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Nothing works for prostate cancer

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Nov 5, 2019, 10:14:44 PM11/5/19
Supplements for Men With Prostate Cancer

When it comes to dietary supplements, less is more. Mega-doses suggest a worse outcome or prognosis in patients with cancer.


B12 may be needed if blood tests show a deficiency. Excess B vitamins may promote heart disease and cancer growth. Researchers have not found that Vitamin C helps prevent or treat prostate cancer. For Vitamin D, I generally recommend 1,000 IU daily if the level is below normal. Men with prostate cancer should not take an individual Vitamin E supplement. Higher doses of Multivitamin pills may feed prostate tumors. Taking a children’s multivitamin several times a week, not to exceed one pill a day, makes more sense. Folic acid and Zinc in higher amounts have been associated with a higher risk of aggressive prostate cancer in human studies.

Fish Oil (Omega-3 fatty acids)

Pills containing EPA and DHA may reduce the risk of cardiovascular events and may have anti-arthritic and anti-depressive properties. Some new research suggests it could encourage the growth of some prostate cancers.


500-1,000 mg per day may reduce nausea during and after chemotherapy.

Korean Red Ginseng, MACA, L-arginine, L-citrulline and American Ginseng

Preliminary data shows they improve sexual health. Panax ginseng may help reduce fatigue in cancer patients. American ginseng from the Ginseng Board of Wisconsin is arguably the safest, least expensive, and most effective option for fatigue.

Glucosamine, Pycnogenol, SAM-e, Lycopene and Resveratrol

Show no evidence of anti-prostate cancer activity. The few studies published to date are inconclusive and controversial.


It has been used with some success in chronic nonbacterial prostatitis.

Saw Palmetto & Other BPH Supplements

In two major clinical trials, the most commonly used dosage was safe but did not work better than a placebo.


Supplements may increase the risk of aggressive prostate cancer!

Tea and Tea Supplements

Most forms of tea, including black, green, herbal, and oolong are healthy and have few or no calories, so enjoy drinking them. However, please keep in mind that tea-based dietary supplements or pills (not the drink) have no solid proof from human studies that they do anything against prostate cancer. A large clinical trial of high-dose green tea supplements in patients with advanced cancer showed no real benefit.

Whey Protein or Protein Powder

This can be taken as a powdered drink supplement (never as a pill) for any man needing more high-quality protein for health, weight loss and to support muscle health.


Zinc supplements in high dosages, 80 to 100 mg per day or more, should be avoided. Recent human research has linked higher doses of zinc from dietary supplements to abnormal immune changes, a potential reduction in the impact of bone-building drugs, abnormal changes in cholesterol blood tests, increased risk of urinary tract infections, kidney stones, prostate enlargement, and an increased risk of aggressive prostate cancer.

Marijuana Cures Everything, Dude?!

So, let’s review: Personally, if you are healthy, I think the risks of marijuana outweigh the benefits, unless of course you win the lottery and just want to try it one time to celebrate the fact that you never again have to listen to your boss or some of your annoying coworkers. Marijuana has NOT been proven to be heart-healthy and in fact it could be heart-unhealthy. And the smoke does not make the lung tissue happy, even though you could feel temporarily happy.

I frequently hear, “Marijuana is natural.” So, should I get excited about it? Just because it is natural is not the reason I get excited about diddly squat (aka anything). I mean, poison ivy and arsenic are natural, folks, but I usually do not recommend those things—except to my big brother when he pushed my face in the snow when we were kids…

Do I think it’s possible that marijuana or one of its compounds can fight cancer or encourage the growth of cancer? Yes! But at this point, we have no conclusive evidence one way or the other. It’s dangerous to treat humans unless studies in humans show that it works. In Europe, a laboratory study showed that a certain drug could impact a cannabinoid receptor in the brain. “Experts” were convinced that it would be a great weight-loss drug and it was marketed briefly under the trade name of Acomplia (Google that bad boy). It was removed from the market because of serious side effects such as anxiety, suicidal ideation, nausea, and, in some cases, the development of multiple sclerosis.


Name Removed

Dec 19, 2019, 2:05:39 PM12/19/19
Perhaps the list is the wrong one. There is selenium and there is selenium and I'll suggest inorganic form is were any benefits may show.
Boswellia looks interesting for cancer.
Cholecalciferol also look good.
So does menaquinone.
And I'll suggest ratios between estrogens and androgens are important and that the conventional approach of androgen suppression is crude and ultimately dead orifice wrong especially after a couple of years.
And I'll suggest ginger maybe useful.
I see no references.
I see something of an appeal to an authority I don't yet fully accept.

Edward Montague

Dec 22, 2019, 10:44:30 PM12/22/19
You're very courageous to discuss this.

Browsing the web I encounter rather a lot of superficial information
on this topic. There's mention of Green Laser surgery, whether this
is used for partial removal of the affected area isn't mentioned.

There are, as always, various drugs undergoing trials for this condition; most, unfortunately, appear to be at the later stages of the
disease. I have yet to discover any preventative medications.

Professor Linus Pauling, Nobel recipient, died of prostate cancer.
His recommendation was copious amounts of Vitamin C, he also said
that this didn't work in his instance because he didn't start taking
Vitamin C early enough. Vitamin D3 may also be of value.

Now Prof Pauling was born in 1901 and passed away in 1994, he was
of note from 1931 onward.

So you're right to ask why hasn't some group researched this type of
cancer and found a preventative measure, apart from surgery.

A little off topic, the Human Papiloma Virus is responsible for a cancer of the cervix. The general notion that cancers are induced by
viruses was proposed, in the 70s, by another Nobel recipient; Dr Howard . Temin . Dr H. Temin eventually died of a adenocarcinoma, induced by
the associated virus. He, and Dr Baltimore, also researched the HIV,
Temin developing what is known as the Western Blot Test.

The notion about viruses is that they insert code into the DNA of the
recipient, in some instances this finds its way into the germ line
and may, under certain conditions, result in the expression of a cancer.

To this very day, most of the medical profession are unwilling to
acknowledge this as a possibility.

Now in response to this I adopted the stance of precision medicine,
down to the level of the genome, where even supposedly non coding
genes are relevant. I developed this notion a considerable time before
it was publicly mentioned by the likes of politicians.

The computational power required for this, using current algorithms,
is only now becoming available at the exascale; and beyond.
The slow pace of supercomputer development over the last decade is
another topic.

With sufficient computational power and the appropriate software,
drug development can be hastened, even at the preclinical and regulatory level; what appears to be lacking is the motivation on the
part of pharma and perhaps deeply entrenched groups.

With more space flights scheduled, cancer may require even more urgent investigation.

Of course tobacco and alcohol consumption can lead to lung cancer and
spleen cancer; respectively.

This is where we discover that there's more to health than technology, as mentioned many times at the yahoo group site, intent and
fulfilled motivation are also required.

Edward Montague

Jan 1, 2020, 6:17:34 AM1/1/20
On Wednesday, November 6, 2019 at 4:14:44 PM UTC+13, Taka wrote:
You may want to check this out.

Fighting Cancer differently

Don't know how readily available this is around the world,
not many details about what the pharmacueticals were or how

Somehow the person of interest generated a family of his own.

Said that his disease was genetic, ancestral viral infections
and current environmental factors may of resulted in his present

Two interesting approaches to treatment that are improving in
efficacy are RNA Antisense and DNA vaccines; not certain of the
readiness of these for treatment and possibly prevention.

Jan 15, 2020, 10:06:57 PM1/15/20
Xanthohumol has potent anticancer effects killing cancer cells based on epigenetic modulation of many pathways.

Fitoterapia. 2015 Jun;103:71-82. doi: 10.1016/j.fitote.2015.03.007. Epub 2015 Mar 12.
Isoxanthohumol--Biologically active hop flavonoid.
Żołnierczyk AK1, Mączka WK1, Grabarczyk M1, Wińska K1, Woźniak E1, Anioł M2.
Author information
Isoxanthohumol (IXN), apart from xanthohumol (XN) and 8-prenylnaringenin (8PN), is one of the most important prenylflavonoids found in hops. Another natural source of this compound is a shrub Sophora flavescens, used in traditional Chinese medicine. Main dietary source of IXN is beer, and the compound is produced from XN during wort boiling. In the human body, the compound is O-demethylated to 8PN, the strongest known phytoestrogen. This process takes place in the liver and in the intestine, where it is mediated by local microflora. It has been reported in some studies that even though beer contains small amounts of hops and its preparations, these compounds may affect the functioning of the human body. IXN exhibits an antiproliferative activity against human cell lines typical for breast cancer (MCF-7), ovarian cancer (A-2780), prostate cancer (DU145 and PC-3), and colon cancer (HT-29 and SW620) cells. It strongly inhibits the activation of the following carcinogens: 2-amino-3-methylimidazol-[4,5-f]quinoline and aflatoxin B1 (AFB1) via human cytochrome P450 (CYP1A2). It also inhibits the production of prostate specific antigen (PSA). IXN significantly reduces the expression of transforming growth factor-β (TGF-β) in the case of invasive breast cancer MDA-MB-231. It interferes with JAK/STAT signaling pathway and inhibits the expression of pro1inflammatory genes in the monoblastic leukemia cell line (MonoMac6). It activates apoptosis in human umbilical vein endothelial cells (HUVEC) and human aortic smooth muscle cells (HASMCs). In addition, IXN shows an antiviral activity towards herpes viruses (HSV1 and HSV2) and bovine viral diarrhea virus (BVDV).

Copyright © 2015 Elsevier B.V. All rights reserved.

Angiogenesis; Antiproliferative activity; Antitumor activity; Isoxanthohumol; Prenylflavonoids

PMID: 25771121 DOI: 10.1016/j.fitote.2015.03.007
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Int J Mol Sci. 2016 Jun 22;17(6). pii: E837. doi: 10.3390/ijms17060837.
Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand-Induced Apoptosis in Prostate Cancer Cells after Treatment with Xanthohumol-A Natural Compound Present in Humulus lupulus L.
Kłósek M1, Mertas A2, Król W3, Jaworska D4, Szymszal J5, Szliszka E6.
Author information
TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) is an endogenous ligand, which plays role in immune surveillance and anti-tumor immunity. It has ability to selectively kill tumor cells showing no toxicity to normal cells. We tested the apoptotic and cytotoxic activities of xanthohumol, a prenylated chalcone found in Humulus lupulus on androgen-sensitive human prostate adenocarcinoma cells (LNCaP) in combination with TRAIL. Cytotoxicity was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide tetrazolium reduction assay (MTT) and lactate dehydrogenase assay (LDH). The expression of death receptors (DR4/TRAIL-R1 and DR5/TRAIL-R2) and apoptosis were detected using flow cytometry. We examined mitochondrial membrane potential (ΔΨm) by DePsipher reagent using fluorescence microscopy. The intracellular expression of proteins was evaluated by Western blotting. Our study showed that xanthohumol enhanced cytotoxic and apoptotic effects of TRAIL. The tested compounds activated caspases-3, -8, -9, Bid, and increased the expression of Bax. They also decreased expression of Bcl-xL and decreased mitochondrial membrane potential, while the expression of death receptors was not changed. The findings suggest that xanthohumol is a compound of potential use in chemoprevention of prostate cancer due to its sensitization of cancer cells to TRAIL-mediated apoptosis.

TRAIL; apoptosis; prostate cancer cells; xanthohumol

PMID: 27338375 PMCID: PMC4926371 DOI: 10.3390/ijms17060837
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Mol Med. 2012 Dec 6;18:1292-302. doi: 10.2119/molmed.2012.00174.
Xanthohumol impairs human prostate cancer cell growth and invasion and diminishes the incidence and progression of advanced tumors in TRAMP mice.
Venè R1, Benelli R, Minghelli S, Astigiano S, Tosetti F, Ferrari N.
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Despite recent advances in understanding the biological basis of prostate cancer, management of the disease, especially in the phase resistant to androgen ablation, remains a significant challenge. The long latency and high incidence of prostate carcinogenesis provides the opportunity to intervene with chemoprevention to prevent or eradicate prostate malignancies. In this study, we have used human hormone-resistant prostate cancer cells, DU145 and PC3, as an in vitro model to assess the efficacy of xanthohumol (XN) against cell growth, motility and invasion. We observed that treatment of prostate cancer cells with low micromolar doses of XN inhibits proliferation and modulates focal adhesion kinase (FAK) and AKT phosphorylation leading to reduced cell migration and invasion. Oxidative stress by increased production of reactive oxygen species (ROS) was associated with these effects. Transgenic adenocarcinoma of the mouse prostate (TRAMP) transgenic mice were used as an in vivo model of prostate adenocarcinoma. Oral gavage of XN, three times per week, beginning at 4 wks of age, induced a decrease in the average weight of the urogenital (UG) tract, delayed advanced tumor progression and inhibited the growth of poorly differentiated prostate carcinoma. 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.

PMID: 22952060 PMCID: PMC3521786 DOI: 10.2119/molmed.2012.00174
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Anticancer Res. 2010 Sep;30(9):3333-9.
Growth inhibitory and apoptosis-inducing effects of xanthohumol, a prenylated chalone present in hops, in human prostate cancer cells.
Deeb D1, Gao X, Jiang H, Arbab AS, Dulchavsky SA, Gautam SC.
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Promotion of apoptosis in cancer cells could potentially lead to the regression and improved prognosis of hormone-refractory prostate cancer. Xanthohumol (XN), a prenylated chalcone-derived from hops, has shown strong antitumorigenic activity towards diverse types of cancer cells. In the present study, the growth-inhibitory and apoptosis-inducing activity of XN was tested in hormone-sensitive and hormone-refractory human prostate cancer cells lines. Cell growth/viability assay (MTS) demonstrated that prostate cancer cells are highly sensitive to XN at a concentration range of 20-40 μM. The primary mode of tumor cell destruction was apoptosis as demonstrated by the binding of annexin V-FITC, cleavage of PARP-1, activation of procaspases -3, -8, and -9, mitochondrial depolarization and release of cytochrome c from mitochondria. 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.

PMID: 20944105 PMCID: PMC3846352
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FASEB J. 2010 Aug;24(8):2938-50. doi: 10.1096/fj.10-155846. Epub 2010 Mar 24.
Xanthohumol-induced transient superoxide anion radical formation triggers cancer cells into apoptosis via a mitochondria-mediated mechanism.
Strathmann J1, Klimo K, Sauer SW, Okun JG, Prehn JH, Gerhäuser C.
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Oxidative stress and increased release of reactive oxygen species (ROS) are associated with apoptosis induction. Here we report ROS-mediated induction of apoptosis by xanthohumol (XN) from hops. XN at concentrations of 1.6-25 microM induced an immediate and transient increase in superoxide anion radical (O(2)(-*)) formation in 3 human cancer cell lines (average+/-SD EC(50) of maximum O(2)(-*) induction=3.1+/-0.8 microM), murine macrophages (EC(50)=4.0+/-0.3 microM), and BPH-1 benign prostate hyperplasia cells (EC(50)=4.3+/-0.1 microM), as evidenced by the O(2)(-*)-specific indicator dihydroethidium. MitoSOX Red costaining and experiments using isolated mouse liver mitochondria (EC(50)=11.4+/-1.8 microM) confirmed mitochondria as the site of intracellular O(2)(-*) formation. Antimycin A served as positive control (EC(50)=12.4+/-0.9 microM). XN-mediated O(2)(-*) release was significantly reduced in BPH-1 rho(0) cells harboring nonfunctional mitochondria (EC(50)>25 microM) and by treatment of BPH-1 cells with vitamin C, N-acetylcysteine (NAC), or the superoxide dismutase mimetic MnTMPyP. In addition, we demonstrated a rapid 15% increase in oxidized glutathione and a dose-dependent overall thiol depletion within 6 h (IC(50)=24.3+/-11 microM). Respiratory chain complexes I-III were weakly inhibited by XN in bovine heart submitochondrial particles, but electron flux from complex I and II to complex III was significantly inhibited in BPH-1 cells, with IC(50) values of 28.1 +/- 2.4 and 24.4 +/- 5.2 microM, respectively. Within 15 min, intracellular ATP levels were significantly reduced by XN at 12.5 to 50 microM concentrations (IC(50)=26.7+/-3.7 microM). Concomitantly, XN treatment caused a rapid breakdown of the mitochondrial membrane potential and the release of cytochrome c, leading to apoptosis induction. Pre- or coincubation with 2 mM NAC and 50 microM MnTMPyP at various steps increased XN-mediated IC(50) values for cytotoxicity in BPH-1 cells from 6.7 +/- 0.2 to 12.2 +/- 0.1 and 41.4 +/- 7.6 microM, and it confirmed XN-induced O(2)(-*) as an essential trigger for apoptosis induction. In summary, we have identified mitochondria as a novel cellular target of XN action, resulting in increased O(2)(-*) production, disruption of cellular redox balance and mitochondrial integrity, and subsequent apoptosis.

PMID: 20335224 DOI: 10.1096/fj.10-155846
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Int J Mol Sci. 2009 Dec 24;11(1):1-13. doi: 10.3390/ijms11010001.
Chalcones enhance TRAIL-induced apoptosis in prostate cancer cells.
Szliszka E1, Czuba ZP, Mazur B, Sedek L, Paradysz A, Krol W.
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Chalcones exhibit chemopreventive and antitumor effects. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a naturally occurring anticancer agent that induces apoptosis in cancer cells and is not toxic to normal cells. We examined the cytotoxic and apoptotic effect of five chalcones in combination with TRAIL on prostate cancer cells. The cytotoxicity was evaluated by the MTT and LDH assays. The apoptosis was determined using flow cytometry with annexin V-FITC. Our study showed that all five tested chalcones: chalcone, licochalcone-A, isobavachalcone, xanthohumol, butein markedly augmented TRAIL-mediated apoptosis and cytotoxicity in prostate cancer cells and confirmed the significant role of chalcones in chemoprevention of prostate cancer.

TRAIL (tumor necrosis factor-related apoptosis-inducing ligand); apoptosis; chalcones; chemoprevention; prostate cancer

PMID: 20161998 PMCID: PMC2820986 DOI: 10.3390/ijms11010001
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Phytother Res. 2008 Feb;22(2):197-203.
Treatment of PC-3 and DU145 prostate cancer cells by prenylflavonoids from hop (Humulus lupulus L.) induces a caspase-independent form of cell death.
Delmulle L1, Vanden Berghe T, Keukeleire DD, Vandenabeele P.
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Xanthohumol (X), isoxanthohumol (IX), 8-prenylnaringenin (8PN) and 6-prenylnaringenin (6PN), prenylflavonoids from hop (Humulus lupulus L.), were investigated for their cytotoxicity and the mechanism by which they exert cell death when incubated with prostate cancer cell lines PC-3 and DU145. All compounds induced cell death in the absence of caspase-3 activation and typical apoptotic morphological features. The general pan-caspase inhibitor zVAD-fmk could not protect this form of cell death. In addition, the formation of vacuoles was observed in PC-3 cells treated with IX and 6PN, and in DU145 treated with IX, 8PN and 6PN, which could suggest the induction of autophagy and consequent cell death. The results indicate that hop-derived prenylflavanones (IX, 8PN, 6PN), but not prenylchalcones (X) induce a caspase-independent form of cell death, suggested to be autophagy. Therefore, IX, 8PN and 6PN appear to be promising candidates for further investigation in prostate anticancer therapy.

PMID: 17726738 DOI: 10.1002/ptr.2286
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Cancer Lett. 2007 Feb 8;246(1-2):201-9. Epub 2006 Mar 24.
Xanthohumol, a prenylflavonoid derived from hops induces apoptosis and inhibits NF-kappaB activation in prostate epithelial cells.
Colgate EC1, Miranda CL, Stevens JF, Bray TM, Ho E.
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There is increasing evidence that certain natural compounds found in plants may be useful as cancer chemopreventive or chemotherapeutic agents. Limited in vitro studies indicate that several prenylated flavonoids present in the hop plant (Humulus lupulus) possess anticarcinogenic properties. The purpose of this study was to investigate the anti-tumorigenic effects of xanthohumol (XN), the major prenylflavonoid in hops, on prostate cancer and benign prostate hyperplasia. BPH-1 and PC3 cell lines were used in our study to represent both non-tumorigenic hyperplasia and malignant prostate cancer. In both BPH-1 and PC3 cells, XN and its oxidation product, XAL, decreased cell viability in a dose dependent manner (2.5-20 microM) as determined by MTT assay and caused an increase in the formation of early and late apoptotic cells as determined by Annexin V staining and multicaspase assays. XN and its oxygenated derivative also induced cell cycle changes in both cells lines, seen in an elevated sub G1 peak at 48h treatment. Western blot analysis was performed to confirm the activation of proapoptotic proteins, Bax and p53. XN and its derivative caused decreased activation of NFkappaB. This work suggests that XN and its oxidation product, XAL, may be potentially useful as a chemopreventive agent during prostate hyperplasia and prostate carcinogenesis, acting via induction of apoptosis and down-regulation of NFkappaB activation in BPH-1 cells.

PMID: 16563612 DOI: 10.1016/j.canlet.2006.02.015
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Edward Montague

Mar 23, 2020, 2:35:49 AM3/23/20
On Wednesday, November 6, 2019 at 4:14:44 PM UTC+13, Taka wrote:
A fair while ago I read an article by one of the co founders
of Intel Corp, probably Andy Groves; who was diagnosed in his
50's. He passed away 29 years later, apparently from Parkinson's
In the article he mentions how the medics were using a i286
based scanner.Intel had stopped producing that I.C fifteen years

So thirty three years later and numerous generations since the
i286, an Intel employee with prostate cancer who has been on a
mission to find a cure, and many are still waiting.

Edward Montague

Mar 31, 2020, 1:35:00 AM3/31/20
On Wednesday, November 6, 2019 at 4:14:44 PM UTC+13, Taka wrote:
Hispanic populations don't succumb to prostate cancer as much
as others, conceivably because of a diet that has less dairy.

May seem a little off topic.
The bat genome may contain useful information as they're so
resilient against cancer.

Aug 28, 2020, 2:10:52 AM8/28/20
I tend to browse the web, quite often I watch a few movies, other times I
look for interesting articles like these; well interesting to some readers of
this forum.

Using your own immune systems T cells, after genetic enhancement, to destroy
cancer cells.

One company that has run, with only partial success, phase one trials is
Poseida Therapeutics .
They encountered a fatality with one of their test subjects, the others
didn't exhibit any untoward symptons.

A possible improvement is implied by this approach, Co-LOCKR.

Don't get over optimistic.

Aug 30, 2020, 10:01:33 AM8/30/20
Also one of possibly many considerations , is mentioned in this article.

The Judge

Aug 31, 2020, 9:43:13 AM8/31/20
There is hope. A new 2 pronged approach has shown 100% tumor removal in mice! Nothing I have read has ever shown 100% success.
Read it here:

Sep 4, 2020, 6:17:00 PM9/4/20
On Tuesday, September 1, 2020 at 1:43:13 AM UTC+12, The Judge wrote:
> There is hope. A new 2 pronged approach has shown 100% tumour removal in mice! Nothing I have read has ever shown 100% success.
This is what's really required. We're not aware of all of the carcinogens
in the environment, nor their consequences for our health . I was wondering a wee while ago as to whether a probe might be made for our
mobile phones that let us monitor pollutants in the environment.

On another related matter, were you caught unawares when your doctor
told you about your illness. Whose responsibility is it to forewarn and
prepare you for these possibilities. If you'd known about this possibility
might you have put in a concerted effort to prevent or prepare; done
something different with your life.
Considering how uses private compute power from
a multitude of individuals, and provides information to the public, the
knowledge is everywhere; except, perhaps, in the doctors clinic.

Sep 20, 2020, 9:16:04 PM9/20/20

Sep 20, 2020, 9:19:13 PM9/20/20
On Saturday, September 5, 2020 at 10:17:00 AM UTC+12, wrote:
A little unfamiliar with the posting procedures of this site.

Might be of some interest, also allows me to have a record of developments.

Using gold nanoparticles of the right size the large leaky vessels that feed
tumours are selectively targeted, whilst the smaller veins of the rest of the
body are avoided.

Then infra red light, possibly from a laser, is applied. This results in
the ablation of the cancerous material, what remains might then be suceptiblle
to immunotherapy.
Angiogenesis in tumours has been known and studied for decades.

That's the theory, these are some of the results.

Sep 22, 2020, 12:40:20 AM9/22/20
Considering the availability of different treatment options, all with different efficacies, toxicities;
the construction of a decision tree, or an if...then...else statement seems appropriate.

Then another possibility is a neural network that has, and does, learn from clinical outcomes.
At this level this might not be as complicated as at the drug discovery level.
And of course, all the while, for the patient, doing no harm.

Now clinical trials involve a degree of risk, the FDA is there to regulate these risks and
determine the safety of medications. Time, I think, for them to provide functioning mini
organs in a support medium, derived from the volunteers stem cells, or at least for the
initial screening, something generic.
Maybe after thirty years they're still not up to the task.

Sep 25, 2020, 11:58:50 PM9/25/20
Car t cells certainly are effective for some cancers, as are other types of immunotherapy.
A consideration though , is damage to cells that have similar binding sites protruding
from their lipid membranes, this is where a selection for multiple and unique binding sites
becomes essential; there are a few approaches to this.
To check on the selectivity , a screening for exclusive binding is required; in a medium.

If solid tumours aren't completely eliminated then the possibility of metastatic cancers from
these is always present, how effectively car t cell therapies are going to be against the various
forms of these is, at this time, an unknown.

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