT1 267 121 55
    DNAJB1-PRKACA 186 107 6 xxx Liver Patient
    PAX7-FOXO1 981 100 56
    FUS-CREB3L2

    ETV6-NTRK3 1059 144
    TPM3-NTRK1_ENST00000392302 629 32
    LMNA-NTRK1_ENST00000392302 38 2
    QKI-NTRK2 96 2
    TFG-NTRK1_ENST00000392302 495 2
    NACC2-NTRK2 96 1
    TP53-NTRK1_ENST00000392302 38 1

    KIAA1549-BRAF 1383 612

  9. D, LOXO-101 is very impressive.

    When you look at page numbered 10 in the pdf, you see 6 patients who had tumor growth.
    If you notice on the bottom of the page numbered 15, there are 6 patients who never achieved a response and stopped treatment
    even before 1.8 months. These patients must have been severely ill. Most trials would not accept them.

    Without these patients almost everyone would have achieved at least a response.
    When they get this out to real world patients the treatment will do even better.
    Think what happens when these patients could be treated at stage 2 or 3!

  10. I am posting this here as it seems the most appropriate place, and the information may help someone else.
    Standard PET/CT has low sensitivity for prostate cancer, making it difficult to determine the extent and location of early spread. There is a need for more accurate scanning techniques when PET/CT and bone scans are inconclusive. We used the C-11 acetate scan after standard imaging was inconclusive and were then able to determine the exact location of mets. At that time, the Axumin scan had not yet been FDA approved, but now it is, so that one may be the easiest to access.

    Axumin PET (aka Fluciclovine F18/ FACBC): http://paact.help/new-pet-scan-approved-for-prostate-cancer-for-psa-recurrence-after-treatment/
    Similar accuracy to C-11 Acetate PET. Now FDA approved, availability is becoming more wide spread.

    C-11 Acetate PET: http://www.phxmi.com/ (only offered in phoenix)
    We had a C-11 acetate scan done in Phoenix and found it accurate and extremely helpful. It can confirm or refute questionable CT and bone scan findings, and show additional lesions that CT/bone scan were unable find. Dr. Almeda, who reads them, has interpreted over 1,500 scans.

    Choline C-11 PET: http://www.mayoclinic.org/tests-procedures/choline-c-11-pet-scan/home/ovc-20156994 (Only offered at Mayo clinic)
    Same idea as the C-11 acetate PET, but the C-11 acetate is more sensitive

    Galium 68 PMSA PET: http://www.pet.theclinics.com/article/S1556-8598(16)30138-9/fulltext
    The Prostate Oncologist I spoke to believes this scan is more sensitive and accurate than the others. It is available through clinical trials and through UCLA:http://urology.ucla.edu/psma-pet-imaging
    https://clinicaltrials.gov/ct2/results?term=gallium+pet&Search=Search

    1. As an update, Ga 68 PSMA PET is outperforming other PET scans for prostate cancer. Although it is still not widely available, this article has a map of locations that offer it as well a comparison of performance with other novel prostate PET scans: https://www.sciencedirect.com/science/article/pii/S1879850017302060
      This type of scan can be imperative for those who are considering targeted therapy instead of just generalized chemo and androgen deprivation. There are some nice studies coming out on the treatment of oligometastatic prostate cancer using Stereotactic Body Radiation Therapy, with even some reported “cures” (5 years with PSA <0.2 not on ADT). I will post on that later today. My best to everyone.

      1. For those with oligometastatic prostate cancer (early metastasis with only a handful of lesions) androgen deprivation and chemo used to be the main treatment with radiation used only for palliative care. Now studies are showing that a specific type of radiation called Stereotactic Body Radiation Therapy (SBRT) with an intention to cure, is providing very good outcomes.

        In this study half of individuals who received a single treatment of SBRT where able to avoid androgen deprivation for at least two years: https://www.europeanurology.com/article/S0302-2838(18)30429-9/abstract?ct=t(EMAIL_CAMPAIGN_7_13_2018_14_40)&goal=0_bc8795358a-78c2b5df4d-199203717&mc_cid=78c2b5df4d&mc_eid=2cf1d76790

        This study concluded: “SBRT offers high local cancer control rates in bone oligometastases of PC and should be evaluated with the aim of curation or to delay modification of systemic treatment.”
        https://bmccancer.biomedcentral.com/articles/10.1186/s12885-017-3341-2

        This study took a multimodal aggressive approach to oligometastatic prostate cancer, including SBRT and concluded that: “A sequentially applied multimodal treatment strategy can eliminate detectable disease in selected patients with metastatic spread at diagnosis. The endpoint of undetectable PSA after testosterone recovery should be considered when evaluating new approaches to rapidly set priorities for large-scale testing in early metastatic disease states and to shift the paradigm from palliation to cure.”
        They actually had long-term ADT-free remissions, including 5 years.
        https://www.goldjournal.net/article/S0090-4295(16)30850-0/abstract

        There are additional supportive studies for this treatment approach for prostate cancer, and for other cancers. I wanted to post this because many doctors do not stay informed of the latest literature, so it is up to us to be informed. For example, when we brought the possibility of SBRT up with my husband’s radiologist, he became angry and refused to see us if we pursued such a “foolish” treatment. Needless to say, we found another doctor. The point is that we must inform ourselves of the latest and most promising treatments for our situation and not assume that our oncologist is aware of the best options.

  11. Advanced prostate cancer (and other cancers too) can have two tumor suppressors silenced, PTEN and p53. Loss of PTEN leads to activation of the oncogenic PI3K/Akt/mTOR pathway. Deguelin and Rotenone selectively kill PTEN null cells.
    Mitochondrial Complex I Inhibitors Expose a Vulnerability for Selective Killing of Pten-Null Cells. PMID: 29617673

  12. Hi Daniel-
    Thanks for your June, 2019 update to this post. I found this reference particularly useful:
    The Metabolic Phenotype of Prostate Cancer https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5474672/
    After a year of being off of androgen deprivation (zytiga and lupron) my husband’s PSA went from <0.006 to 0.029. He had also discontinued most of his supplements, despite my protest. He is now back on them and we are retesting PSA in a few days. This article was useful in deciding which pathways to prioritize if we need to start ramping up our therapy. We suspect he is still androgen deprivation responsive, but are going to try to avoid androgen deprivation, if possible. Also finding the HCA+ALA, Cholesterol synthesis inhibition and Zinc ionophor posts very helpful in formulating a plan. I will post here what we implement and the results or if I have questions for all of you.

    On a side note, we tried the supplement Prostasal, my husband's reaction was similar to when he tried an estrogen patch while on androgen deprivation in an attempt to support bones, memory and help with hot flashes. Specifically, he began to have breast tenderness, mood swings, fatigue and weight gain immediately and discontinued because he felt the side-effects outweighed the benefits. We also have a friend who believes it controlled his low grade, confined prostate cancer for 8 years (he also had estrogen like side-effects). Looking at the ingredients, I wonder if it isn't contaminated with a synthetic estrogen. This is just an informational post, no need to respond, please focus your energies on those who have greater need.

    Warmly,

    Shanti

    1. Hi dear Shanti,

      Thank you for the update. Indeed Prostasol and Nutrition 2000 seem to lead to similar side effects as you mentioned. I also know some people who experienced this as well but also a PSA reduction. Normally, I would expect this could be the results of Regrestrol components, but the reaction seems to be much stronger, indicating, as you said, possible contamination with estrogen. If I can help with anything please let me know.

      Kind regards,
      Daniel

  13. Hi All-
    I would like your thoughts on this initial protocol for stage IV prostate cancer. Anything I should add or take away? My husband’s PSA has started to increase. It is believed he has a low PSA producing cancer, so it makes increases more significant, and, so far, his doubling time is about a month. Here is his history in a nut shell:
    62 yo Male
    Oct 2016 PSA 10, Gleason 9
    Feb 2017 radical prostatectomy
    April 2017 post prostatectomy PSA 5
    May 2017 C11-Acetate Scan reveals 1 met to left lung, 1 met to sacrum and multiple positive pelvic and abdominal lymph nodes
    May 2017- May 2018- Zytiga+Lupron+Prednisone+Xgeva, PSA is less than 0.006 but side effects are eroding quality of life
    May 2018-May 2019- We decide to take a break from ADT and are using only supplements. PSA is less than 0.006 for 1 year
    June 2019, PSA 0.029. July 2019 PSA 0.058

    We would like to avoid androgen deprivation for as long as possible AND want to find something that works before the dreaded androgen deprivation resistance sets in. Right now, the androgen deprivation (assuming he is still sensitive) can serve as a re-set button if needed. The main metabolic pathways we are focusing on are: Zinc metabolism, copper depletion, lipid use and synthesis, and mitochondrial inhibition.

    Altered Zinc metabolism of prostate cancer:
    Clioquinol 3% cream -1g twice a day (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6392423/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6578577/- Thank you J)
    Chloroquine 250mg/day
    zinc -50mg twice a day

    Copper depletion:
    Silver 10ml/day (zinc should work synergistically)

    Lipid use and synthesis:
    HCA 1.5g twice a day
    Lipoic acid 300mg extended release twice a day
    Tocotrienols 1 twice a day https://www.lifeextension.com/Vitamins-Supplements/item01400/Super-Absorbable-Tocotrienols
    Atorvastatin 10mg

    Mitochondrial Inhibition:
    Metformin 1000mg extended release
    Berberine 1000mg twice a day
    Doxycyclin 100mg /day

    Other:
    Honopure, Ursolic acid, Xanthumol

    We are also considering adding IVC and oral vitamin C to synergize with the Doxycycline (we have used IVC before, but not combined with Doxy). Maybe also Artemisinin/Artemisia (one week on-one week off). If everything is tolerated, we may also add in Dipyridamole and Fenbendazol or Mebendazol and dutasteride.

    He currently takes:
    Berberine 1000mg
    Lycopene 45mg
    Pomi-T
    Aspirin 82mg
    CoQ10 200mg
    PQQ 20mg
    Metatrol 2/day
    Apigenin 50mg bid
    Grape Seed Extract 100mg
    Pectasol 2 scoops
    Tart Cherry
    Luteolin 50mg
    Mega Green Tea 45% EGCG
    Vitamin D 6000IU, 1 oz Juiced turmeric (about 5 roots)
    Basentabs
    resveratrol 150mg/ day
    Diet: Vegan diet that is mostly vegetables, nuts, beans and green juices

    In the past he has tried and not tolerated: Cimetidine, vitamin K2 and K3, Prostasal, Diclofenac
    Thank you all for any thoughts and help!
    -Shanti

    1. Hi Shanti,
      could you tell us more about your husband’s supplements plan; when did he start each supplement, does he take all supplements continuously, etc.
      Best Regards,
      Johan

      1. Hi Johan,
        Thank you for your reply. He took all supplements continuously from Feb 2017 through March 2019, at which point all but the vitamin D were discontinued (my husband doesn’t like taking them and the undetectable PSA gave a false sense of security). I do not know if discontinuing coincided with the PSA increase. We reinitiated all supplements with the June PSA reading of 0.029 and approximately 3 weeks passed between supplement reinitiation and the July reading of 0.053.
        His supplement regimen has had some variation in it, and at various times he has used artemisinin (1 week on/one week off), shark liver oil, xanthohumol, Coriolus, and reishi.
        Warmly,
        Shanti

    2. Hi Shanti,
      you might want to consider the following:
      -In hormone-sensitive cancers, the flavonoids apigenin, quercetin, and genistein may act in a biphasic manner.
      -Resveratrol, again the biphasic properties of this compound should be noted:
      https://tandfonline.com/doi/abs/10.1080/01635581.2017.1359309
      -Myricetin:
      https://www.karger.com/Article/FullText/492009
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631581/
      -Sodium phenylbutyrate antagonizes prostate cancer through the induction of apoptosis and attenuation of cell viability and migration
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4869668/

      Best Regards,
      Johan

      1. Hi Johan,
        I very much appreciate your responding providing these links. We previously eliminated quercetin and genistein from our supplement regimen due to this type of conflicting information. I had read a study in which a minority of prostate cancers had androgen receptors that could use genistein for growth, so we decided not to take chance. Daniel has a post on high dose (in the gram range) genistein and I did order a kilo in case we need to try it as a strategy at some point. I will spend some time reading the links you sent this evening and adjust our regimen accordingly.
        Thanks again,
        Shanti

        1. Hi Shanti,
          It’s impossible to know if the rise in PSA has anything to do with discontinuing the supplement plan, but at least the rise in PSA can’t be attributed to those supplements. The fact he took those supplements for an extended period of time without a rise in PSA does add confidence the supplement cocktail is(was) beneficial. That said, the PSA levels now continue to rise after reintroducing the supplements.

          As mentioned in my previous reply below(or above), there’s a case to be made to exclude apigenin and resveratrol from the supplement plan, or to use in rotation (for example one or two months on/off).
          In combination with Artemisinin, Resveratrol does seem to produce synergy in anticancer activity. PMID: 25048878

          When taking Coq10, consider adding β-glucan.

          Combination Therapy with Glucan and Coenzyme Q10 in Murine Experimental Autoimmune Disease and Cancer. PMID: 29848676

          When taking lycopene, consider adding sulforaphane.

          Combinations of Tomato and Broccoli Enhance Antitumor Activity in Dunning R3327-H Prostate Adenocarcinomas

          A phase II study of sulforaphane-rich broccoli sprout extracts in men with recurrent prostate cancer. PMID: 25431127

          Consider adding IP6

          Inositol Hexaphosphate Inhibits Tumor Growth, Vascularity, and Metabolism in TRAMP Mice: A Multiparametric Magnetic Resonance Study
          http://cancerpreventionresearch.aacrjournals.org/content/6/1/40

          Consider taking Magnesium

          Magnesium Chloride increases apoptosis and decreases prostate cancer cells migration
          https://www.ffhdj.com/index.php/ffhd/article/view/368/699

          Honokiol + Artemisinin synergy
          https://www.researchgate.net/publication/285726504_Experimental_studies_of_honokiol_in_combination_with_artemisinin_on_anti-tumor_effect_of_SPC-A-1_cells_in_vitro

          Consider using liposomal curcumin, in addition or to rotate with the turmeric juice.

          Consider adding flax seeds to his diet.

          Best Regards,
          Johan

          1. Hi Johan,
            Thanks again for the great links. We removed resveratrol from our regimen… too risky https://www.nutraingredients-usa.com/Article/2010/07/20/Researchers-Resveratrol-a-double-edged-sword-for-prostate-cancer. I couldn’t find any negative studies on apigenin, if you have a link, I would be grateful. Thank you also for the link to the phenylbutyrate, interesting that this is also used by the controversial Dr. Burzynski. Your second post came through in my email notifications, so I will take a look at it now.
            Warmly,
            Shanti

            1. Hi, I’ve posted over at the forum if you don’t mind, I’ve posted so many times here without getting through 🙂

            2. phenylbutyrate is indeed used by dr.burzynski, we used his A10 antineoplastons back in 2003 (when sodium is metabolized in the body it produces byproducts, also called antineoplastons) along with tamoxifen, melatonin, and lomustine, which resulted in a recurrent glioblastoma to shrink and eventually disappear.

          2. Hi Johan,
            That is an amazing testimonial! It is hearing about such cases that give us hope. Do you think Burzynski’s success with phenylbutyrate came because of the way he combined it with other medications and chemo? The studies I saw on it not authored by him seem to show minimal success, but I am learning that the power is often in how things are combined rather than a single agent.

            1. Hi Shanti, I think back then Burzinsky was mainly treating patients with antineoplastons, I got the impression he was trying to find the most effective dosage, and at high dosages, the sodium is a big problem. Nowadays he also uses low dose chemo and many of the drugs we now know can be used against cancer e.g. metformin. I believe he is a pioneer in the field of repurposing drugs for cancer treatment. Going to his clinic in Texas wasn’t an option for my father-in-law but back then he was selling A10 antineoplastons in a product called Aminocare A10. It still exists but no longer has the antineoplastons, as he isn’t allowed to sell it anymore.

    3. Dear Friends,
      Good news 🙂
      After implementing the following (in addition to the supplements he already takes):
      2.5mg HCA bid
      300mg ALA bid
      Tocotrienols bid
      500mg SR metformin bid
      50mg zinc
      3% clioquinol cream 1g topically/day (zinc ionophore)
      15ml 10ppm silver (sovereign silver) bid
      Nebulization of silver, water, sodium bicarb solution bid x 7 min

      My husband’s PSA has held steady at 0.051 (May= <0.006 // June, 20 = 0.029 //July 11 =0.053 // Aug 2 = 0.051). This means we are on the right track!
      We have also made some minor adjustments to our supplement list (which can be viewed in an earlier post), thank you Johan for your suggestions. We will be adding other tactics as tolerated, my husband did not do well with chloroquine or fenbendazole (diarrhea, nausea, cramping, fatigue). We are considering adding in LDN as it has synergy with ALA. Daniel posted elsewhere that it is important for a cancer to express TLR4 when considering LDN, which prostate cancer does: https://www.ncbi.nlm.nih.gov/pubmed/29928275. I will be researching this afternoon, but would be interested if anyone has thoughts or experience with LDN and prostate cancer.
      I am eternally grateful to all of you for your help and support,
      Shanti

      1. Dear Shanti,

        I thought I responded to your kind and positive comment here but somehow I probably forgot to push “reply” as I did it while travelling. I was happy to read the positive news and I wish you continued success. Indeed, LDN is a good one to add to the cocktail. (Looking at the silver dose you mentioned you are using, I realised it is about 10x lower compared to what the man in the case report cited in the silver post used.).
        If you have questions about other subjects where I could help, please let me know. I am now back home and should be able to find the time (as I promised earlier).

        Kind regards,
        Daniel

        1. Hi D,
          Your comment on the silver dosing is noted. I was going off of the “dosing section” in the blog post, but I can appreciate why you give the dosing as you did in that section with encouragement to consider higher dosing with active cancer. I think we will continue with our current dosing and increase pending our upcoming scan and PSA reading.
          By the way, my husband’s baseline ceruloplasmin in May was 16.9 mg/dL (range 16-31), after a month of silver and 50mg zinc once or twice a day it hasn’t changed and is at 17. We probably need higher silver dosing or dosing for a longer time period to bring it down. We also tested our water for copper, which was negative. I could start him on TM since it is best with low volume disease, but his consistently low WBC stop me from doing so (last reading WBC 2.5 range 3.4-10.8).
          Glad to have you back 😊,
          Shanti

        1. Thanks Johan, I think I was so relieved the PSA didn’t go up last month that I got over-enthusiastic, I still think it is because of what we are doing, but will take more time to confirm.
          -Shanti

      2. Husband’s Axumin PET was negative for active cancer. Our oncologist was concerned it had morphed into a non-PSA producing aggressive prostate cancer of the neuroendocrine variety. Thankfully that is not the case. We are holding at PSA of 0.051, off of all ADT for 1 year.

  14. We are now ALSO considering 3BP (https://www.ncbi.nlm.nih.gov/pubmed/30928407- Thank you Jcancom). I need to reread the 3BP sections of this site and figure out how to work it in and what of the items we are using it doesn’t work with (MCT1 inhibitors, glutathione regenerators etc). J also pointed out that the fact that my husbands mets were brightly lit on an acetate scan increases the chance they will respond to 3BP. My concern with 3BP is reports of tumor being made very aggressive without a complete response-I would love insight on this.

    1. Hi Shanti,

      If you are interested in 3BP, when I come back from holiday please remind me to contact a man with whom I was in contact 4 years ago. He was using first DCA and after 3BP to control/suppress his PSA. He first used DCA and that was helping his PSA but he experienced nephropathy so he had to stop and switch to 3BP. He was taking it orally. His job at that time was as a cancer scientist in a pharma company working on chemo in France as I remember, so he could also do studies in the lab. He claimed good results with 3BP and he gave me all the details on how he was using it. I remember one-two years after our first contact on Cancer Compass he was still using it.

      Kind regards,
      Daniel

  15. Hi Daniel,
    Yes, I am very interested in anything that may work and would very much appreciate being in contact with such an individual. I will reach out to you in a few days when you are back. We briefly used DCA along with 2DG (both oral) and some other meds, but discontinued as PSA was undetectable on ADT.
    Thank you,
    Shanti

  16. Hi All-
    As my husband also has two small mets to his left lung, we are also looking into what we can do with getting substances in direct contact with the lung mets via nebulization. As his PSA recently started to increase, the same persistent cough he had before androgen deprivation began to return. It has actually gone away since implementing some of the items outlined in the protocol I posted above. We won’t know if this is related to an improvement in the cancer until later this month with a PSA and PET. I know 3BP can be nebulized, but we aren’t using that at the moment. Does anyone have experience nebulizing therapeutic substances for lung mets? There is anecdotal evidence for nebulized sodium bicarbonate, H202 and colloidal silver for use in cancer. All of these have a history of nebulization for use in COPD, asthma, pneumonia, infection etc and I think their use is relatively safe as long as one stays with in the established dose based on collective experience.

    Here is some info on dosing:
    http://healyourselfathome.com/HOW/THERAPIES/SODIUM_BICARBONATE/sodium_bicarbonate_nebulizing.aspx
    http://www.healyourselfathome.com/HOW/THERAPIES/H2O2/nebulizing_H2O2.aspx
    https://livelovefruit.com/nebulize-colloidal-silver-support-lung-health/
    https://mountainwellbeing.com/nebulizing-colloidal-silver-support-lung-health/

    1. Dear Shanti,

      I do have experience with nebulizers. My wife did used DMSO, DMSO+3BP (extremly low dose), and also tried Methyl Jasmonate a little. I also considered H202 and colloidal silver. Nebulizing Helleborus niger from Helixor may also help.It’s very affordable and can be found at German pharmacies. I always thought nebulizing is a very relevant treatment route for lung tumors (and others). Please let me know if I can help with anything on this line. I may not remember all the details but I can always look back at my notes. All what we did was safe with no side effects.

      Regarding the cough, I do not expect that is related to the lung ments since those are very small to my understanding. What I also find a relevant idea for those who deal with lung tumours is to have a vaccine such as Pneumococcal conjugate vaccine done (Pneumococcal infections are an important cause of infections in cancer patients).

      Kind regards,
      Daniel

  17. Hi Daniel,
    If we begin to use 3BP, we will most certainly do some of the application via nebulization. We started on Sat with nebulization of colloidal silver and 2% sodium bicarbonate solution for 5-10mg and this has been well-tolerated with my husband reporting a decrease in respiratory/nasal inflammation, but it is early in the treatment. Thank you for the additional suggestions, I will look into them.

    For those who have interest, here is an article on why chemo is not delivered via nebulization (which was something I was wondering). In short, there are multiple challenges including lung toxicity, only reaching the periphery of the tumor, contamination of the environment with vapor escaping from the nebulizer, among others.
    https://www.mdpi.com/2072-6694/11/3/329/pdf

    Warmly,
    Shanti

  18. Hi All-

    For those who have challenges following a vegan plant based diet, the low polyamine diet could be a viable alternative. Best results would likely be achieved by following a low polyamine+vegan diet. This study is from 2010, but I hadn’t seen it posted and the hormone-refractory men on the low-polyamine diet appear to have a doubling of survival time.

    “Median cancer-specific survival times for the intervention groups as a whole compared to controls are 36 months versus 17 months, respectively (P = 0.004)”

    Polyamine reduced diet (PRD) nutrition therapy in hormone refractory prostate cancer patients.
    https://www.ncbi.nlm.nih.gov/pubmed/20106631

    Abstract
    BACKGROUND:
    Reducing polyamine uptake by selecting low polyamine-containing foodstuffs and reducing bacterial gut production can improve performance status and pain control in hormone refractory prostate cancer (HRPC) patients. Long term PRD observance and tolerance were assessed. Cancer specific survival was studied in function of PRD and time of PRD initiation.

    METHODS:
    Twenty-six volunteers, age: 68+/-10 years with metastatic HRPC accepted a polyamine reduced diet and partial gut decontamination with oral neomycin or nifuroxazide (750 mg daily, one week out of two). Time from HRPC to PRD initiation was 10+/-8 months. WHO performance status, EORTC pain scale, body weight, blood counts and serum proteins were regularly assessed. Sixteen other HRPC patients eating a normal diet served as “controls”.

    RESULTS:
    Mean diet observance is 25+/-24 months. Tolerance is good. WHO performance status and EORTC pain scales were significantly improved respectively at 3 months (0.5+/-0.7 vs 0.7+/-0.9: p=0.03) and 6 months (0.5+/-0.8 vs 1+/-1.3, p=0.02) compared to initial values. Median cancer specific survival times after HRPC and PRD initiation are respectively 36 and 21 months. Eleven PRD patients started the diet before a 9 months cut-off period (after HRPC) and 15 patients after. Median cancer specific survival times for these two groups of patients are respectively 44 and 34 months, p=0.014. Median cancer specific survival times (after HRPC) for PRD patients compared to controls are 36 vs 17 months (p=0.004).

    CONCLUSIONS:
    Polyamine-reduced diet is well observed and tolerated. It seems to improve and/or maintain quality of life for HRPC patients. Early PRD initiation in HRPC is promising and may impact favorably cancer specific survival. These results open a rationale for PRD in HRPC management and warrant further investigation.

    The Denver Naturopathic Clinic has put together a nice listing of low/moderate/high polyamine foods:
    http://www.denvernaturopathic.com/EclairDiet.htm.

    Group 3 foods, the foods with the highest polyamine content and that were most important to avoid included:
    Calamari, oysters, muscles, crab, scallops, liver mousse, chitterlings, duck-liver pate´, pork liver pate´ garlic, chervil, tarragon, cabbage, broccoli, parsley, mushrooms, green peas, eggplant, tomatoes, bone marrow, oranges, hazelnuts, almonds, pistachios, peanuts, bananas, wheat, mustard, tinned gherkins, tomato paste, instant mashed potatoes, minced spinach, lentils, chickpeas, ratatouille, and sauerkraut.

    Group 2 foods that contain moderate levels of polyamine:
    fresh salmon, beef and ox tongue, chicken, rabbit, veal, lamb, beef, ham, garlic sausage, paella, red beans, radish, chicory, leek, endives, potatoes with skin, spring potatoes, Brussels sprouts, lettuce, cucumber, melon, goat cheese, oat, rye and whole breads, ketchup, grapefruit and orange juices.

    Group 1 foods with the lowest polyamine content that could be consumed freely:
    scampi, crayfish, hake, cod, whiting, smoked and canned salmon, tinned tuna, bacon, sausages, chipolata, pork, turkey, chorizo, minced pork, salami, onions, celery, carrots, green cabbage, beetroot, skinned potatoes, sorrel, string beans, small tomatoes, peppers, canned vegetable soup, raisins, apples, prunes, pears, avocado, peach, dates, pineapple, grapes, kiwi, lemon, strawberries, fruit salad, butter, cream, milk, yoghurt, soft cheese, Emmental, goat cheese without rind, pasteurized brie, grated cheese, camembert, eggs, rice, semolina, pasta, white bread, sugar, pancakes, chocolate eclair, honey, cookies, pound cake, chocolate, lemon pie, strawberry pie, apricot, strawberry, prune and raspberry jams, salt, pepper, oils, vinegar, coffee, tea, cider, cola, whisky, cognac, port, wine [God Bless the French! TK], apple, grape and apricot juices, beer, tropical fruit cocktail, and tomato juice.

    The list somewhat flies in the face of convention on what a prostate cancer patient should eat. Polyamines likely play a role in other cancer types as well: https://www.ncbi.nlm.nih.gov/pubmed/?term=polyamine+%5Bti%5D+cancer

  19. Hi All-

    For those who have challenges following a vegan plant based diet, the low polyamine diet could be a viable alternative. Best results would likely be achieved by following a low polyamine+vegan diet. This study is from 2010, but I hadn’t seen it posted and the hormone-refractory men on the low-polyamine diet appear to have a doubling of survival time.

    “Median cancer-specific survival times for the intervention groups as a whole compared to controls are 36 months versus 17 months, respectively (P = 0.004)”

    Polyamine reduced diet (PRD) nutrition therapy in hormone refractory prostate cancer patients.
    https://www.ncbi.nlm.nih.gov/pubmed/20106631

    Abstract
    BACKGROUND:
    Reducing polyamine uptake by selecting low polyamine-containing foodstuffs and reducing bacterial gut production can improve performance status and pain control in hormone refractory prostate cancer (HRPC) patients. Long term PRD observance and tolerance were assessed. Cancer specific survival was studied in function of PRD and time of PRD initiation.

    METHODS:
    Twenty-six volunteers, age: 68+/-10 years with metastatic HRPC accepted a polyamine reduced diet and partial gut decontamination with oral neomycin or nifuroxazide (750 mg daily, one week out of two). Time from HRPC to PRD initiation was 10+/-8 months. WHO performance status, EORTC pain scale, body weight, blood counts and serum proteins were regularly assessed. Sixteen other HRPC patients eating a normal diet served as “controls”.

    RESULTS:
    Mean diet observance is 25+/-24 months. Tolerance is good. WHO performance status and EORTC pain scales were significantly improved respectively at 3 months (0.5+/-0.7 vs 0.7+/-0.9: p=0.03) and 6 months (0.5+/-0.8 vs 1+/-1.3, p=0.02) compared to initial values. Median cancer specific survival times after HRPC and PRD initiation are respectively 36 and 21 months. Eleven PRD patients started the diet before a 9 months cut-off period (after HRPC) and 15 patients after. Median cancer specific survival times for these two groups of patients are respectively 44 and 34 months, p=0.014. Median cancer specific survival times (after HRPC) for PRD patients compared to controls are 36 vs 17 months (p=0.004).

    CONCLUSIONS:
    Polyamine-reduced diet is well observed and tolerated. It seems to improve and/or maintain quality of life for HRPC patients. Early PRD initiation in HRPC is promising and may impact favorably cancer specific survival. These results open a rationale for PRD in HRPC management and warrant further investigation.

    The Denver Naturopathic Clinic has put together a nice listing of low/moderate/high polyamine foods:
    http://www.denvernaturopathic.com/EclairDiet.htm.
    The list somewhat flies in the face of convention on what a prostate cancer patient should eat. Polyamines likely play a role in other cancer types as well: https://www.ncbi.nlm.nih.gov/pubmed/?term=polyamine+%5Bti%5D+cancer

  20. Yesterday I came across this article:
    https://www.ncbi.nlm.nih.gov/pubmed/23671572/
    From an objective of rectifying mitochondrial defects in cancer cells and to establish mitochondria as a potential anticancer drug target, understanding the role of functional mitochondria in reversing oncogenic properties under a cancer nuclear background is very important. Here we analyzed the potential reversal of oncogenic properties of a highly metastatic cell line with the introduction of non-cancerous mitochondria. Cybrids were established by fusing the mitochondria DNA depleted 143B TK- ρ0 cells from an aggressive osteosarcoma cell line with mitochondria from benign breast epithelial cell line MCF10A, moderately metastatic breast cancer cell line MDA-MB-468 and 143B cells. In spite of the uniform cancerous nuclear background, as observed with the mitochondria donor cells, cybrids with benign mitochondria showed high mitochondrial functional properties including increased ATP synthesis, oxygen consumption and respiratory chain activities compared to cybrids with cancerous mitochondria. Interestingly, benign mitochondria could reverse different oncogenic characteristics of 143B TK(-) cell including cell proliferation, viability under hypoxic condition, anti-apoptotic properties, resistance to anti-cancer drug, invasion, and colony formation in soft agar, and in vivo tumor growth in nude mice. Microarray analysis suggested that several oncogenic pathways observed in cybrids with cancer mitochondria are inhibited in cybrids with non-cancerous mitochondria. These results suggest the critical oncogenic regulation by mitochondrial-nuclear cross talk and highlights rectifying mitochondrial functional properties as a promising target in cancer therapy.
    —- we have been talking about the different metabolism in prostate cancer cells from other types of cancer… Well, what if it is the same problem? The normal mitochondria in prostate cancer cells are not supposed to oxidate citrate but cancerous cells do… And mitochondria from other cancer types are suppose to use oxidative phosporylation yet they don’t do it… Then the mitochondria are the real problem and the focus should be on making them functional again

  21. Hi Yudiatheska,
    Based on this paper and other that have been published, I agree, dysfunctional mitochondria play a huge role in cancer initiation and progression. Cancer universally shows dysfunction or altered metabolism as part of its strategy to survive and multiply. It is certainly odd that prostate cancer ramps up the kreb cycle in early cancer, only becoming highly glycolytic in later stages. It is certainly something we have taken into consideration as we have designed our approach to my husband’s prostate cancer. I think it useful for everyone to investigate their cancer’s “metabolic phenotype” to help choose strategies and find out if there are any “Achilles heel”. I love the idea of returning mitochondria to normal function and found this paper outlying some strategies: https://isom.ca/article/mitochondrial-correction-new-therapeutic-paradigm-cancer-degenerative-diseases/. Nonetheless, it seems our most effective tools are still weakening the cancer cell through metabolic therapies and then trying to kill them while defenses are low. The mitochondria seem unwilling to revert back to normal easily.
    Warmly,
    Shanti

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