Prevent and cure cancer

#121

Attia does low dose CT scan, to my knowledge. I think the radiation isn’t something to worry about, in the context of life in general

I would have to assume so, but I think it would be super difficult to prove with a trial. But in general, people who are sedentary get more cancer, people who are active get less, and now we have like the joining part, where people with cancer have better outcomes with exercise. So IMO it’s likely that exercise ticks box boxes.

What I’d be really interested in is knowing the dose and type of exercise. For example, I wonder if resistance training would qualify under the 4 hours per week.

And FWIW, I find it really hard to believe there’s any sort of “one size fits all” general statement for cancer. I’m sure lactate and mitochondria are important, but you get foetuses with cancerous growths in the womb, or really young kids tragically getting fatal cancers. It’s hard to imagine they have metabolic health or mitochondrial problems, and if they did, how that wouldn’t have been determined already.

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#122

That’s like the trial that could be powered to detect any effect in cancer prevention. But if prospective cohort studies show a reduction in cancer as well, I’d act as if it is causal until further evidence. It’s like cholesterol lowering meds only being powered to detect effects in people with high risk of CVD. We still believe it will be the case in those with low risk over time. But we have genetic studies as well, I don’t know if that could be established for exercise → cancer. Maybe future studies can find a biomarker that exercise improves and which explains the reduction in cancer, which there’s genetic variation in that exposure. Then it’d be easy to see if it’s causal and even have an important biomarker to track. Pharma would probably find a way to drug it as well.

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#124

Yes, but you’d need an enormous population. These people already had cancer, and there’s a very high percentage of reoccurrence. If you grabbed random people from the general population, the general chance of cancer within the trial period is pretty low.

As for exercise biomarkers, you might be interested in this: https://www.motrpac.org They’ve published a ton of papers now, omics (transcriptomic, proteomic, kinome, metabolome etc) datasets etc showing acute responses to exercise.

#125

Awesome paper from a team at UCLA: Serotonin transporter inhibits antitumor immunity through regulating the intratumoral serotonin axis (Cell, 2025)

Identifying additional immune checkpoints hindering antitumor T cell responses is key to the development of next-generation cancer immunotherapies. Here, we report the induction of serotonin transporter (SERT), a regulator of serotonin levels and physiological functions in the brain and peripheral tissues, in tumor-infiltrating CD8 T cells. Inhibition of SERT using selective serotonin reuptake inhibitors (SSRIs), the most widely prescribed antidepressants, significantly suppressed tumor growth and enhanced T cell antitumor immunity in various mouse syngeneic and human xenograft tumor models. Importantly, SSRI treatment exhibited significant therapeutic synergy with programmed cell death protein 1 (PD-1) blockade, and clinical data correlation studies negatively associated intratumoral SERT expression with patient survival in a range of cancers. Mechanistically, SERT functions as a negative-feedback regulator inhibiting CD8 T cell reactivities by depleting intratumoral T cell-autocrine serotonin. These findings highlight the significance of the intratumoral serotonin axis and identify SERT as an immune checkpoint, positioning SSRIs as promising candidates for cancer immunotherapy.

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#126

Many Lung Cancers Are Now in Nonsmokers. Scientists Want to Know Why.

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#127

Any thoughts on Dr Aubrey de Grey’s theory of telomerase being more active in cancers and the solution to cancer is to actually turn telomerase off and do stem cell replacement of cells to over one a lack of telomerase?

Hopefully I didn’t butcher that. I read it in one of his books.

#128

Long-term use of low-dose aspirin for cancer prevention: A 20-year longitudinal cohort study of 1,506,525 Hong Kong residents

Long-term use of low-dose aspirin has been demonstrated to reduce cancer risk, but the duration of necessary medication use remains uncertain. This study aimed to investigate the long-term chemoprotective effect of aspirin among the Chinese population. This population-based study included all aspirin users between 2000 and 2019. Aspirin users were age-sex matched with non-users at a 1:2 ratio. Cancer incidence and mortality were the main outcomes measured. Survival analyses with the Fine-Gray modelling were performed. The chemoprotective effects were measured by the sub-distribution hazard ratios (SHR) with control for the competing risks. A total of 538,147 aspirin users and 968,378 non-users were included, with a mean age of 64.8 years, 9,543,399 person-years of follow-up and 90% of users with 80 mg aspirin. The long-term use of aspirin was associated with a reduced risk of cancer (SHR 0.92, 95% CI 0.91-0.94) and a reduced risk of cancer mortality (SHR 0.80, 95% CI 0.79-0.82). Stronger chemopreventive effects were observed among those who used aspirin for more than 10 years, including risk reductions for lung (SHR 0.56, 95% CI 0.51-0.60), breast (SHR 0.34, 95% CI 0.29-0.38) and colorectal (SHR 0.37, 95% CI 0.33-0.40) cancers, but not for bladder cancer and leukaemia. Low-dose use of aspirin was associated with lower risk of cancer among Chinese. The association was even stronger for those using aspirin for more than 10 years. Prescription of aspirin may be started as early as at age of 40, as the chemoprotective effect also applied for early cancers.

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#129

An abortion drug for breast cancer is being blocked by moral and political interests

A group of experts says that conservative politics have hampered research on mifepristone. ‘It’s scary to investigate it and look pro-abortion’

On December 1, 2006, the journal Science flagged up a promising development. “In the future, perhaps, drugs can be used to prevent breast cancer,” the article predicted. Almost 20 years later, that hasn’t happened. The ‘maybes’ in scientific journals should be written in capital letters. Science advances slowly and there are many obstacles in its path: lack of funding, errors, dead ends… But in this case, the research has also been impeded by moral prejudice and political bias.

The drug Science was talking about is called mifepristone and is used to induce abortions. And this is a problem. “It’s scary to investigate it and look pro-abortion,” Swedish researcher Kristina Gemzell Danielsson, from the Karolinska Institutet, explains. Danielsson is one of the signatories of a recent editorial published in The Lancet denouncing the situation. “We have very promising data, but no efforts are being made to continue with the research,” she explains. “Mifepristone is also extremely expensive to use for research and the regulatory hurdles are absurd, probably because it is associated with induced abortion.”

Squelching Progesterone’s Signal May Prevent Breast Cancer

Lee’s team also showed that mifepristone, a drug that induces abortions by inhibiting the progesterone receptor, blocks the development of mammary tumors in mice that have had the rodent version of BRCA1 inactivated in their mammary glands. “The paper has a mechanism [of BRCA1 activity] and has clinical implications. It’s potentially important,” says Eliot Rosen of Georgetown University School of Medicine in Washington, D.C., who is also studying the interaction between BRCA1 and progesterone.

Read the full article:

https://www.science.org/doi/10.1126/science.314.5804.1370

The potential role of mifepristone in breast cancer prevention: beyond medical abortion

Breast cancer is the leading cause of cancer-related deaths among women globally. Yet, current management strategies emphasise detection and treatment over primary prevention. For groups at high risk of breast cancer, such as carriers of BRCA1 or BRCA2 pathogenic variants, salpingo-oophorectomy and mastectomy are risk-reducing surgical options, but these approaches affect quality of life and evidence for a mortality benefit is sparse. Non-surgical treatments, such as selective oestrogen receptor modulators, have low efficacy against breast cancers with poor prognosis (eg, triple-negative cancers), and toxicity can often lead to poor adherence. Emerging evidence indicates that progesterone plays a part in breast carcinogenesis, particularly in carriers of BRCA1 pathogenic variants. Mifepristone, a selective progesterone receptor modulator, has shown potential to reduce breast epithelial proliferation. However, the association of this drug with medical abortion, besides long-standing availability and patent restrictions, has hindered its development for breast cancer prevention. Regulatory, political, and legal barriers, along with minimal pharmaceutical investment, have further restricted research. Collaborative efforts are needed to accelerate research on mifepristone as a non-surgical risk-reducing option. Overcoming current barriers is essential to expand prevention strategies, particularly for women at high risk of breast cancer worldwide.

https://www.thelancet.com/journals/lanogw/article/PIIS3050-5038(25)00013-5/abstract

ChatGPT:

Identify the research papers that suggest that mifepristone may be helpful against breast cancer

Here’s a concise, citation-backed list of peer-reviewed papers (plus a few registered trials) that have reported signals suggesting mifepristone (RU-486) could be helpful against breast cancer—either directly as an anti-tumor agent or by enhancing other therapies.

Clinical and translational studies in humans

  • MIPRA trial (biomarker-selected neoadjuvant study).
    Single-arm window-of-opportunity trial showing Ki-67 reductions and molecular responses to short-course mifepristone in patients whose tumors had a high PR-A:PR-B isoform ratio (PRA-H)—supporting antiprogestins in a selected subset. (PMC)

  • Randomized phase I (nab-paclitaxel ± mifepristone) in advanced breast cancer.
    Demonstrated feasibility and signals of activity (including complete and partial responses) when pretreating with mifepristone; rationale was glucocorticoid receptor (GR) antagonism to overcome chemo-resistance. (PMC)

  • Randomized phase II (nab-paclitaxel ± mifepristone) in advanced TNBC.
    Under-accrued study; no PFS benefit overall, but responders were seen and authors note the need for biomarker-driven selection for GR/PR targeting. Useful as context for where mifepristone may (or may not) help. (PMC)

  • Single-agent phase II in metastatic PR-positive disease (1990s).
    Early trials of mifepristone (and related antiprogestins) in metastatic breast cancer reported modest activity in small cohorts—important historically for the antiprogestin concept. (PubMed)

  • Short-term exposure study in healthy/premenopausal women.
    50 mg/day mifepristone for 3 months reduced breast epithelial proliferation (Ki-67), a prevention-relevant endpoint. (Oxford Academic)

  • Case reports suggesting benefit.
    Isolated reports describe marked clinical responses with mifepristone, including a complete remission after short exposure; these are hypothesis-generating only. (IIAR Journals)

Preclinical/mechanistic work underpinning benefit

  • GR antagonism as a strategy in TNBC.
    Foundational lab paper showing that mifepristone blocks GR-mediated pro-survival signaling and enhances taxane-induced apoptosis in GR-positive triple-negative models—providing the mechanistic basis for clinical combinations.

  • TNBC xenograft study (Theranostics).
    Additional in-vivo work supporting mifepristone’s anti-proliferative and anti-metastatic effects in TNBC models. (PMC)

Ongoing/related clinical efforts (context)

  • Pembrolizumab + mifepristone (HER2-negative metastatic breast cancer).
    Phase II trial exploring GR blockade with immunotherapy; abstracted results presented (safety/efficacy signals). (ASCO Publications, ClinicalTrials.gov, Cancer.gov)

  • Enzalutamide ± mifepristone vs. physician’s choice in AR-expressing disease.
    A current phase II design testing whether adding mifepristone can improve outcomes; included here to show how investigators are operationalizing the hypothesis. (ClinicalTrials.gov, Cancer.gov)

How to read this evidence

  • The strongest positive human signal so far is biomarker-selected (PRA-H in the MIPRA study).
  • Attempts to use mifepristone broadly (e.g., unselected TNBC with nab-paclitaxel) have not yet shown clear PFS benefit, reinforcing the need for selection by PR isoforms and/or GR activity. (PMC)

If you want, I can filter these into a mini-bibliography (APA/AMA) or pull out key data (dose, schedule, endpoints, effect sizes) for the papers most relevant to your use case.

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#130

Old post I missed, purple Owsley blotter was quite popular in my day :slight_smile:

For a couple years my buddies and I would take a trip every couple months :slight_smile: We went on one run doing it every weekend for about 3 months in 1972. As a bunch of farmer boys most of our trips were at a cabin we built in the woods.

Green Frog and Yellow Sunshine and a few other come to mind but that was 50+ years ago.

The stories I could tell.

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#131

I kept searching mycotherapy §(medicinal mushrooms) for cancer prevention. The recurring combo for cancer prevention (as sell as cure adjuvant) seems to be:

  1. Turkey tail (Trametes or Coriolus versicolor)
  2. Reishi (Ganoderma lucidum).

My concern is whether it is acceptable in prevention to take them intermittently, for example, one or two months on and two off. For various reasons, including cost: high-quality powders and extracts are not inexpensive.

Here’s a concise, prevention‑focused snapshot of what the medical and pre‑clinical literature says about Coriolus versicolor (Trametes versicolor) and Ganoderma lucidum (Reishi) when the goal is reducing cancer risk rather than treating established disease.

:seedling: Biological rationale for prevention

  • Immune surveillance support:
  • Anti‑inflammatory effects:
  • Antioxidant activity:
  • Direct anti‑proliferative actions:

:books: Selected preventive‑relevant findings

  • Colorectal adenoma suppression: A water‑soluble extract from G. lucidum mycelia inhibited the development of colorectal adenomas in a small human study, suggesting possible chemopreventive activity in the colon.
  • Immune modulation in healthy or at‑risk adults: Pilot trials and observational studies report increased NK‑cell activity and T‑cell subsets after supplementation, which could translate into improved cancer immunosurveillance.
  • Synergistic potential: Reviews note that combining G. lucidum and C. versicolor may broaden the spectrum of bioactive compounds, potentially enhancing preventive effects through complementary mechanisms.

In summary: Laboratory and early human data suggest that Coriolus versicolor and Ganoderma lucidum may help reduce cancer risk by modulating immunity, lowering inflammation, and protecting against oxidative DNA damage. While promising, these findings need confirmation in robust, long‑term prevention trials before firm recommendations can be made.

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