Clival chordoma research
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Cannabinoids

Research agent report, 4 September 2026, from PubMed, guideline bodies and published trials. Gaps marked. No prognosis figures. Where a statement is inference or clinical judgement rather than citation it is labelled as such.

Patient context: 34-year-old woman, 2 x 3 cm right cavernous sinus mass, working diagnosis chordoma (chondrosarcoma the main lookalike), biopsy pending, expected pathway endoscopic surgery then proton beam therapy. Continuous right trigeminal-distribution pain, poor sleep, weight loss. Partner concerned about drug effects on her thinking. Family has asked about high-THC and CBD products as a post-operative therapy after hearing of people who did well. UK.

1. What is being claimed and by whom

The lay case runs: cannabinoids kill cancer cells in the laboratory; some people with cancer who took high-THC oil (often "Rick Simpson oil", a crude solvent extract taken in gram quantities) report their tumours shrank or stayed away; therefore cannabis treats cancer. The claim is spread mainly by patient testimony on social media, by Rick Simpson himself (whose own claim concerns skin lesions he treated at home, never documented by a doctor, and basal cell carcinoma is a tumour type that can regress on its own), and by some cannabis retailers and clinics with a commercial interest. Medscape, "Rick Simpson Oil: Cancer Cure or Pipe Dream?", 2019, https://www.medscape.com/viewarticle/909178; Medical News Today, https://www.medicalnewstoday.com/articles/325612.

Why the anecdotes are weak evidence, without dismissing the people telling them:

None of this means the people are wrong about how they felt. Cannabinoids do relieve some symptoms (section 3), and feeling better is real. The problem is the step from "I felt better and I am still here" to "it treated the tumour", which no anecdote can carry.

Honest note on chordoma specifically: the online chordoma community (Chordoma Foundation forums, Facebook groups) contains cannabis testimonies like every other cancer community. I found no published case report of chordoma responding to cannabinoids. Absence of a published case is not proof of nothing; it is absence of evidence.

2. Anti-tumour evidence, tiered by strength

2a. Chordoma and chondrosarcoma specifically

PubMed search on 4 September 2026 for (chordoma) AND (cannabinoid OR cannabidiol OR tetrahydrocannabinol OR cannabis): no results. There is no published study of any cannabinoid in any chordoma cell line (U-CH1, U-CH2, UM-Chor1, MUG-Chor1, JHC7 or others), in chordoma xenografts, or in chordoma patients. The Chordoma Foundation's disease-model pages list drug screens run on these lines and cannabinoids are not among them. https://www.chordomafoundation.org/researchers/disease-models/

Chondrosarcoma: the same search returned two records, one irrelevant (a turmeric oleoresin study on osteoarthritis chondrocytes, Ghiselli 2024, PMID 39717553). The other is the only relevant paper:

Related but not the same tissue: CBD above about 4 micromolar reduces viability of normal human articular chondrocytes (Winklmayr 2019, Cannabis Cannabinoid Res, PMC6899975). This is a toxicity finding in normal cartilage cells, not an anti-tumour finding.

Bottom line for 2a: nothing exists for chordoma; one in vitro chemosensitisation paper exists for chondrosarcoma. Any claim that cannabinoids act on chordoma is extrapolation from other tumour types.

2b. Brain and skull base tumours (glioma and glioblastoma)

This is where the laboratory case is strongest, and it is worth being clear that glioblastoma is a glial tumour of the brain itself, biologically unrelated to chordoma (a notochordal remnant tumour of bone) except that both sit in the head.

Preclinical, Madrid group (Guzmán, Velasco, Sánchez and colleagues): - Galve-Roperh 2000, Nature Medicine: THC and a synthetic cannabinoid caused regression of C6 glioma in rats via ceramide accumulation and ERK activation. https://www.nature.com/articles/nm0300_313 - Sánchez 2001, Cancer Research: CB2 receptor activation inhibited glioma growth in vivo. - Carracedo 2006, Cancer Cell: cannabinoids induce ER stress and autophagy-mediated cell death in glioma cells. Salazar 2009, J Clin Invest: same mechanism confirmed, autophagy upstream of apoptosis. - Blázquez 2003 and 2004: cannabinoids inhibit glioma angiogenesis and VEGF signalling. - Torres 2011, Molecular Cancer Therapeutics: THC plus temozolomide had synergistic anti-tumour effect in glioma xenografts, and submaximal THC plus CBD also synergised with temozolomide. - Marcu 2010, Molecular Cancer Therapeutics: CBD enhances the inhibitory effects of THC on glioblastoma cell proliferation and survival. https://pmc.ncbi.nlm.nih.gov/articles/PMC2806496/ - Review: Velasco, Sánchez, Guzmán, "Towards the use of cannabinoids as antitumour agents", Nature Reviews Cancer 2012. https://www.nature.com/articles/nrc3247

Cannabinoids with radiotherapy in glioma models: - Scott KA, Dalgleish AG, Liu WM. "The combination of cannabidiol and delta9-tetrahydrocannabinol enhances the anticancer effects of radiation in an orthotopic murine glioma model." Molecular Cancer Therapeutics 2014;13:2955-2967. DOI 10.1158/1535-7163.MCT-14-0402. In GL261 mouse glioma cells and in an orthotopic mouse model, THC plus CBD plus irradiation shrank tumours more than either alone, with increased markers of autophagy and apoptosis. The doses used were pre-treatment with cannabinoids before radiation; this is a mouse model with a mouse tumour line. - Ivanov VN, Wu J, Hei TK. "Regulation of human glioblastoma cell death by combined treatment of cannabidiol, gamma-radiation and small molecule inhibitors of cell signaling pathways." Oncotarget 2017. PMID 29088769. CBD 5 to 40 micromolar reduced GBM cell survival and 10 Gy irradiation increased the effect; CBD appeared to spare neural stem cells and astrocytes relative to tumour cells. In vitro. - Kosgodage / Wang and colleagues, "Cannabidiol inhibits RAD51 and sensitizes glioblastoma to temozolomide in multiple orthotopic tumor models", Neuro-Oncology Advances 2022;4(1):vdac019. https://academic.oup.com/noa/article/4/1/vdac019/6530332. CBD suppressed RAD51 (a homologous recombination repair protein) and increased temozolomide effect, selectively in MGMT-methylated tumours, in mice. Mechanistically a RAD51 inhibitor would also be expected to radiosensitise, but that was not tested here.

Human studies in glioblastoma: - Guzmán M, Duarte MJ, Blázquez C, et al. "A pilot clinical study of delta9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme." British Journal of Cancer 2006;95:197-203. https://www.nature.com/articles/6603236. Nine patients, THC infused directly into the tumour cavity through a catheter. Safe. Reduced proliferation markers in tumour tissue in two of nine. No control group, no survival claim that can be interpreted. Its value is as a safety and mechanism study, not an efficacy study. - Twelves C, Sabel M, Checketts D, et al. "A phase 1b randomised, placebo-controlled trial of nabiximols cannabinoid oromucosal spray with temozolomide in patients with recurrent glioblastoma." British Journal of Cancer 2021;124:1379-1387. PMID 33623076. https://www.nature.com/articles/s41416-021-01259-3. 27 patients; the randomised part was 12 nabiximols versus 9 placebo, all on dose-intense temozolomide. Primary aim was safety: no new safety concerns and no effect on temozolomide pharmacokinetics. Commonest adverse events vomiting, dizziness, nausea, fatigue, headache. At one year 10 of 12 on nabiximols were alive versus 4 of 9 on placebo (p = 0.042). The authors themselves say the trial was not powered for survival, that two placebo patients died within 40 days which suggests baseline imbalance, and that the result "should be interpreted with caution and justify further exploration in an adequately powered randomised controlled trial." That is the correct reading: a hypothesis, not a finding. - ARISTOCRAT (NCT05629702), the UK phase II follow-up, run from the University of Birmingham CRCTU with University of Leeds, funded by The Brain Tumour Charity: double-blind, placebo-controlled, nabiximols plus temozolomide in recurrent MGMT-methylated glioblastoma at about 15 NHS sites, 2:1 randomisation, target 120 (reduced from an original 234). Status checked 4 September 2026 on the ClinicalTrials.gov API: still recruiting, estimated primary completion September 2026, study completion April 2027, last record update 5 May 2026, no results posted. https://clinicaltrials.gov/study/NCT05629702; https://www.birmingham.ac.uk/research/crctu/trials/aristocrat. So as of today there is still no adequately powered randomised evidence that a cannabinoid improves any outcome in any brain tumour. - Commentary: "Cannabinoids in glioblastoma multiforme: hype or hope?" British Journal of Cancer 2021. https://www.nature.com/articles/s41416-021-01265-5.

What this means for the patient: even if ARISTOCRAT is positive in 2027, it will be a result in glioblastoma given with temozolomide. It would not transfer to chordoma without separate evidence, because the mechanisms proposed (CB1/CB2 receptor density in glial tumours, ceramide signalling, interaction with alkylating chemotherapy) have not been shown in notochordal tumours. That is inference from the biology, stated plainly.

2c. Other cancers: the broad picture, including the negative findings

Preclinical effects reported across many tumour types (breast, prostate, lung, pancreas, colon, lymphoma, melanoma): induction of apoptosis, autophagy, cell-cycle arrest, reduced angiogenesis, reduced invasion and metastasis. Reviews: Velasco 2012 (above); Hinz and Ramer, "Cannabinoids as anticancer drugs: current status of preclinical research", British Journal of Cancer 2022, https://www.nature.com/articles/s41416-022-01727-4; Kis 2019 review of the concentration problem, Cannabis Cannabinoid Res, https://journals.sagepub.com/doi/full/10.1089/can.2022.0344.

Two problems with translating this:

  1. Concentration. Most anti-tumour effects in dishes appear at 5 to 40 micromolar cannabinoid. Blood levels after oral or vaporised cannabis are typically in the low nanomolar to low tens of nanomolar range for THC, which is one hundred to one thousand times lower, and brain or bone concentrations at the tumour are unknown. This is the single most important reason dish results have not turned into treatments (Hinz and Ramer 2022, above; ASCO 2024 guideline, below).

  2. Direction of effect is dose-dependent and can reverse. Hart S, Fischer OM, Ullrich A. "Cannabinoids induce cancer cell proliferation via tumor necrosis factor alpha-converting enzyme (TACE/ADAM17)-mediated transactivation of the epidermal growth factor receptor." Cancer Research 2004;64:1943-1950. https://cancerres.aacrjournals.org/content/64/6/1943. At nanomolar (physiological) concentrations THC and other cannabinoids increased proliferation of lung, glioblastoma and other cancer lines through EGFR transactivation; only at high micromolar concentrations did they kill cells. The concentrations reached by taking cannabis by mouth are the ones in the proliferation range, not the killing range.

Immune suppression. McKallip RJ, Nagarkatti M, Nagarkatti PS. "Delta-9-tetrahydrocannabinol enhances breast cancer growth and metastasis by suppression of the antitumor immune response." Journal of Immunology 2005;174:3281-3289. https://journals.aai.org/jimmunol/article/174/6/3281/8507. In mice, THC increased growth and metastasis of a breast tumour that lacked cannabinoid receptors, by suppressing the immune response through CB2. Cannabinoids are broadly immunosuppressive (reduced Th1 responses, T-cell proliferation and cytokine production), which is the basis of their study in autoimmune disease.

Human observational data on cannabis with immunotherapy (checkpoint inhibitors): - Taha T, Meiri D, Talhamy S, et al. "Cannabis impacts tumor response rate to nivolumab in patients with advanced malignancies." The Oncologist 2019;24:549-554. https://academic.oup.com/oncolo/article/24/4/549/6439154. Retrospective, 140 patients. Response rate 37.5 percent without cannabis versus 15.9 percent with (odds ratio 3.13, p = 0.016). No significant difference in progression-free or overall survival. - Bar-Sela G, Cohen I, Campisi-Pinto S, et al. "Cannabis consumption used by cancer patients during immunotherapy correlates with poor clinical outcome." Cancers 2020;12:2447. Prospective observational, 102 patients. Cannabis users had shorter time to progression and shorter overall survival. Note: a 2025 comment in the same journal (Cancers 2025;17:2754, PMC12427464) identified inconsistencies between methods and results and arithmetic errors in the paper, and a correction was published in 2022. The signal is real enough to be taken seriously but the paper is contested. A 2025 systematic review (Supportive Care in Cancer 2025, https://link.springer.com/article/10.1007/s00520-025-09218-x) and a 2024 preprint (medRxiv 2024.01.26.24301817) find the evidence limited and confounded. - Relevance: immunotherapy is not standard for chordoma, so this is not a direct interaction for the patient. It matters because it is the best human evidence that cannabis can blunt an anti-tumour immune response, which is the mechanism by which it could in principle be unhelpful rather than neutral.

Positive randomised human trials of cannabinoids as a cancer treatment: none exist for any cancer as of September 2026. The Twelves phase 1b is the only randomised placebo-controlled signal and its authors do not claim efficacy.

2d. Systematic reviews and position statements

3. Symptomatic evidence (stronger, but more modest than the lay picture)

Pain

Nausea and vomiting

Appetite and weight

Sleep

Anxiety

4. Safety in this patient

Cognitive effects of THC

Interactions with the drugs she is on or likely to be on

Appetite and weight

THC stimulates appetite acutely; the cancer trials (section 3) did not show weight gain. Long-term regular cannabis users have, on average, lower BMI in population studies, so the effect is not simple. Not a reliable route to weight restoration.

Psychiatric effects

Cardiovascular effects

Around surgery and anaesthesia

Around radiotherapy (proton or photon)

What is licensed and what the NHS will prescribe

Private clinics

Private prescribing by a specialist on the GMC Specialist Register is legal and is the route almost all UK medical cannabis patients use (roughly 60,000 plus patients by 2025 by industry estimates). Clinics are CQC-registered. Main clinics: Curaleaf Clinic (formerly Sapphire Medical Clinics, the first CQC-registered cannabis clinic; runs the UK Medical Cannabis Registry), Mamedica, Releaf, Alternaleaf, Integro, Lyphe, CB1 Medical and others. Typical 2026 fee structures, from clinic price pages and the MCPH comparison (https://mcph.org.uk/uk-medical-cannabis-clinic-comparison-2026/):

Medication is on top and is the main cost. Flower averages about 7 pounds a gram (range 3 to 13); oils 2 to 10 pounds per ml, a 30 ml bottle about 135 pounds. A typical balanced or THC-dominant prescription costs 150 to 250 pounds a month; a CBD-dominant oil prescription 100 to 150 pounds a month. Total realistic outlay 100 to 300 pounds a month. https://medicalcannabis.co.uk/the-price-of-cannabinoids-in-the-uk/; https://releaf.co.uk/blog/the-price-of-medical-cannabis-in-the-uk.

Clinics require evidence that two conventional treatments have been tried (this is a professional convention from the industry guidance, not law), and take a full history; many now prescribe for cancer symptom control, pain, insomnia and anxiety. Prescribing is by a consultant, usually a pain, psychiatry or oncology specialist, after video consultation; a summary care record or GP letter is normally required. The prescription is a private one, dispensed by a specialist pharmacy and posted.

Products: flower (vaporised with a medical device, not smoked), oils (sublingual or swallowed), soft-gel capsules, pastilles, vape cartridges. Cannabinoid ratios range from CBD-dominant (for example 50 mg/ml CBD with under 1 mg/ml THC), through balanced (roughly 10:10 or 20:20 mg/ml), to THC-dominant oils and flowers of 15 to 30 percent THC. A clinic can start CBD-dominant and titrate, which is the relevant point for the patient.

Over-the-counter CBD

CBD products sold as food supplements (oils, gummies, drinks) are legal if THC content is below the 1 mg per container limit (Home Office) and they are on the FSA public list of novel food applications; no CBD food has yet received full novel food authorisation but listed products may stay on sale in England and Wales. FSA precautionary advice since October 2023: healthy adults should take no more than 10 mg CBD a day from foods, based on liver and thyroid signals in the safety assessment. https://www.food.gov.uk (consumer advice); https://www.food-safety.com/articles/8958-based-on-new-evidence-uk-fsa-advises-consuming-no-more-than-10-mg-cbd-per-day-from-foods. The FSA advises that people taking any medication should not take CBD foods without medical advice. 10 mg a day is far below the doses used in any clinical study of CBD for pain, sleep or anxiety (typically 100 to 800 mg), and far below the concentrations in any anti-tumour study. Shop CBD is therefore, at best, a placebo at the advised dose and an unregulated interaction risk at higher doses. Independent testing repeatedly finds shop CBD products mislabelled for content.

Illegal products

High-THC oils, flowers and edibles bought outside a prescription are Class B controlled drugs. Rick Simpson oil and similar are unstandardised (THC content in tested samples varies several-fold, and contaminants including solvents, pesticides and heavy metals are found), and no one can dose them reliably. Possession carries up to five years, supply up to fourteen. For a family with young children, and with the household about to be under social and clinical scrutiny during a serious illness, this route should be off the table for reasons beyond the medicine.

6. Honest bottom line for the family

What the evidence supports: - Cannabinoids can help some people with sleep, and to a smaller and less certain degree with neuropathic pain and anxiety, as an add-on to standard treatment. The effects are modest (roughly one in six to one in eleven people get a meaningful pain benefit; sleep benefit is more consistent but the trials are weak), and side effects are common (about one in twenty-five stop because of them; one in ten have a psychiatric side effect such as anxiety, confusion or low mood). - Nabilone works for chemotherapy sickness, which is not expected to be part of the patient's treatment.

What it does not support: - Treating chordoma or chondrosarcoma, or reducing the chance of it coming back. There is no study, in a dish, in an animal, or in a person, of any cannabinoid in chordoma. Nothing. The glioblastoma work is real science but it is a different tumour, its one randomised human signal is from 21 patients whose own investigators say it needs confirming, and the confirming trial (ARISTOCRAT) has not reported. The best-documented human effect of cannabis on a cancer treatment (immunotherapy) is in the wrong direction. - Weight gain: the cancer trials were negative. - Replacing any of the standard treatment. Nothing in this file argues for delaying biopsy, surgery or proton therapy.

If the family wants to try a cannabinoid for symptoms, the conditions under which that is reasonable: 1. After histology is back and the treatment plan is fixed, not before. Before then it adds an unknown to a picture that is already complicated enough. 2. Not in the two weeks before surgery and not until the surgical team says recovery is complete. Nothing that could raise heart rate, alter anaesthetic requirement, or cloud her neurological checks. [Corrected 11 Oct 2026: the two weeks is my judgement, not guidance, and stopping suddenly in a regular user puts withdrawal on the operation. See research 31 and corrections.tsv.] 3. With the neurosurgeon, the clinical oncologist and whoever prescribes her pain medicines told in writing what she is taking, at what dose, and from which pharmacy. This is not a formality; it is because of the drug interactions in section 4, particularly with any anticonvulsant used for the facial pain, with opioids and with dexamethasone. 4. Through a legal prescribed product from a CQC-registered clinic, so the dose is known, the product is tested, and there is a doctor accountable for it. 5. CBD-dominant or balanced, started low, rather than high-THC. This follows directly from the partner's concern about her thinking: THC is the component that impairs memory and attention while it is being taken, and the component with psychiatric and cardiovascular risk. CBD alone will do little for pain but has the better safety and cognition profile; a low-THC balanced oil at night is the usual clinic starting point for sleep. High-THC flower is the product with the least evidence and the most downside for her specific situation. 6. With a defined trial period and a measurable goal (sleep hours, pain score, morphine use) and a decision to stop if it is not met, exactly as with any other drug trial. 7. Budget: expect 100 to 250 pounds a month privately. Nothing on the NHS.

Questions to ask the treating team: - Are there any drugs in her plan (anticonvulsants, dexamethasone, anticoagulants, antiemetics) that CBD would interact with, and would you want levels checked? - What is your policy on cannabinoids around the operation and during proton therapy? (Ask both the neurosurgical team and the proton centre.) - If she uses a prescribed cannabinoid for sleep or pain after recovery, will you note it in her record and let her GP know? - Would the pain team consider nabilone or a cannabinoid at all under NG144 if conventional neuropathic pain treatment fails, or is the private route the only one? - Is there a cannabinoid trial she could be eligible for? (Honest answer today: none for chordoma. ARISTOCRAT is glioblastoma only.)

7. Sources

Chordoma and chondrosarcoma - PubMed search (chordoma) AND (cannabinoid OR cannabidiol OR tetrahydrocannabinol OR cannabis), 4 Sep 2026: zero results. - Aydın D, et al. Naunyn-Schmiedeberg's Arch Pharmacol 2026, PMID 42362763, DOI 10.1007/s00210-026-05551-y. - Chordoma Foundation disease models: https://www.chordomafoundation.org/researchers/disease-models/ - Winklmayr M, et al. Cannabis Cannabinoid Res 2019, PMC6899975 (CBD toxicity in chondrocytes).

Glioma and glioblastoma - Galve-Roperh I, et al. Nature Medicine 2000;6:313-319. - Carracedo A, et al. Cancer Cell 2006;9:301-312. Salazar M, et al. J Clin Invest 2009;119:1359-1372. - Torres S, et al. Mol Cancer Ther 2011;10:90-103. - Marcu JP, et al. Mol Cancer Ther 2010;9:180-189. https://pmc.ncbi.nlm.nih.gov/articles/PMC2806496/ - Velasco G, Sánchez C, Guzmán M. Nat Rev Cancer 2012;12:436-444. https://www.nature.com/articles/nrc3247 - Scott KA, Dalgleish AG, Liu WM. Mol Cancer Ther 2014;13:2955-2967. DOI 10.1158/1535-7163.MCT-14-0402. - Ivanov VN, Wu J, Hei TK. Oncotarget 2017;8:74068. PMID 29088769. - Neuro-Oncology Advances 2022;4:vdac019 (CBD, RAD51, temozolomide). https://academic.oup.com/noa/article/4/1/vdac019/6530332 - Guzmán M, et al. Br J Cancer 2006;95:197-203. https://www.nature.com/articles/6603236 - Twelves C, et al. Br J Cancer 2021;124:1379-1387. PMID 33623076. https://www.nature.com/articles/s41416-021-01259-3 - ARISTOCRAT NCT05629702: https://clinicaltrials.gov/study/NCT05629702 (status 4 Sep 2026: recruiting, no results); https://www.birmingham.ac.uk/research/crctu/trials/aristocrat - Br J Cancer 2021 editorial, "Cannabinoids in glioblastoma multiforme: hype or hope?" https://www.nature.com/articles/s41416-021-01265-5

Other cancers and negative findings - Hinz B, Ramer R. Br J Cancer 2022;127:1-13. https://www.nature.com/articles/s41416-022-01727-4 - Hart S, Fischer OM, Ullrich A. Cancer Res 2004;64:1943-1950. https://cancerres.aacrjournals.org/content/64/6/1943 - McKallip RJ, Nagarkatti M, Nagarkatti PS. J Immunol 2005;174:3281-3289. https://journals.aai.org/jimmunol/article/174/6/3281/8507 - Taha T, et al. Oncologist 2019;24:549-554. https://academic.oup.com/oncolo/article/24/4/549/6439154 - Bar-Sela G, et al. Cancers 2020;12:2447; correction 2022 (PMC9031888); comment Cancers 2025;17:2754 (PMC12427464). - Supportive Care in Cancer 2025 systematic review: https://link.springer.com/article/10.1007/s00520-025-09218-x

Position statements - NCI PDQ Cannabis and Cannabinoids (HP): https://www.cancer.gov/about-cancer/treatment/cam/hp/cannabis-pdq - Braun IM, et al. ASCO guideline. J Clin Oncol 2024;42:1575-1593. https://ascopubs.org/doi/10.1200/JCO.23.02596 - Cancer Research UK 2022: https://news.cancerresearchuk.org/2022/05/13/cannabis-cannabinoids-and-cancer-the-evidence-so-far/ - National Academies 2017: https://www.nationalacademies.org/read/24625

Symptoms - Mücke M, et al. Cochrane 2018, CD012182. PMID 29513392. - Andreae MH, et al. J Pain 2015;16:1221-1232. PMID 26362106. - Whiting PF, et al. JAMA 2015;313:2456-2473. https://jamanetwork.com/journals/jama/fullarticle/2338251 - Häuser W, et al. Cochrane 2023, CD014915. PMID 37283486. - NICE NG144: https://www.nice.org.uk/guidance/ng144 - British Pain Society position statement 2019: https://www.britishpainsociety.org/static/uploads/resources/files/BPS_position_statement_25_11_19.pdf - Smith LA, et al. Cochrane 2015, CD009464 (CINV). - Jatoi A, et al. J Clin Oncol 2002;20:567-573. Strasser F, et al. J Clin Oncol 2006;24:3394-3400. - AminiLari M, et al. Sleep 2022;45:zsab234. https://academic.oup.com/sleep/article/45/2/zsab234/6373351 - Black N, et al. Lancet Psychiatry 2019;6:995-1010. - Rosewall T, Feuz C, Bayley A. J Med Imaging Radiat Sci 2020. PMID 32249134. - Liang YC, et al. Curr Drug Targets 2004 (trigeminal neuralgia review). PMID 15578967. - J Oral Maxillofac Surg 2021 orofacial pain review: https://www.sciencedirect.com/science/article/abs/pii/S0266435621002199

Safety - Broyd SJ, et al. Biol Psychiatry 2016;79:557-567. - Scott JC, et al. JAMA Psychiatry 2018;75:585-595. https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2678214 - Di Forti M, et al. Lancet Psychiatry 2019;6:427-436. - Jeffers AM, et al. J Am Heart Assoc 2024;13:e030178. - Storck W, et al. Heart 2025 (meta-analysis of cannabis and MACE). - Epidyolex SmPC (EMA): https://www.ema.europa.eu/en/documents/product-information/epidyolex-epar-product-information_en.pdf - Brown JD, Winterstein AG. J Gen Intern Med 2020. https://link.springer.com/article/10.1007/s11606-020-06504-8 - Gomes T, et al. PLoS Med 2017 (opioids plus gabapentin mortality); PMC9593000 (gabapentinoid plus opioid systematic review). - Shah S, et al. ASRA guideline. Reg Anesth Pain Med 2023;48:97-117. DOI 10.1136/rapm-2022-104013. - J Clin Med 2025;14:858, propofol in cannabis users meta-analysis. PMC11818839. - APSF 2025 update: https://www.apsf.org/article/cannabis-and-anesthesia-a-2025-update-on-perioperative-considerations/ - Int J Radiat Oncol Biol Phys 2024 survey of cannabinoid use during radiotherapy. PMID 38462019. - Bairati I, et al. J Clin Oncol 2005;23:5805-5813 (antioxidants during head and neck radiotherapy).

UK legal and practical - GMC information for doctors: https://www.gmc-uk.org/professional-standards/learning-materials/information-for-doctors-on-cannabis-based-products-for-medicinal-use - NHS England CBPMs: https://www.england.nhs.uk/long-read/cannabis-based-products-for-medicinal-use-cbpms/ - House of Commons Library CBP-8355: https://commonslibrary.parliament.uk/research-briefings/cbp-8355/ - NICE TA614, TA615, TA873 (Epidyolex); NG144 (Sativex, nabilone). - Clinic comparison 2026: https://mcph.org.uk/uk-medical-cannabis-clinic-comparison-2026/ - Curaleaf pricing: https://curaleafclinic.com/pricing/; Mamedica: https://mamedica.co.uk/pricing; Releaf: https://releaf.co.uk/pricing - Product prices: https://medicalcannabis.co.uk/the-price-of-cannabinoids-in-the-uk/ - FSA CBD advice: https://www.food-safety.com/articles/8958-based-on-new-evidence-uk-fsa-advises-consuming-no-more-than-10-mg-cbd-per-day-from-foods - Rick Simpson oil: https://www.medscape.com/viewarticle/909178; https://www.medicalnewstoday.com/articles/325612

Research thread 10 · source file em-research/10-cannabinoids.md · last edited 11 October 2026