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I saw some info about the recent study on Ovarian Cancer and Cannabinoids and it reminded me of Dr. Dedi Meiri's research on Cannabinoid combinations causing cancer cell death. It appears Dr. Meiri is continuing to study this awesome plant.
There’s a claim making the rounds that “non-psychoactive cannabis compounds have been proven to stop aggressive ovarian cancer cells from forming colonies” and that this is a “breakthrough” for people who’ve run out of chemo options.
That sounds amazing.
It’s also not what the science actually says.
The truth is more interesting, more nuanced, and – if anything – points right back to what researchers like Dr. Dedi Meiri at Technion have been showing for years: cannabinoids can hit cancer cells hard, but only in very specific combinations, and we’re still at the preclinical stage.
Let’s unpack it properly.
What the new ovarian cancer study actually found
On December 15, 2025, a paper in Frontiers in Pharmacology reported that CBD (cannabidiol) and THC (delta-9-tetrahydrocannabinol), used together, showed strong anti-cancer activity against ovarian cancer cells in the lab. (Frontiers)
Key points:
Researchers worked with ovarian cancer cell lines SKOV3 and A2780, plus non-cancerous ovarian surface epithelial cells (IOSE) as controls. (ResearchGate)
They tested CBD alone, THC alone, and a CBD:THC combination.
The combination:
Slowed cancer cell growth.
Reduced colony formation (the ability of a few cells to seed new clusters).
Reduced migration, which is a basic lab proxy for metastatic potential. (Inside Precision Medicine)
Crucially, the treatment did minimal damage to healthy IOSE cells at the same concentrations. (ScienceDaily)
Mechanistically, they focused on the PI3K/AKT/mTOR pathway, which is notoriously overactivated in ovarian cancer and tied to cell proliferation, survival, and chemoresistance. The CBD+THC combo appeared to:
Reduce phosphorylation (activation) of key proteins in that pathway.
Restore activity of PTEN, a tumor-suppressor that normally reins that pathway in. (Frontiers)
Put simply: in a petri dish, the cannabinoid combo pushed ovarian cancer cells away from “divide and spread” and toward “stop and die,” while sparing normal cells much of the collateral damage.
That’s big – for a cell-culture study.
What this study does NOT show
Here’s where social media and headlines start to overreach.
This study:
Did not prove that “non-psychoactive cannabinoids alone” can stop aggressive ovarian cancer. THC – a psychoactive compound – was part of the most effective combo. (Frontiers)
Did not test this in animals or humans. There were no patients, no survival curves, no clinical outcomes – only cells in a dish.
Did not demonstrate that this is a working option for people who have “exhausted chemo.” That’s speculation layered on top of preclinical data.
Did not freeze cancer “for good”. It showed a powerful hit to growth and migration under controlled lab conditions. That’s promising, not final.
It’s still early-stage, but it’s not nothing. It’s a serious, peer-reviewed piece of evidence that cannabinoids can target a central growth pathway in ovarian cancer with surprising precision.
And it fits into a much larger pattern of research that’s been emerging for years.
Enter Dr. Dedi Meiri and the Technion data machine
Years ago I wrote about Dr. David “Dedi” Meiri from the Technion – Israel Institute of Technology. He heads the Laboratory of Cancer Biology and Cannabinoid Research and has basically dedicated his career to one question:
Can specific cannabinoid combinations push specific cancer cells into apoptosis (programmed cell death) – and can we map that reliably? (Cancer Biology Lab)
His lab has done three especially important things:
Built detailed cannabinoid fingerprints of different cannabis chemovars.
In 2018 they published a method to comprehensively profile phytocannabinoids via LC-MS, giving them a high-resolution map of what’s actually in each extract – far beyond “THC and CBD.” (Cancer Biology Lab)Shown that whole-plant extracts can selectively kill cancer cells and induce apoptosis.
A 2019 paper by Baram et al. (with Meiri as co-author) showed that some specific cannabis extracts:Impaired survival and proliferation of various cancer cell lines.
Induced apoptosis – not just random toxicity.
Had highly variable effects depending on the exact cannabinoid/terpene profile. (PMC)
Translation: “Cannabis” is not one drug. Some profiles barely touch the cancer; others hit it like a hammer.
Identified a cannabinoid combo that targets NOTCH1-mutated T-cell leukemia.
More recently, Meiri’s group reported that a specific cannabis chemovar – and then a purified trio of phytocannabinoids from it – selectively induced apoptosis in NOTCH1-mutated T-cell acute lymphoblastic leukemia (T-ALL) cells. (eLife)They showed that these cannabinoids:
Interfered with Notch1 maturation, a key driver of that leukemia.
Triggered cell death in the mutated leukemia cells.
Were far less harmful to non-mutated cells.
This is the same general pattern we see in the new ovarian cancer paper: find the signaling pathway the tumor relies on, then hit it with a very specific cannabinoid combo that cancer cells can’t easily dodge.
The pattern: not “cannabis cures cancer,” but targeted combinations
When you line up Meiri’s work with the new ovarian cancer study, three themes repeat:
Specificity matters.
Pathways, not magic.
In leukemia, the combo hits Notch1 signaling. (eLife)
In ovarian cancer, the combo hits PI3K/AKT/mTOR and restores PTEN regulation. (Frontiers)
We’re not talking about a miracle plant that “just knows what to do.” We’re talking about specific molecules modulating very specific biochemical circuits.
Preclinical – not yet standard of care.
Most of this is still:in vitro (cell lines)
sometimes in vivo (animal models)
and only rarely in early human trials
This is exactly the kind of data you want before human trials – but it’s not a substitute for them.
Why this still matters for ovarian cancer
Ovarian cancer is one of the deadliest gynecologic cancers: late diagnosis, high recurrence, brutal side-effects from standard treatment, and limited second-line options. (Inside Precision Medicine)
So when a study shows that:
A CBD+THC combo can:
reduce cell growth,
reduce colony formation,
reduce migration,
and do it while sparing healthy cells, (ScienceDaily)
and it targets one of the major survival pathways (PI3K/AKT/mTOR),
then yes – that is a legit signal we should be following up on. It lines up with Meiri’s broader finding that certain cannabinoids, in the right ratios, can act as genuine anti-cancer agents in the lab.
The honest way to frame it is:
Cannabis-derived compounds are showing reproducible, pathway-level anti-cancer effects in preclinical models, including ovarian cancer. The next step is serious animal and human trials – not Facebook miracles.
Where the online “breakthrough” narrative goes off the rails
Here’s how the social post version usually mutates:
“Non-psychoactive cannabis compound cures ovarian cancer.”
“Cancer cells froze and couldn’t replicate.”
“Game-changer for patients who tried every chemo.”
Reality check:
The most effective combo in the study included THC, which is psychoactive. That doesn’t mean it can’t be used medically; it just means the “non-psychoactive only” claim is false. (Frontiers)
“Frozen for good” is not a measured endpoint. They looked at growth, colony formation, and migration over specific time windows.
No human beings were treated in this paper. No one with recurrent, chemo-resistant ovarian cancer was shown to benefit – yet.
The danger here isn’t hope. Hope is fine. The danger is overselling preclinical data as a proven cure, which:
Sets patients up for disappointment.
Gives ammunition to regulators and skeptics who already dismiss cannabis as “over-hyped.”
Undermines the very real, hard-earned progress people like Meiri and other researchers have been making for years.
What a grounded cannabis-and-cancer conversation should sound like
If we’re going to be honest – and useful – the conversation needs to sound more like this:
There is solid evidence that cannabinoids provide palliative benefits in oncology: nausea control, appetite stimulation, pain relief, sleep, anxiety. (Cancer Biology Lab)
There is growing preclinical evidence that specific cannabinoid combinations can:
induce apoptosis,
slow proliferation,
and interfere with survival pathways in certain cancers (ovarian, leukemias, glioma, breast, etc.). (PMC)
We do not yet have large-scale clinical proof that any cannabinoid protocol “cures” cancer in humans.
The smartest path forward looks like:
mapping cannabinoid profiles the way Meiri’s group is doing,
pairing them with tumor genetics and signaling pathways,
and running properly designed clinical trials, especially in hard-to-treat or chemo-resistant disease.
On the patient side, the only safe answer is:
This is not medical advice.
Anyone considering cannabis alongside cancer treatment needs to be talking with their oncology team, not just the internet.
At the same time, it’s completely legitimate for patients and advocates to push for:
more research,
more access to whole-plant options,
and serious exploration of cannabinoid-based adjuncts in oncology, rather than brushing this off as “anecdotal.”
Bottom line
The December 15, 2025 study is real and important: CBD + THC showed strong, pathway-level anti-cancer effects against ovarian cancer cells in vitro, with limited harm to healthy cells. (Frontiers)
It does not yet translate into a proven treatment for people with ovarian cancer.
Dr. Dedi Meiri’s work at Technion backs up the overall pattern: specific cannabinoid combinations can selectively push certain cancers into apoptosis, but everything depends on the exact profile and the tumor biology. (PMC)
The responsible narrative isn’t “cannabis cures cancer.” It’s:
“Cannabinoid science is maturing. We’re finally mapping which compounds do what, to which cancers, and why. The system needs to stop pretending this is fringe and start funding the trials.”
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