Cannabis and Cancer: What the Evidence Actually Shows

Cannabis helps a lot of people get through cancer treatment. That is not the same thing as treating cancer. Almost all the confusion lives in the gap between those two sentences.

Twenty-five years of laboratory work, two very small human trials aimed at the tumor itself and a British study still recruiting that could finally move the question beyond tiny exploratory human studies. Here is what the evidence supports, and what it does not.

Cancer patients are using cannabis faster than physicians can tell them whether it works.

In 2024, the American Society of Clinical Oncology, the main professional body for cancer doctors in the United States, published its first full guideline on cannabis and cannabinoids in adults with cancer. The panel worked through thirteen systematic reviews and dozens of trials. It opened by conceding the obvious: patient use has run well ahead of the evidence.

Its central recommendation is that cannabis should not be used as cancer-directed treatment, meaning treatment aimed at the tumor itself, outside a clinical trial. On the one hand, there’s a real and growing body of evidence that cannabis helps people endure cancer and its treatment. On the other hand, a claim that has circulated for two decades without a single adequately powered human trial behind it.

What the Evidence Supports

Solid ground is symptom management.

Nausea ranks highest. For patients still vomiting through chemotherapy despite standard anti-nausea drugs, ASCO says cannabinoids can be added to the regimen. This is the oldest formal recognition cannabinoids have in medicine. In 1985, the FDA approved synthetic THC, sold as dronabinol under the brand name Marinol, for chemotherapy-induced nausea. It cleared a second synthetic THC compound the same year, nabilone, sold as Cesamet. Eli Lilly pulled Cesamet from the American market in 1989 for commercial reasons. Valeant Pharmaceuticals bought the drug in 2004 and returned it to US pharmacies in 2006.

So cannabinoids have been part of supportive cancer care for four decades, but they are usually not the first option. Modern anti-nausea regimens remain the standard, while cannabinoids may be added when symptoms persist, balancing potential relief against intoxication and other side effects.

After that, the ground softens.

Appetite is the one everybody assumes is settled, because everybody knows what the munchies are. In 2002, a trial in patients with advanced cancer tested dronabinol head-to-head against megestrol, an older appetite stimulant. Megestrol clearly performed better: 75 percent of patients reported improved appetite, compared with 49 percent on dronabinol, while 11 percent versus 3 percent gained at least 10 percent of their starting weight. Dronabinol helped some patients. It just did not work nearly as well in this trial.

Four years later, a larger Phase 3 trial randomized 243 patients with cancer-related anorexia-cachexia to a standardized cannabis extract, THC alone or placebo, twice daily for six weeks. An independent data review board recommended ending recruitment after an interim analysis found insufficient differences between the groups. In the final analysis, neither the cannabis extract nor THC outperformed placebo on appetite or quality of life, and cannabinoid-related toxicity did not differ significantly among the three groups.

The most revealing numbers in that trial are the ones almost nobody quotes. Increased appetite was reported by 73 percent of patients receiving the cannabis extract, 58 percent receiving THC and 69 percent receiving placebo.

Most patients in every arm felt hungrier, including the ones on placebo.

That is what a control group is for, and it is worth sitting with before dismissing anyone’s story. Patients across all three groups genuinely reported feeling hungrier. What the trial could not show was that either the cannabis extract or THC produced more improvement than placebo.

Stimulating appetite and reversing the metabolic freefall of cancer cachexia, the wasting syndrome that comes with advanced disease, turn out to be different problems. The controlled record here is not large, but it is larger than one study, and at the doses tested, it has not shown that cannabinoids reverse late-stage wasting. That is a different statement from saying an individual patient earlier in treatment cannot find it easier to eat.

Pain is where the record gets uncomfortable. Nabiximols, sold as Sativex, is a mouth spray containing roughly equal parts THC and CBD, and one of the most extensively studied cannabinoid medicines. It went through three Phase 3 trials in cancer pain, the stage of testing intended to confirm whether a treatment works in a larger population. Marie Fallon and colleagues reported two of them in the British Journal of Pain in 2017. The third, led by Aron Lichtman, randomized 199 patients to nabiximols and 198 to placebo and appeared in the Journal of Pain and Symptom Management in 2018.

It did not meet the primary pain endpoint in any of the three trials.

That is a real result and it should be said plainly. It is also worth knowing what the trials were testing: whether adding nabiximols could produce a further reduction in pain among patients with advanced cancer whose pain remained uncontrolled despite optimized opioid therapy. The primary pain scores did not separate significantly from placebo, but some secondary outcomes were more encouraging. In the Lichtman trial, nabiximols outperformed placebo on two of three quality-of-life measures at week three and all three at week five. Post hoc analyses also suggested a benefit in some U.S. subgroups that did not appear in patients elsewhere. Those signals are worth studying, but they do not overturn the primary results.

The newest randomized evidence adds another mixed result. In a trial published in 2025, 144 patients with advanced cancer receiving palliative care were randomized to a one-to-one THC-to-CBD oil or a matched placebo. Total symptom distress improved in both groups, with no significant difference between them. Pain scores improved more in the cannabis group, although the difference was small and the study was not powered to establish benefits on individual symptoms. The cannabis group also reported more psychoactive side effects. On one measure of general well-being, placebo performed better at day 14, though that difference did not persist to day 28. A companion trial from the same group, testing CBD alone, likewise found no improvement over placebo in overall symptom burden.

No overall symptom advantage. A small pain benefit of uncertain clinical importance. More psychoactive side effects. Neither a miracle nor nothing.

Patient experience runs ahead of that record. Many patients report reducing their use of opioids and other pain medications, and some real-world data show the same pattern. A prospective registry study of 358 cancer patients enrolled in the Quebec Cannabis Registry, published in BMJ Supportive & Palliative Care in 2023, found reductions in pain severity, pain interference, opioid use and total medication burden during follow-up. Because the study had no control group, it cannot establish that cannabis caused those changes. Its authors called for confirmation in randomized placebo-controlled trials, and the registry was supported in part by unrestricted grants from licensed cannabis producers. That is what real-world evidence looks like: suggestive, not decisive.

Outside oncology, in chronic pain, a recent systematic review in Annals of Internal Medicine pooled 25 short-term randomized trials covering 2,303 patients, nearly two-thirds of them with neuropathic pain. Compared with placebo, oral THC-only products reduced pain by an average of about 0.78 points on a ten-point scale. Balanced THC-to-CBD oromucosal sprays, the class Sativex belongs to, reduced it by about half a point. Those modest benefits came with increased risks of dizziness, sedation and nausea. Results also diverged sharply within the THC-only category: nabilone reduced pain by 1.59 points more than placebo, while the 0.23-point difference for dronabinol did not demonstrate a meaningful benefit.

Real relief for some people. Modest on a population scale. Both things are true.

What the Lab Shows, and Why It Does Not Prove a Cure

The question underneath all of this is whether cannabis can kill cancer.

In the laboratory, there is genuinely interesting evidence. For twenty-five years, a lab at the Complutense University of Madrid run by Manuel Guzmán has documented how cannabinoids attack tumor cells. THC can trigger a stress response inside a cancer cell that pushes it to digest and destroy itself. In some laboratory and animal models, cannabinoids can choke off the blood supply a tumor needs and blunt its ability to invade neighboring tissue. Glioblastoma, breast, pancreatic, melanoma. In cell cultures and in mice, the compounds do impressive work. And the work has not stopped. In June 2026, a team at Rostock University Medical Center reported that cannabigerol and cannabichromene, two non-intoxicating cannabinoids that get a fraction of the attention paid to THC and CBD, killed lung cancer cells in culture and pushed them into apoptosis, with CBG appearing to act through a receptor called PPARα rather than the cannabinoid receptors everyone assumes are doing the work. That is a cell-culture finding, with everything that implies. It is also a reminder that this field is active, not closed.

Then come the qualifiers, and they are not small ones.

Cell lines and mice are not people. Oncology’s graveyard is full of compounds that cleared tumors in a dish and did nothing in a human body. One common reason is dosage: the concentrations that kill tumor cells in vitro, meaning in glassware rather than in a patient, may be difficult or impossible to reach safely in the human body.

Not every preclinical result points in the same direction. In one 2005 mouse study, THC increased the growth and spread of a breast-cancer model whose cells expressed little or no cannabinoid receptors, apparently by suppressing the antitumor immune response. That does not show that cannabis makes cancer grow in people. It does show that cannabinoid effects can vary by compound, tumor type and biological context. Cancer Research UK describes the laboratory record the same way: some cannabinoids inhibit cancer cells, while under certain conditions others can encourage their growth.

The National Cancer Institute makes the same distinction in its own summary for clinicians: antitumor activity in preclinical models, no approval and no established role in treating cancer in patients.

And when the National Academies of Sciences, Engineering, and Medicine reviewed the entire published literature in 2017, it landed on a phrase worth memorizing. There is insufficient evidence, the report concluded, either “to support or refute” the idea that cannabinoids are an effective treatment for cancers.

What Human Trials Have Actually Found

In humans, the direct anti-tumor evidence fits in a few paragraphs.

Guzmán’s team ran the first one in 2006. Nine patients with terminal recurrent glioblastoma, THC delivered through a catheter directly into the tumor. It was a safety study, and it cleared that bar. The treatment did not appear to accelerate the disease. Median survival was 24 weeks, and two patients survived for approximately a year. Without a control group, the study could not show whether THC extended anyone’s life. Guzmán’s own verdict was measured: the significance, he has said, is little in clinical terms, but the trial offered “some hints towards possible anti-tumoral action of THC in certain patients.”

Guzmán has been more careful about that study than most people who cite it. In a 2013 opinion piece, he wrote that “cannabinoids are efficacious drugs to treat at least some types of cancers in laboratory animals,” but that the anecdotal evidence “remains far from supporting that cannabinoids are efficacious anticancer drugs for large patient populations.” Part of the problem is that “cancer” is not one disease. It is at least 150 histological types and thousands more by molecular profile. Nothing treats all of that, which makes the question of which therapy helps which patient enormously specific.

In 2021, a team led by Chris Twelves at the University of Leeds published the results of GWCA1208, which gave nabiximols alongside chemotherapy to patients with recurrent glioblastoma. One-year survival was 83 percent in the nabiximols group against 44 percent on placebo. Those numbers traveled fast.

What traveled less is the shape of the study. It was a Phase 1b trial built to test safety and tolerability, run in two parts. Part 1 was open-label, with six patients. Part 2 randomized 21 more, twelve to nabiximols and nine to placebo, and the survival figures come from those 21. Two of the placebo patients died within the first 40 days of enrollment. At six months, progression-free survival was identical in both arms, 33 percent. The trial was sponsored by GW Research, which made the drug, and the authors wrote that the survival difference would need testing in an adequately powered randomized controlled trial.

This is why the study to watch is the one still running.

ARISTOCRAT is a Phase 2, double-blind, placebo-controlled trial testing nabiximols plus the chemotherapy drug temozolomide against placebo plus temozolomide in patients with recurrent, MGMT-methylated glioblastoma. It is coordinated by the Cancer Research UK Clinical Trials Unit at the University of Birmingham and funded by The Brain Tumour Charity, with the drug supplied free by Jazz Pharmaceuticals, which now owns the Sativex line. Its primary endpoint is overall survival, the clearest measure of whether the combination extends life. Patients are randomized two to one, with a target enrollment of 120, revised down from an original 234. Per the trial registry, it is still recruiting, with primary completion expected in September 2026.

It is worth being precise about what that would and would not settle. ARISTOCRAT tests one standardized drug, added to one chemotherapy, in one defined group of patients with one cancer. It will not answer whether cannabis treats cancer. It could answer whether adding nabiximols to temozolomide helps these patients live longer, which is more than any previous cannabinoid trial in cancer was designed to establish.

Where the Cure Story Came From

In 2003, according to accounts he has given over the years and to secondary sources including WebMD, a doctor removed a basal cell carcinoma from a Canadian man named Rick Simpson. It is the most common form of skin cancer and is usually highly treatable. Simpson then made a concentrated cannabis oil at home, put it on his bandages and concluded the oil had healed him. High Times could not locate published medical records or pathology documentation supporting the account.

What he did next is the part his critics skip. RSO is not a branded product, and Simpson’s own site explains how to make the oil rather than selling it. The syringes now sitting in dispensary cases across legal markets, dosed in rice grains, are other people’s businesses. By his own account, he gave the method away rather than building one.

The cure claim remains unsupported.

There is no reliable clinical evidence that RSO cures cancer in people. No published clinical trial has established that it does. And according to the secondary accounts reviewed here, the founding story involves a lesion that had already been surgically removed before Simpson applied the oil, making it impossible to determine what caused the outcome.

That does not make the accounts that followed dishonest or imaginary. People who say RSO helped them may be describing real symptom relief, or even a real change in a tumor. What none of those accounts can establish on its own is what caused it, especially when surgery, chemotherapy or radiation were happening at the same time. The problem is not that patients are lying. It is that a story about one person cannot tell you what a drug does.

Some of the strongest warnings about the cure claim have come from clinicians who are not hostile to cannabinoids. Adam Friedman, professor of dermatology at the George Washington School of Medicine and Health Sciences, has co-authored research on their therapeutic potential and has discussed using cannabinoid treatments in dermatology. He has called the spread of unproven RSO cancer claims “terrifying.”

The real risk is what happens when an unproven cure claim changes medical decisions. A patient may delay treatment with established benefits, or use cannabis alongside treatment without discussing it with the oncology team. That can leave drug interactions, product contamination and treatment-specific risks harder to assess. One unresolved concern is whether cannabis might interfere with some immunotherapies. Observational studies have reported poorer outcomes among cannabis users receiving immune-checkpoint inhibitors, but the findings are disputed and cannot establish that cannabis caused the difference. The evidence remains uncertain. It is concerning enough, however, that patients receiving immunotherapy should tell their oncology team what they are taking.

This is not a fringe issue. In a cross-sectional survey of patients and survivors at the Hollings Cancer Center at the Medical University of South Carolina, where cannabis remains illegal, 26 percent reported using cannabis since their diagnosis and 15 percent were current users.

Ethan Zohn, the Survivor: Africa winner and co-producer of the High Times docuseries Kicking Back, who survived Hodgkin lymphoma twice, described exactly that gap in a recent interview for this magazine. He said that when he used cannabis to manage chemotherapy side effects, none of his doctors could tell him how to use it safely. The only guidance he recalls receiving was not to smoke it.

What the Government Now Admits

For more than fifty years, the United States kept cannabis in Schedule I, the category defined in statute as having no currently accepted medical use. Heroin’s shelf. That was a political artifact rather than a scientific finding, and the government’s own machinery has now said so in writing.

In August 2023, the Department of Health and Human Services, drawing on the FDA and NIDA, formally recommended moving cannabis to Schedule III. The FDA review behind that recommendation counted more than 30,000 licensed practitioners recommending marijuana across 43 jurisdictions to more than six million registered patients for at least fifteen conditions. For scheduling purposes, it found some credible scientific support for marijuana in pain, anorexia related to a medical condition, and nausea and vomiting, including chemotherapy-induced nausea and vomiting.

The same three symptom domains that the trials keep pointing at. Not the tumor.

In April 2024, the Justice Department’s Office of Legal Counsel concluded that the DEA is bound by the scientific and medical determinations HHS reached. The agency that spent five decades insisting cannabis had no medical value was told by its own department’s lawyers otherwise.

Then, on April 23, 2026, the DOJ issued a final order moving two categories into Schedule III: cannabis contained in an FDA-approved drug product, and cannabis subject to a state medical marijuana license. It took effect five days later, the first time cannabis has moved out of Schedule I since the Controlled Substances Act became law in 1970.

It is also narrower than the headlines suggested. Everything outside those two categories, including all adult-use cannabis, remains in Schedule I. A DEA administrative hearing on broader rescheduling ran from June 29 to July 15, 2026. Chief Administrative Law Judge Derek Julius set August 17 as the deadline for post-hearing briefs, after which he issues a recommendation and the DEA Administrator makes the final call. No timeline for that decision has been announced. Schedule III is a meaningful change for research access and for the tax treatment of medical operators. It is not the end of federal prohibition.

Where That Leaves Patients

Here is the honest accounting.

Cannabis helps some people endure cancer treatment. Nausea is the firmest clinical case. Patients also commonly report help with sleep, anxiety and the general siege of being sick, even where formal trials lag behind.

Cannabinoids might eventually earn a role against certain tumors. That possibility rests on twenty-five years of laboratory work that keeps producing results and one carefully caveated survival signal in a study too small to prove anything. Unproven is not the same as disproven, and the distance between them is exactly what a trial is for. ARISTOCRAT is the strongest study yet designed to answer even a narrow version of the question.

What nobody can responsibly claim today is that cannabis has been shown to treat cancer in people. The scientist who ran the first human trial says so himself, and says it more cautiously than most of the people who quote him. He has not stopped working on the question, and neither has the field.

What is beyond dispute is that many people with cancer are using a plant with documented medical value without clear, evidence-based guidance on products, doses and interactions. That is a scientific problem made worse by decades of restrictive policy.

The Brain Tumour Charity raised the £450,000 needed for ARISTOCRAT through a public fundraising appeal, and Jazz Pharmaceuticals supplies the drug. Much of what it took to answer the question came from the people who most wanted it answered. They passed the hat.

Editorial note: Some earlier High Times coverage presented laboratory findings about cannabis and cancer more definitively than the human evidence supported. This article replaces that coverage, clarifies the distinction between preclinical research and established treatment in patients, and will be updated as stronger clinical evidence emerges.

Last reviewed and updated: July 29, 2026.

This article is for informational purposes only and is not medical advice. Cannabis can interact with cancer treatments. Patients should tell their oncology team about any cannabis or cannabinoid products they use and should not start, stop or change cancer treatment based on this article.