What does the research say?
It is not possible to test whether cannabis changes cancer risk by randomly assigning people to use cannabis and following them for years, so all of the evidence comes from observational studies. Case-control studies compare the past cannabis use of people diagnosed with cancer with that of people without cancer; cohort studies follow users and non-users for years; and Mendelian randomization uses genes that make people more likely to use cannabis as a kind of natural experiment. In these studies, seeing two things together does not show that one causes the other. The biggest difficulty is tobacco: most people who smoke cannabis also smoke cigarettes, in some regions cannabis is smoked mixed with tobacco, and few people smoke only cannabis. Use is mostly based on self-report, and newer registry studies measure not the amount used but a diagnosis of 'cannabis use disorder' in health records.
Laboratory comparisons found that cannabis smoke contains many substances that can cause cancer and that are also found in tobacco smoke, and that the physical and chemical properties of the two kinds of smoke are largely similar. On the other hand, THC itself did not cause cancer in a two-year rat study in which it was given by mouth; in mice there was only an 'equivocal' finding in the thyroid that was not dose-related. Taken together, these two findings suggest that the main concern for lung and head and neck cancers may be the products of burning; but this has not been tested directly in people. For the link seen with the testis, which smoke does not reach directly, researchers are discussing the role of both cannabinoids and the other substances in smoke.
Lung cancer: In an international analysis that combined data from six studies and included 2159 people with lung cancer, the risk did not increase in habitual cannabis smokers, and no increase was seen in people who had never smoked cigarettes either. The New Zealand study in the same pool, however, had on its own reported an increase with heavy use. In a Swedish study that followed around 49,000 men aged 18–20 for 40 years, the risk was more than twice as high in those who had smoked cannabis more than 50 times in their youth. In a 2026 US study based on health records, the risk was about four times higher in people with cannabis use disorder; but the amount of tobacco smoked is not known in these records, and letters questioning the method were published. In North Africa, where cannabis is smoked mixed with tobacco, the risk was high, but all cannabis smokers there also smoked cigarettes. A study using genetic predisposition showed a small increase in squamous cell lung cancer. A comprehensive 2019 review found the evidence for the lung insufficient, while the 2017 report of the US National Academies saw moderate evidence of no association. These two assessments were made before the newer registry studies that report an increase. A 2026 meta-analysis that reported an increase was not included in the table: two numbers that drive its result for cohorts do not match the source study's own results. The evidence is mixed and very weak.
Head and neck and oral cancers: In a large analysis that combined data from 4029 patients in five studies, smoking cannabis did not increase the risk of head and neck cancer, and there was no increase in people who had never used cigarettes or alcohol either. In another pool of nine studies, a slight increase was seen in the tonsil and base-of-tongue area of the throat (oropharynx), but this increase disappeared once HPV infection was taken into account; for tongue cancer, the risk was lower. Meta-analyses also found no overall increase, the 2017 report of the US National Academies also saw moderate evidence of no association, and a 2025 meta-analysis reported a lower risk of oral cancer. In contrast, in 2024 and 2025 US studies based on health records, any head and neck cancer was about 3.5 times and oral cancer 2.5–3.3 times more common in people with cannabis use disorder (higher for the larynx); these records do not show the amount of tobacco and alcohol used or HPV status. An increase seen in another hospital registry disappeared once alcohol or smoking was taken into account. In North Africa, the link with cancer of the upper throat behind the nose (nasopharynx) was clearer for cannabis smoked mixed with tobacco. The evidence is conflicting and very weak.
Testicular cancer: This is the type of cancer with the most consistent finding. In meta-analyses that combined the same three US case-control studies (so they do not count as independent evidence from one another), long-term (more than 10 years), frequent (at least weekly) or current use was linked to about a 1.4–1.9-fold increase in testicular germ cell tumors; the link was stronger for nonseminoma tumors. In Swedish men followed for 42 years, use more than 50 times in youth was linked to a higher risk, while ever having used was not. In a 2026 study from France, an increase was seen with daily or regular use in young adulthood, but this time the link appeared for seminoma rather than nonseminoma tumors; in a large UK cohort no link was found, but there participants were aged 40–69 and there were only 29 testicular cancers. The comprehensive 2019 review rated the strength of evidence as low, and the 2017 report of the US National Academies considered it 'limited' for the nonseminoma type. Because testicular cancer is rare, relative increases add up to a small absolute risk: in the Swedish study it occurred in 119 of 45,000 men over 42 years.
Bladder, prostate and kidney cancers: The findings point in two directions. In a California study that followed about 84,000 men for 11 years, bladder cancer was less common in those who used only cannabis; in a UK study that followed more than 150,000 people, prostate and kidney cancer was also less common in those who had used cannabis before. In contrast, in a 2025 US study based on health records, bladder, kidney and prostate cancer were more common in people with cannabis use disorder. In a 1997 US cohort, there was an increase in prostate cancer only among non-smokers. For the bladder, the only systematic review found few and conflicting studies. The evidence is insufficient.
Brain tumors: In a single cohort in California that followed more than 133,000 people for up to 21 years, the risk of glioma (a type of brain tumor) was about three times higher in those who smoked cannabis at least once a month, but the risk did not rise with more use; a study using genetic predisposition showed no causal link for glioma. The evidence is insufficient.
Use during pregnancy and childhood cancers: In five case-control studies carried out in the US between 1989 and 2006, the mother's use of marijuana or other recreational drugs around the time of pregnancy (in one, the father's as well) was linked to a type of leukemia, rhabdomyosarcoma (a soft tissue cancer) and neuroblastoma in the child; the increase seen for astrocytoma (a brain tumor) was not statistically significant. However, the largest study, done to test the first report on childhood leukemia, did not confirm the increase. These studies were small, use was reported from memory years later, and in some studies marijuana had been used together with other drugs; no new cohort study was found. The 2017 report of the US National Academies also assessed these studies and found the evidence insufficient. The evidence is insufficient. Cannabis use during pregnancy was, however, more consistently linked to other outcomes such as low birth weight; these estimates were not adjusted for confounders.
All cancers and findings in the opposite direction: In a 1997 cohort that followed a young population for an average of 8.6 years, there was no increase among cannabis users when all cancers were considered. A 2025 cancer-specific umbrella review wrote that the links between cannabis and cancer are 'suggestive rather than conclusive' and that the closest association was seen with nonseminoma testicular cancer; in another umbrella review from 2023 that assessed 101 meta-analyses, no cancer-related association reached the strong evidence class. Some studies reported that bladder, prostate, kidney, oral or pancreatic cancer was less common in cannabis users; a 2021 meta-analysis also found a lower overall risk when some studies were excluded. These opposite findings are also observational and should be read with care: in some, adjustment for confounders was limited, in one the follow-up of cannabis users was shorter, and the meta-analysis result depended on which studies were excluded. It has not been shown that cannabis or CBD prevents cancer. In most studies using genetic predisposition, there was either no link or a very small one.
Pure CBD: No study was found that looked at cancer risk from CBD oil or pure CBD in people. The US and European product information describe the two-year animal studies of the approved pure CBD medicine in different detail. According to the US label, there was no statistically significant increase in tumors in rats; benign liver tumors increased in male mice at the highest dose, and at one dose lower, the blood CBD level was close to that at the highest doses of the medicine used in people. According to the European product information, however, benign liver tumors increased in male mice at all doses and in female mice at the highest dose; in male rats, overgrowth and benign tumors of the Leydig cells in the testis increased at all doses, including the lowest dose, at which the blood CBD level was lower than in people, and a malignant tumor was seen in one rat at the highest dose. The European product information states that the relevance of the Leydig cell tumors in rats to humans is generally considered limited; neither document explains the reason for the difference between them. CBD was negative in genotoxicity (genetic damage) tests. In 2026, the European Food Safety Authority wrote that, despite publications suggesting that pure CBD itself does not cause genetic damage, manufacturing and formulation may introduce new hazards, and that the effects of long-term use are unknown. The effect of CBD on the course of an existing cancer is covered on the site's 'Cancer Treatment and CBD' page.
Strength of evidence: ○○○○ Insufficient evidence. Finding: Not studied enough. What does this mean?
Ongoing research on this topic
No ongoing CBD trial on this topic appears on ClinicalTrials.gov right now. All ongoing trials
Possible side effects and drug interactions
Because this page describes a risk rather than a treatment, 'side effect' here means the harms of cannabis use other than cancer. In an umbrella review that assessed more than one hundred meta-analyses, the strongest evidence was found for use during pregnancy and low birth weight and small-for-gestational-age babies, for crashes among people who drive, and for psychosis in the general population; in randomized trials of cannabis-based medicines, nervous system side effects such as dizziness and drowsiness, as well as psychiatric side effects, also increased. The effects of smoked cannabis on the heart and blood vessels and on mental health are covered separately on the related pages of the site.
For pure CBD, the European Food Safety Authority reported consistent liver effects in animal studies and, in human studies, a possibility of liver harm, especially when used together with other medicines. CBD can slow the breakdown of some medicines in the body; it is important for people who take medicines regularly, especially those being treated for cancer, to talk to their doctor before starting.
To check interactions with the medicines you take: CBD drug interaction checker.
How was CBD used in studies?
This page describes a risk, not a treatment, so there is no tested or recommended dose. The studies measured cannabis use in different ways: joint-years (use equal to smoking one joint a day for one year), the number of times used over a lifetime (e.g., more than 50 times), at least weekly or daily use, duration of use (e.g., more than 10 years), or a diagnosis of 'cannabis use disorder' in health records.
In studies that found an increase, the link was mostly seen with long-term, frequent or heavy use (for testicular cancer, use for more than 10 years or at least weekly; in the Swedish studies, more than 50 times over a lifetime for lung and testis); in most studies, ever having used was not linked to risk. Because there are no human studies of cancer risk with pure CBD, no amount can be called safe or risky. In animal studies, according to the US label, the increase in male mice was seen at the highest dose (300 mg per kilogram per day), and at one dose lower the blood CBD level was about 1–2 times that at the highest human doses of the approved medicine. According to the European product information, however, the increase was seen in male mice at all doses (at the highest dose, the blood level was about 3 times that at the human dose) and, in the testes of male rats, also at the lowest dose, at which the blood level was lower than at the human dose. These are animal study doses, not personal recommendations.
Study details (for health professionals)
On the question of cannabis and cancer risk, there are no randomized controlled trials and none are expected; the evidence comes from case-control, cohort and Mendelian randomization studies and reviews of them. Testis: in meta-analyses of the same three US case-control studies, current use (OR 1.62), at least weekly use (1.92) and use for more than 10 years (1.50; 1.36 and 'low' strength of evidence in Ghasemiesfe 2019) were linked to testicular germ cell tumors, especially the nonseminoma type; in the Swedish cohort, HR 2.57 (1.02–6.50) with heavy use; in the 2026 French study, the link was with seminoma; no link in UK Biobank (HR 0.85; 29 cases, participants aged 40–69); NASEM 2017 saw 'limited' evidence for the nonseminoma type. Lung: in the ILCCO pool (2159 cases), OR 0.96 (0.66–1.38) for habitual use and 1.03 in never-tobacco-smokers; in the Swedish cohort, HR 2.12 (1.08–4.14) with heavy use; in the US registry cohort, RR 3.87 (3.43–4.38; method disputed) with use disorder; in the North African pool, OR 2.4 (all cannabis smokers also smoked tobacco); in Mendelian randomization, OR 1.22 for the squamous type; Ghasemiesfe 2019 found the evidence insufficient, and NASEM 2017 saw moderate evidence of no association (both before the registry cohorts). Head and neck: in the INHANCE pool (4029 cases), OR 0.88 (0.67–1.16); NASEM 2017: moderate evidence of no association; 1.02 and 1.26 in meta-analyses (not significant); 1.24 for the oropharynx (0.99 with HPV adjustment), 0.47 for tongue cancer; 0.66 in an oral cancer meta-analysis; in US registry cohorts, RR 3.49 and OR 3.25 with use disorder, but in one hospital registry the link disappeared after adjusting for alcohol and smoking; in North Africa, OR 1.83 for nasopharyngeal cancer (1.54 after adjusting for cigarette smoking, not significant). Bladder, kidney, prostate: a decrease in prospective cohorts (bladder HR 0.55; kidney 0.61; prostate 0.83), an increase in a registry cohort (bladder RR 4.21; kidney 3.70; prostate 2.80). Glioma: 2.8-fold in a single cohort. Childhood cancers: in five small case-control studies between 1989 and 2006, 2–11-fold associations with the mother's or father's marijuana use (in one, any mind-altering drug) (not significant for astrocytoma; NASEM 2017: insufficient evidence); in the largest leukemia study, no link or a link in the opposite direction. In chronic pancreatitis, pancreatic cancer HR 0.26 (less detection). In most Mendelian randomization studies, no link or a very small one. Umbrella reviews summarize the evidence as 'suggestive rather than conclusive' (Nargis 2025) and find no strong evidence class for cancer (Solmi 2023). Pure CBD: no studies of cancer risk in people; in 2-year animal studies of the approved medicine, according to the US label, an increase in hepatocellular adenoma in male mice at the highest dose and no significant increase in tumors in rats; according to the European product information, hepatocellular adenoma increased in male mice at all doses and in female mice at the highest dose, Leydig cell hyperplasia and adenoma increased in male rats at all doses, and 1 Leydig cell carcinoma was seen at the highest dose (according to the document, the relevance of Leydig tumors in rats to humans is generally limited); genotoxicity tests negative; EFSA 2026 wrote that data gaps remain for genotoxicity and long-term use. THC itself was not carcinogenic in a 2-year rat study and equivocal in mice (thyroid adenoma, not dose-related). October 2026 search (PubMed, Cochrane, ClinicalTrials.gov, Europe PMC): no randomized controlled trials on this question; no human study of cancer risk with pure CBD was found. For smoked cannabis, 2 umbrella reviews, 1 institutional assessment (NASEM 2017), 8 systematic reviews and meta-analyses, 4 Mendelian randomization studies, 12 cohort or registry studies, 4 pooled case-control analyses and 7 case-control studies were found; for pure CBD, 1 institutional assessment and 1 animal study (the approved medicine's US and European product information); for THC, 1 animal study; all are in the table below. Two 2026 meta-analyses were not included in the table: the results of the testicular meta-analysis were identical to earlier meta-analyses of the same three studies, and the cohort result of the lung meta-analysis rested on two numbers that did not match the source study. No Cochrane review, no study from Turkey and no ongoing study on ClinicalTrials.gov examining this question was found.
Evidence assessment: Pure CBD: Insufficient (no human studies of cancer risk; only two-year animal studies of the approved medicine and the European Food Safety Authority assessment)
CBD alone
No study was found that looked at cancer risk from pure CBD or CBD oil in people. The US and European product information summarize the two-year animal studies of the approved pure CBD medicine in different detail. According to the US label, benign liver tumors (hepatocellular adenoma) increased in male mice at the highest dose (300 mg per kilogram per day), and there was no statistically significant increase in tumors in rats. According to the European product information, however, these liver tumors increased in male mice at all doses and in female mice at the highest dose; in male rats, overgrowth and benign tumors of the Leydig cells in the testis increased at all doses, and a malignant Leydig cell tumor was seen in one rat at the highest dose; the document states that the relevance of these rat tumors to humans is generally considered limited. CBD and its two main breakdown products were negative in genotoxicity (genetic damage) tests. The European Food Safety Authority (2026) wrote that, despite publications suggesting that pure CBD itself does not cause genetic damage, manufacturing and formulation may introduce new hazards, and that the effects of long-term use are unknown. It has not been shown that CBD either raises or lowers cancer risk.
Products containing THC
The findings come almost entirely from smoking marijuana and differ by type of cancer. Testis: a link with testicular germ cell tumors after long-term (more than 10 years) or frequent use; meta-analyses of the same three US case-control studies (OR about 1.4–1.9), the Swedish cohort (HR 2.57 with heavy use) and the 2026 French study showed an increase, but the tumor type affected differed between studies, and there was no link in the UK cohort with older participants and few cases; the US National Academies in 2017 saw 'limited' evidence for the nonseminoma type (weak evidence). Lung: no increase in the pooled analysis of 2159 patients or in never-smokers, and the US National Academies (2017) saw moderate evidence of no association; an increase with heavy use in the Swedish cohort (HR 2.12) and the US registry cohort (RR 3.87); hard to separate from tobacco (mixed, very weak). Head and neck and oral: no increase in large pooled analyses and meta-analyses, a lower risk in some (US National Academies 2017: moderate evidence of no association); in US registry cohorts, with use disorder, any head and neck cancer about 3.5-fold and oral cancer 2.5–3.3-fold, but in one hospital registry the link disappeared after adjusting for alcohol and smoking (conflicting, very weak). Bladder, prostate, kidney: findings in two directions (insufficient). Brain (glioma): a single cohort (insufficient). Childhood cancers (use during pregnancy): small and conflicting case-control studies (insufficient). There are no human cancer data for THC taken by mouth (as a medicine); THC did not cause cancer in a two-year rat study, and in mice there was an equivocal finding in the thyroid that was not dose-related.
Evidence: Smoked cannabis and THC-containing products: Weak evidence on whether they raise cancer risk (only observational studies and Mendelian randomization; the most consistent signal is for testicular cancer, with low strength of evidence; conflicting and very weak for lung and head and neck; insufficient for bladder, prostate, kidney, brain and childhood cancers; no human data for oral THC)
Dose range in studies
No treatment dose (risk page). Exposure measures in human studies: ever having used; joint-years (≥10, ≥60); number of lifetime uses (>50 times, ≥2000 times); at least weekly or daily use; ≥10 years of use; a diagnosis of cannabis use disorder in records. Animal studies (2 years): pure CBD 30–300 mg/kg/day in mice and 15–150 mg/kg/day in rats; THC 12.5–50 mg/kg in rats and 125–500 mg/kg in mice (5 days a week); these are study doses, not personal recommendations
Starting dose and titration
Not applicable: the studies measured a usage habit, not a treatment; there is no dose adjustment
These are doses researchers gave under medical supervision; they are not a recommended dose for you. "mg/kg/day" means milligrams per kilogram of body weight per day.
| Study | Participants | Product | Dose and titration | Duration | Result | Source |
|---|---|---|---|---|---|---|
| Nargis 2025 Umbrella review (review of the global epidemiological evidence on cannabis and cancer risk) | Not reported (in the abstract; full text could not be read) Cannabis users in the general population | Cannabis use (mostly recreational, smoked) | Not applicable | Varies by publication | According to the authors, the links between cannabis and cancer risk are 'suggestive rather than conclusive'. The cancer most closely linked to cannabis use is nonseminoma testicular cancer; 'emerging evidence' of an increase was reported for squamous cell lung and head and neck cancers and for oral, breast, liver, cervical, laryngeal, pancreatic, thyroid and childhood cancers. The authors wrote that new studies free of confounding, misclassification and errors in exposure measurement are needed | PMID 39427677, doi:10.1016/S2468-2667(24)00223-8, PMID 40921170, 10:e814, its content could not be read) |
| Solmi 2023 Umbrella review (101 meta-analyses: 50 observational, 51 of RCTs; evidence classes for observational evidence, GRADE for RCTs) | 101 meta-analyses; cancer-related results from 4 meta-analyses (Ghasemiesfe 2019, Gurney 2015, de Carvalho 2015, Zhang 2015) General population and various patient groups; cancer risk results in the general population | Cannabis, cannabinoids and cannabis-based medicines | Not applicable | Search through February 9, 2022 | Of 119 cannabis-related associations in the general population, those concerning cancer were in the 'weak' or no-evidence class in the main analysis; when the criterion of more than 1000 cases was removed, three associations for testicular cancer moved up to the 'suggestive' class. The strongest ('convincing') evidence class included use during pregnancy with small-for-gestational-age babies (equivalent OR 1.61; 95% CI 1.41–1.83) and low birth weight (1.43; 1.27–1.62; both estimates not adjusted for confounders), and crashes among drivers (1.27; 1.21–1.34); psychosis in adolescents (1.71; 1.47–2.00) was 'highly suggestive' in the main analysis and 'convincing' when only cohorts were included. The authors supported avoiding cannabis during adolescence and young adulthood, in people prone to mental illness, during pregnancy, and before and while driving | PMID 37648266, doi:10.1136/bmj-2022-072348, PROSPERO CRD42018093045, PMID 37722728 |
| Ghasemiesfe 2019 Systematic review and meta-analysis (observational studies; strength-of-evidence grading) | 25 studies (19 case-control, 5 cohort, 1 cross-sectional); only 2 at low risk of bias Adult cannabis users and nonusers | Cannabis (mostly smoked) | Exposure: ever use (at least 1 joint-year; 1 joint-year = one joint a day for a year) and duration of use | Publications 1973–April 2019 | Testis: use for more than 10 years was associated with testicular germ cell tumors (OR 1.36; 95% CI 1.03–1.81; 3 case-control studies), more clearly for the nonseminoma type (1.85; 1.10–3.11); no association for seminoma (0.98; 0.47–2.06); ever use not associated (1.11; 0.81–1.53); strength of evidence 'low'. For head and neck squamous cancer (1.26; 0.88–1.80; 4 studies) and oral cancer (1.22; 0.95–1.56; 2 studies), ever use was not associated. Lung: the results of 8 studies were mixed and could not be pooled; evidence 'insufficient'. Bladder, prostate, cervical, glioma, lymphoma, Kaposi sarcoma, nasopharyngeal, laryngeal, esophageal and other cancers: only isolated studies; evidence 'insufficient' for all. Very few people smoked only cannabis, exposure was low and poorly defined | PMID 31774524, doi:10.1001/jamanetworkopen.2019.16318, PMID 31940033, does not change the results). PROSPERO CRD42018102457 |
| Clark 2021 Scoping review and meta-analysis (observational studies; US-focused) | 55 risk ratios from 34 studies (50 in the analysis) Cannabis users and nonusers; various cancer types | Cannabis use | Not applicable | Search through August 2019 | When all data were combined, cancer risk did not differ significantly in cannabis users (RR 0.90; p > 0.06; high heterogeneity, I² 72%). When the authors excluded the North African data (where cannabis is smoked mixed with tobacco) and data not adjusted for tobacco or with few cases, the risk came out lower (RR 0.86; p < 0.017; 24 data points); RR 0.83 for head and neck cancers. For testicular cancer, RR 1.12 (not significant). Heterogeneity remained high, and separate results from the same study (e.g., men and women) were counted as independent data points; the authors wrote that they had 'low confidence' in the result. The excluded North African studies (including Berthiller 2008, Voirin 2006 and Feng 2009) had reported increases; this inverse result is sensitive to the selection decisions | PMID 33998861, doi:10.1089/can.2019.0095 |
| NASEM 2017 (US National Academies report) Expert committee report (US National Academies of Sciences, Engineering, and Medicine; assessment based on good- and fair-quality systematic reviews and selected primary studies; five-level evidence grading) | In the cancer chapter, 3 systematic reviews (one a pooled analysis) and 3 primary studies; primary case-control studies for childhood cancers Adult cannabis users; children whose mother or father used cannabis | Cannabis (mostly smoked) | The committee's conclusions: moderate evidence of no statistical association between smoking cannabis and lung cancer (5-1) and between cannabis use and head and neck cancers (5-2); limited evidence of an association between current, frequent or chronic cannabis smoking and nonseminoma testicular germ cell tumors (5-3); insufficient evidence for esophageal, prostate, cervical cancer, glioma, non-Hodgkin lymphoma, penile, anal and bladder cancer and Kaposi sarcoma (5-4, 5-5), and for parental cannabis use and leukemia, rhabdomyosarcoma, astrocytoma and neuroblastoma in the child (5-6). The newest publications in the chapter date from 2015; the registry cohorts and Mendelian randomization studies published after 2017 are not in the report | PMID 28182367, doi:10.17226/24625, National Academies Press, chapter 5 'Cancer' (nationalacademies.org/read/24625/chapter/7, read on October 28, 2026), the NCBI Bookshelf copy (NBK425767) could not be opened because of bot verification. The same report also appears in the Glaucoma and Irritable Bowel and Stomach Problems tables | ||
| Mehra 2006 Systematic review (no meta-analysis) | 19 studies Cannabis smokers over 18 | Smoking cannabis | Not applicable | Publications 1966–October 2005 | Increased tar exposure, impaired lung macrophage function, oxidative stress and precancerous changes in the bronchial lining were reported in cannabis smokers; however, observational studies could not show a significant association between cannabis and lung cancer after adjustment for tobacco. Main problems: selection bias, small samples, young participants (not enough time for cancer to develop) and lack of adjustment for tobacco | PMID 16832000, doi:10.1001/archinte.166.13.1359 |
| de Carvalho 2015 Systematic review and meta-analysis (matched case-control studies) | 6 articles (9 case-control studies) Patients with head and neck cancer and controls; 12.6% of cases and 14.3% of controls had used cannabis | Cannabis (lifetime use) | Exposure: ever use | Not reported (in the abstract) | In models adjusted for age, sex, race and tobacco, lifetime cannabis use was not associated with head and neck cancer (OR 1.02; 95% CI 0.91–1.14; p = 0.72). Because the data were presented in different ways, no dose or duration analysis could be done | PMID 26433192, doi:10.1016/j.archoralbio.2015.09.009, PMID 27449844, title 'insufficient evidence to support or refute the association') |
| Ibrahim Mohammad 2025 Systematic review and meta-analysis (case-control studies; random effects) | 6 case-control studies; 4686 cases, 10,370 controls People with oral cancer (ICD-10 C00–C06) and controls | Cannabis use | Exposure: ever use; subgroups by duration and age at starting | Search through August 2025 | Cannabis use was associated with a lower risk of oral cancer (OR 0.66; 95% CI 0.50–0.87; p = 0.003; I² 47%); three studies showed a significant decrease, three showed no significant difference; no dose-response relationship was seen. The authors wrote that the results should be interpreted with caution because of methodological limitations, differences in exposure measurement and conflicting new evidence. An inverse (lower-risk) finding; case-control studies do not show cause and effect | PMID 41236922, doi:10.1080/15332640.2025.2581692 |
| Song 2020 Systematic review and meta-analysis (epidemiological studies; random effects) | 4 studies for cannabis, 12 for tobacco People with testicular germ cell tumors and controls | Cannabis use (tobacco smoking for comparison) | Exposure: ever use | Not reported (in the abstract) | Ever cannabis use was associated with nonseminoma testicular tumors (summary OR 1.71; 95% CI 1.12–2.60); tobacco smoking was associated with all testicular germ cell tumors (1.18; 1.05–1.33). According to the authors, the data are consistent with a role for both cannabinoids and other substances in smoke; studies are needed that separate combined tobacco and cannabis use and smokeless sources of cannabinoids | PMID 32409200, doi:10.1016/j.urolonc.2020.03.013 |
| Gurney 2015 Systematic review and meta-analysis (case-control studies; random effects) | 3 case-control studies; 719 cases, 1419 controls (all US, data mostly from the 1990s) Men aged 18–50 | Cannabis use (self-reported) | Exposure: current use, at least weekly use and use for more than 10 years | Publications January 1, 1980–May 13, 2015 | Current use (OR 1.62; 95% CI 1.13–2.31), at least weekly use (1.92; 1.35–2.72) and use for more than 10 years (1.50; 1.08–2.09) were associated with testicular germ cell tumors; the result for ever use was uncertain (1.19; 0.72–1.95). The association was stronger for the nonseminoma type (2.09; 1.29–3.37 for current use; 2.59; 1.60–4.19 for at least weekly use); evidence for seminoma was insufficient. In two studies, response rates differed greatly between cases and controls; use is based on self-report | PMID 26560314, doi:10.1186/s12885-015-1905-6, PMID 19204904, PMID 20925043, PMID 22965656, PMID 23233189, PMID 41188200, which re-pooled the same studies, was not given a separate row: its current-use result (OR 1.62, 1.13–2.31) is identical to this meta-analysis and its nonseminoma result (1.71, 1.12–2.60) is identical to Song 2020 |
| Mehrnoush 2022 Systematic review (qualitative synthesis; Newcastle-Ottawa scale) | 3 studies (the search was not limited to human studies) Bladder cancer | Cannabis use | Not applicable | Not reported (in the abstract) | The relationship between cannabis and bladder cancer has been studied very little; the results of the few studies found are contradictory: both carcinogenic and protective effects were reported. The authors wrote that new, well-designed studies are needed | PMID 35775355, doi:10.4081/aiua.2022.2.248 |
| Baumeister 2021 Two-sample Mendelian randomization (a 'natural experiment' using genetic liability) | Genetic data on lifetime use from 184,765 people; use disorder 17,068 cases and 357,219 controls; lung cancer 29,266 cases and 56,450 controls Adults of European ancestry (international consortia, 23andMe, UK Biobank) | Genetic liability to lifetime cannabis use and to cannabis use disorder | Not applicable | Not applicable (genetic data) | Genetic liability to lifetime cannabis use was associated with an increased risk of squamous cell lung cancer (OR 1.22; 95% CI 1.07–1.39; p = 0.003, q = 0.025); pleiotropy-robust methods and control analyses showed no bias. No other significant associations are reported in the abstract. According to the authors, the finding suggests a possible causal relationship; it needs confirmation by observational studies and other methods | PMID 33852959, doi:10.1016/j.jtho.2021.03.025 |
| Niu 2024 Two-sample Mendelian randomization | Genetic data: ICC, UK Biobank and 23andMe (lifetime use); Psychiatric Genomics Consortium, iPSYCH and deCODE (use disorder); 9 cancer types Adults of European ancestry | Genetic liability to lifetime cannabis use and to cannabis use disorder | Not applicable | Not applicable (genetic data) | Genetic liability to lifetime use was not associated with cancers other than breast cancer; in breast cancer the risk was slightly lower (OR 0.981; p = 0.016). Liability to use disorder was associated with an increased risk of breast (OR 1.007; p = 0.007) and lung cancer (OR 1.122; p = 0.014). Effect sizes are small; no confidence intervals in the abstract. It uses largely the same genetic data sources as Huang 2023 (Mendelian randomization); for breast cancer the two studies' results point in opposite directions | PMID 37947877, doi:10.1007/s00508-023-02303-3 |
| Huang 2023 (Mendelian randomization) Two-sample Mendelian randomization | Genetic data on cannabis use (genome-wide meta-analysis in people of European ancestry); cancer data from UK Biobank and GliomaScan; 9 cancer types Adults of European ancestry | Genetic liability to cannabis use | Not applicable | Not applicable (genetic data) | Genetic liability to cannabis use was associated with cervical cancer (OR 1.0013; 95% CI 1.0004–1.0022; p = 0.005); suggestive evidence for laryngeal (OR 1.0004; p = 0.03) and breast cancer (1.0037; p = 0.047); no evidence of a causal relationship for melanoma, colorectal, oral, oropharyngeal or esophageal cancer, or glioma. The reported odds ratios are very close to 1; their clinical meaning is unclear | PMID 37099198, doi:10.1007/s00432-023-04807-x |
| Su 2025 Two-sample Mendelian randomization (FinnGen and UK Biobank) | Not reported (in the abstract) Adults of European ancestry | Genetic liability to cannabis use disorder (opioid use disorder was also studied) | Not applicable | Not applicable (genetic data) | No evidence of a causal relationship was found between cannabis use disorder and any of the cancer types studied (p > 0.05 for all). The associations found for opioid use disorder (an increase in bladder cancer, decreases in acute myeloid leukemia and ovarian cancer) were not significant after correction for multiple comparisons | PMID 40178608, doi:10.1007/s00213-025-06781-3 |
| Gallagher 2026 Retrospective matched cohort (US electronic health records, 67 health care organizations, 20 years; propensity score matching) | 149,632 per group (with and without a cannabis use disorder diagnosis) Adults over 18 | Cannabis (heavy use; use disorder diagnosis in the record) | Exposure: cannabis use disorder diagnosis in the record (amount and route of use unknown) | 20 years of records; plus analyses after 1 and 5 years | People with cannabis use disorder had a higher risk of lung and bronchus cancer (RR 3.87; 95% CI 3.43–4.38); the risk remained higher after 1 and 5 years; increases in all types: small cell (2.70; 1.31–5.58), adenocarcinoma (2.54; 1.59–4.08) and squamous cell (2.90; 1.41–5.95). Matching was based on demographics and lung cancer risk factors; because it is record-based, the amount of tobacco and how cannabis was used cannot be measured. Two letters published in the same journal questioned the clarity of the methods and the interpretation; the authors replied | PMID 42044619, doi:10.1016/j.lungcan.2026.109421, PMID 42172736, PMID 42442866, PMID 42372382 |
| Gallagher 2024 Retrospective multicenter cohort (US electronic health records, 64 health care organizations; propensity score matching) | 116,076 people diagnosed with a cannabis-related disorder and 3,985,286 without the diagnosis; 115,865 per group after matching US adults with an outpatient record and no previous head and neck cancer | Cannabis (cannabis-related disorder diagnosis in the record) | Exposure: cannabis-related disorder diagnosis in the record (amount, frequency and form unknown) | 20 years of records (through April 2024) | People with a cannabis-related disorder had a higher risk of any head and neck cancer (RR 3.49; 95% CI 2.78–4.39): oral (2.51; 1.81–3.47), oropharyngeal (4.90; 2.99–8.02) and laryngeal (8.39; 4.72–14.90). Matching included age, race and ethnicity, alcohol use disorder and tobacco use (by diagnosis code); the amount of tobacco and alcohol, HPV and tumor type were not included. The authors noted that dose-response could not be examined and that cannabis use may be underrecorded in the records. A commentary was published in the same issue, followed by two letters asking for clarification | PMID 39115834, doi:10.1001/jamaoto.2024.2419, PMID 40014339, PMID 39636626, PMID 39636627, PMID 39636616, the texts of the commentary and letters could not be read |
| Davis 2025 Retrospective matched cohort (US, TriNetX health records, 2004–2024; separate propensity score matching for each cancer) | 74,642 people diagnosed with cannabis abuse or dependence and 4,709,585 without the diagnosis (numbers after matching vary by cancer) US adults with no previous genitourinary cancer | Cannabis (abuse or dependence diagnosis in the record) | Exposure: diagnosis code in the record (amount unknown) | Records from 2004–2024 | After matching, cannabis abuse or dependence was associated with an increased risk of bladder (0.14% vs 0.03%; RR 4.21; 95% CI 2.70–6.57), kidney (RR 3.70; 2.52–5.43) and prostate cancer (RR 2.80; 2.19–3.58); no significant association with upper urinary tract, testicular or penile cancer (because these cancers are rare, an association cannot be ruled out). Matching was based on demographics, tobacco use, nicotine dependence, other substance use disorders and each cancer's risk factors; no dose information | PMID 40484779, doi:10.1016/j.urolonc.2025.05.010 |
| Maan 2026 Retrospective multicenter matched cohort (TriNetX; propensity score matching) | 6858 patients with chronic pancreatitis per group after matching (before matching, 10,864 with and 42,160 without cannabis use disorder) Adults with chronic pancreatitis (a group already at high risk of pancreatic cancer) | Cannabis (use disorder diagnosis in the record) | Exposure: diagnosis code in the record | Mean follow-up 736 days (with the disorder) and 896 days (without) | Fewer pancreatic cancers were detected during follow-up in people with cannabis use disorder (67 vs 274 cases; HR 0.26; 95% CI 0.20–0.34); there was a slight increase in acute pancreatitis attacks (HR 1.10; 1.04–1.17). Follow-up was shorter in people with the use disorder; the authors interpret the finding as 'less detection during follow-up' and call for prospective confirmation. An inverse (lower-risk) finding, in a specific patient group | PMID 41533288, doi:10.1007/s12029-025-01383-w, PMID 41779300 |
| Cuomo 2025 Retrospective cohort (health records of 6 academic centers of the University of California) | 45,129 people; 949 (2.1%) diagnosed with cannabis use disorder during follow-up Adults screened for substance use disorder with no previous oral cancer | Cannabis (use disorder diagnosis in the record) | Exposure: new diagnosis code during follow-up | 5-year follow-up (baseline 2012–2019; records through December 2024) | Oral (lip or tongue) cancer occurred in 0.74% of people with cannabis use disorder and 0.23% of those without; after adjustment for age, sex, body mass index and smoking, the odds were about three times higher (OR 3.25; 95% CI 1.47–7.17; HR 3.25; 1.48–7.13). Few cases in the disorder group (0.74% of 949 people); there were no data on alcohol, HPV or socioeconomic status. The authors wrote that routine oral exams may be useful in this group | PMID 40746396, doi:10.1016/j.pmedr.2025.103185 |
| Katz 2026 Retrospective hospital database study (i2b2, ICD-10 codes; logistic regression) | Not reported (in the abstract) Patients with head and neck cancer and cannabis users in a hospital database | Cannabis use (diagnosis code) | Not applicable | Not reported (in the abstract) | In cannabis users, the odds of oropharyngeal cancer were 3.12 times and of oral cancer 2.38 times higher in the crude analysis; they remained significant after adjustment for age, sex and race, but significance was lost after adjustment for alcohol (oropharynx 1.07; oral 0.7) or smoking (0.87; 0.62); with adjustment for HPV vaccination, oropharynx 1.02. According to the authors, alcohol and smoking rather than cannabis may explain the association | PMID 40935384, doi:10.1111/jop.70055 |
| Huang 2023 (UK Biobank) Prospective population cohort (UK Biobank) and Mendelian randomization | 151,945 people (33,449 had used cannabis); testicular and prostate analyses in 64,730 men UK adults aged 40–69 | Cannabis use (questionnaire; past and current use separated) | Exposure: 1–2, 3–10, 11–100 or more than 100 lifetime uses; in the analysis, never vs past use | Enrollment 2006–2010, follow-up through May 2020 | Past use was associated with a lower risk of kidney cancer (HR 0.61; 95% CI 0.40–0.93) and prostate cancer (HR 0.83; 0.74–0.94; 0.82 in the abstract); a nonsignificant decrease in bladder cancer (0.77; 0.58–1.02), significant in women (0.43; 0.21–0.86); no association with testicular cancer (0.85; 0.37–1.97; only 29 cases, participants aged 40–69). All urological cancers were more common in current users; according to the authors, this may reflect use for treatment after diagnosis (reverse causation). Mendelian randomization suggested a possible decrease in kidney cancer. Tobacco smokers were more common among cannabis users; the bladder and kidney analyses were adjusted for tobacco, the prostate analysis only for age and family history. An inverse (lower-risk) finding | PMID 35975633, doi:10.1002/cam4.5132 |
| Callaghan 2017 Prospective population cohort (Swedish military conscription, 42-year follow-up; linkage with national registries) | 49,343 men (45,250 in the analysis; 119 testicular cancers) Swedish men aged 18–21 who underwent military conscription in 1969–1970 | Cannabis use (non-anonymous questionnaire at conscription) | Exposure: lifetime use; more than 50 times counted as 'heavy' | 1970–2011 | Ever use was not significantly associated with testicular cancer (adjusted HR 1.42; 95% CI 0.83–2.45); more than 50 uses was associated with an increased risk of testicular cancer (HR 2.57; 1.02–6.50). Analyses were adjusted for tobacco, alcohol and other factors. Use was asked about only once, in youth; use in later years is unknown | PMID 29093004, doi:10.1158/1055-9965.EPI-17-0428 |
| Callaghan 2013 Prospective population cohort (Swedish military conscription, 40-year follow-up; linkage with national registries) | 49,321 men (44,284 in the analysis) Swedish men aged 18–20 | Smoking cannabis (questionnaire at conscription) | Exposure: more than 50 lifetime uses counted as 'heavy' (1.7% of participants) | 1969–1970 to 2009 | Heavy use (more than 50 lifetime uses) was associated with a more than twofold increase in lung cancer risk over 40 years (HR 2.12; 95% CI 1.08–4.14); adjusted for baseline tobacco and alcohol use, respiratory conditions and socioeconomic status. Results for lower levels of use are not in the abstract. Use was asked about only once; tobacco and cannabis use in later years is unknown | PMID 23846283, doi:10.1007/s10552-013-0259-0 |
| Thomas 2015 Prospective cohort (California Men's Health Study; questionnaire and electronic health records) | 84,170 men; 279 bladder cancers Multiethnic men aged 45–69 | Cannabis use (questionnaire, 2002–2003) | Exposure: ever use | 11 years | In people who used cannabis only, bladder cancer risk was 45% lower (HR 0.55; 95% CI 0.31–1.00); in those who smoked tobacco only, it was higher (1.52; 1.12–2.07); in those who used both, not significant (1.28; 0.91–1.80). According to the authors, cause and effect cannot be established; adjustment was limited to age, race and body mass index (according to Ghasemiesfe 2019, there was not enough adjustment for important confounders). An inverse (lower-risk) finding | PMID 25623697, doi:10.1016/j.urology.2014.08.060, PMID 25623698, PMID 25623699, PMID 26292856, their texts could not be read |
| Efird 2004 Prospective cohort (Kaiser Permanente, Northern California) | 133,811 people Health plan members over 25 with no previous brain tumor | Smoking cannabis (questionnaire) | Exposure: smoking cannabis at least once a month | Up to 21 years of follow-up (enrollment 1977–1985) | In people who smoked cannabis at least once a month, after adjustment for cigarettes and other factors, the risk of adult-onset malignant glioma (a type of brain tumor) was 2.8 times higher (95% CI 1.3–6.2); no dose-response relationship was seen. Ghasemiesfe 2019 rated the evidence as insufficient, noting that the amount of use was not measured | PMID 15174522, doi:10.1023/b:neon.0000024746.87666.ed |
| Sidney 1997 Retrospective cohort (Kaiser Permanente health checkups, San Francisco and Oakland) | 64,855 people People aged 15–49 attending health checkups | Cannabis use (questionnaire) | Exposure: ever or current use; fewer than 7 lifetime uses counted as 'experimentation' | Mean follow-up 8.6 years (enrollment 1979–1985, follow-up through 1993) | No increase in all cancers combined (men RR 0.9; women 1.0; 95% CI 0.8–1.1); no association with tobacco-related cancers or with colorectal, lung, melanoma, prostate, breast or cervical cancer. Among nonsmokers of tobacco, prostate cancer (RR 3.1; 1.0–9.5) and, borderline, cervical cancer (1.4; 1.0–2.1) were more common in cannabis users. Participants were young and follow-up was short | PMID 9328194, doi:10.1023/a:1018427320658, PMID 31940033 |
| Zhang 2015 Pooled case-control analysis (International Lung Cancer Consortium; individual data from 6 studies) | 2159 lung cancer cases, 2985 controls (370 cases and 1358 controls had never smoked tobacco) Adults from the US, Canada, the United Kingdom and New Zealand | Smoking cannabis | Exposure: habitual use; at least 1 joint-equivalent a day; at least 10 joint-years | Studies 1999–2013 | Habitual cannabis smokers did not have an increased risk of lung cancer (OR 0.96; 95% CI 0.66–1.38); no increase for at least one joint a day (0.88; 0.63–1.24) or at least 10 joint-years (0.94; 0.67–1.32) either. No association in people who had never smoked tobacco (1.03; 0.51–2.08). A nonsignificant trend toward an increase in adenocarcinoma (1.73; 0.75–4.00 and 1.74; 0.85–3.55); according to the authors, possible harm from heavy use cannot be ruled out. The New Zealand study in the pool had on its own reported an increase with heavy use (more than 10.5 joint-years) (RR 5.7; 1.5–21.6) | PMID 24947688, doi:10.1002/ijc.29036, Studies in the pool include the Los Angeles (Hashibe 2006, PMID 17035389, PMID 18238947, PMID 18238942, PMID 18591344, 18757709) studies |
| Marks 2014 Pooled case-control analysis (INHANCE consortium; individual data from 9 studies) | 1921 oropharyngeal cancer cases, 356 tongue cancer cases, 7639 controls Adults from the US and Latin America | Smoking cannabis | Exposure: ever use; frequency and duration | Varies by study | People who had ever smoked cannabis had a slightly higher risk of oropharyngeal cancer (tonsil and base of tongue area) (adjusted OR 1.24; 95% CI 1.06–1.47) and a lower risk of tongue cancer (0.47; 0.29–0.75). In a sensitivity analysis adjusted for HPV, the oropharyngeal association disappeared (0.99); in the 4 studies with known HPV antibody status there was no association to begin with (0.89; 0.65–1.19). In people who had never used tobacco or alcohol, 2.11 (0.97–4.62) for the oropharynx. According to the authors, the association may vary by tumor site; confounding by HPV and misclassification of exposure need to be ruled out | PMID 24351902, doi:10.1158/1055-9965.EPI-13-0181 |
| Berthiller 2009 Pooled case-control analysis (INHANCE consortium; individual data from 5 studies) | 4029 head and neck cancer cases, 5015 controls Studies from Los Angeles, Seattle, Tampa, Houston and Latin America | Smoking cannabis (self-reported) | Exposure: ever use; frequency, duration and cumulative use | Varies by study (1985–2000s) | Ever smoking cannabis did not increase head and neck cancer risk (OR 0.88; 95% CI 0.67–1.16); risk did not rise with frequency, duration or cumulative use. No increase in people who had never used tobacco (0.93; 0.63–1.37) or who had never used tobacco or alcohol (1.06; 0.47–2.38). Because frequent users were few in most studies, a moderate increase cannot be ruled out | PMID 19423532, doi:10.1158/1055-9965.EPI-08-0845, Studies in the pool include Los Angeles (Hashibe 2006, PMID 17035389, PMID 15173020 |
| Berthiller 2008 Pooled case-control analysis (Tunisia, Morocco, Algeria; 3 hospital-based studies) | 430 lung cancer cases, 778 controls (men only) Men from North African countries where cannabis is widely used and produced | Smoking cannabis (in the region, mostly mixed with tobacco) | Exposure: ever use; joint-years | Not reported (in the abstract) | All cannabis smokers also smoked tobacco. After adjustment for country, age, tobacco and occupational exposure, ever smoking cannabis was associated with an increased risk of lung cancer (OR 2.4; 95% CI 1.6–3.8; 2.3; 1.5–3.6 with adjustment for lifetime pack-years). In tobacco smokers who did not smoke cannabis, OR 10.9 (6.0–19.7); in those who smoked both tobacco and cannabis, 18.2 (8.0–41.0). Risk rose with joint-years, but not with dose or duration. According to the authors, residual confounding by tobacco may explain part of the increase | PMID 19057263, doi:10.1097/JTO.0b013e31818ddcde, PMID 17409920, OR 4.1, PMID 19057257 |
| Coste 2026 (TESTIS) Nationwide hospital-based case-control study (France) | 454 cases, 670 controls Men with testicular germ cell tumors and controls | Cannabis use (timing and frequency in adolescence and young adulthood) | Exposure: weekly equivalent score; daily, weekly and persistent use | Not reported (in the abstract) | Overall, cannabis use was not consistently associated with testicular tumor risk. Daily use in young adulthood was associated with increased risk (OR 1.50; 95% CI 1.02–2.19), especially for seminoma (OR adjusted for tobacco, alcohol and education 1.93; 1.13–3.31); weekly use throughout ages 12–25 had an adjusted OR of 1.85 (1.11–3.07). There was a dose-response relationship in young adulthood (p = 0.046; 0.016 for seminoma). No association with use in adolescence or with the nonseminoma type; this does not match the association with nonseminoma seen in older US studies; the authors wrote that the subtype results need independent confirmation | PMID 42447513, doi:10.1016/j.ejca.2026.116939 |
| Feng 2009 Multicenter case-control study (Algeria, Morocco, Tunisia) | 636 patients, 615 controls (cannabis analysis in men) People with nasopharyngeal cancer and controls | Cannabis (mostly smoked as 'kif', mixed with tobacco) | Exposure: ever use; more than 30 times a month; more than 2000 times in a lifetime | 2002–2005 | In men, ever cannabis use was associated with nasopharyngeal cancer (OR 1.83; 95% CI 1.04–3.22), but significance was lost after adjustment for cigarettes per day (1.54; 0.86–2.76); 2.62 (1.00–6.86) for more than 2000 lifetime uses. A stratified permutation analysis showed an association independent of cigarettes. 97% of cannabis users also smoked cigarettes; the trend toward an increase was in those who smoked cannabis mixed with tobacco (kif) (adjusted for cigarettes 1.94; 0.96–3.92), not in those who smoked it without tobacco (0.97; 0.37–2.52) | PMID 19724280, doi:10.1038/sj.bjc.6605281 |
| Bluhm 2006 Case-control study (US, Children's Oncology Group) | Mothers of 538 children with neuroblastoma and 504 controls Children diagnosed with neuroblastoma (a childhood cancer of nerve tissue) and age-matched controls | Maternal use of marijuana and other recreational drugs around pregnancy (self-reported) | Exposure: the month before pregnancy and the periods of pregnancy | Diagnosed 1992–1994 | Use of any illegal drug around pregnancy was associated with an increased risk of neuroblastoma (OR 1.82; 95% CI 1.13–3.00); the clearest was marijuana use in the first trimester (4.75; 1.55–16.48). Use in the month before pregnancy did not increase risk; the association was stronger in children diagnosed before age one. Adjustment was only for age at diagnosis and income; use is based on retrospective recall | PMID 16633913, doi:10.1007/s10552-005-0580-3 |
| Trivers 2006 Matched case-control study (US and Canada, Children's Cancer Group) | 517 cases, 610 controls Children under 18 diagnosed with acute myeloid leukemia (AML) | Maternal and paternal marijuana use (telephone interview) | Exposure: lifetime; 3 months before and during pregnancy | Diagnosed 1989–1993 | Maternal lifetime marijuana use was not associated with AML in the child (OR 0.89; 95% CI 0.66–1.19); use in the 3 months before or during pregnancy was inversely associated (0.43; 0.23–0.80); paternal use was not associated. The previously reported increase was not confirmed; the authors wrote that the low odds ratios may be due to recall bias (ORs adjusted for misclassification 0.82–1.40) | PMID 16466429, doi:10.1111/j.1365-3016.2006.00700.x |
| Grufferman 1993 Matched case-control study (US, national) | 322 cases, 322 controls Children and young people aged 0–20 diagnosed with rhabdomyosarcoma (a soft tissue cancer) | Maternal and paternal marijuana and cocaine use (telephone interview) | Exposure: the year before the child's birth | Not reported (in the abstract) | Maternal marijuana use in the year before birth was associated with a 3-fold (OR 3.0; 95% CI 1.4–6.5) and paternal use with a 2-fold (2.0; 1.3–3.3) increase in rhabdomyosarcoma risk. Marijuana and cocaine use, and maternal and paternal use, were highly correlated with each other; the effects could not be separated | PMID 8318638, doi:10.1007/BF00051316 |
| Kuijten 1990 Matched case-control study (US; Pennsylvania, New Jersey, Delaware) | 163 matched pairs Children under 15 diagnosed with astrocytoma (a brain tumor) | Marijuana exposure during pregnancy (reported by the mother) | Exposure: use during pregnancy | Diagnosed 1980–1986 | Marijuana exposure during pregnancy was associated with a borderline, not statistically significant increase in childhood astrocytoma (OR 2.8; p = 0.07). Use of antinausea medicine during pregnancy (OR 2.0) and a family history of cancer were also risk factors; alcohol and tobacco during pregnancy were not | PMID 2328486 |
| Robison 1989 Matched case-control study (US, Children's Cancer Study Group) | 204 case-control pairs Children diagnosed with acute nonlymphoblastic leukemia (ANLL) | Maternal use of mind-altering drugs just before or during pregnancy (marijuana in the title) | Exposure: just before and during pregnancy | Not reported (in the abstract) | Maternal use of mind-altering drugs just before or during pregnancy was associated with an 11-fold increase in risk of this type of leukemia in the child (p = 0.003); children exposed to marijuana were diagnosed at a younger age and were concentrated in certain subtypes (myelomonocytic, monocytic). Small number of cases; the larger 2006 study (Trivers 2006) did not confirm this association | PMID 2649219 |
| EFSA 2026 (European Food Safety Authority statement) Agency assessment (safety of CBD as a novel food; animal and human literature and application dossiers from the 2022 statement through June 2024) | Literature review; for the dose calculation, 5 good laboratory practice (GLP) 90-day rat studies General population who would use CBD as a food supplement | Pure CBD (purity at least 98%) | Not applicable (agency assessment) | Studies published through June 2024 | The panel wrote that the data gaps it identified in 2022 remain. Genetic damage (genotoxicity): although a new study suggests that pure CBD itself does not cause genetic damage, the panel concluded that each product needs to be assessed separately, because the manufacturing process, contaminants and formulation (e.g., nanoparticles) may introduce new hazards. The effects of long-term use on the liver, nervous system, reproduction and immune system are uncertain; because the dose calculation is based on 90-day studies, an additional uncertainty factor (2) was applied for extrapolation to long-term use. The statement does not separately address carcinogenicity or cancer risk. Safety could not be established in people under 25, pregnant and breastfeeding people, and people taking medicines Side effects: Consistent liver effects in animal studies; in human studies, possible liver injury, especially with other medicines; gastrointestinal effects at high doses | PMID 41668771, doi:10.2903/j.efsa.2026.9862, EFSA Journal 2026, 24(2):e9862, previous statement: EFSA NDA Panel 2022 |
| Epidiolex US label 2026 (animal studies) Animal: 2-year carcinogenicity studies (mouse and rat) and genotoxicity (genetic damage) tests; US label of the approved pure CBD medicine, Section 13.1, and European product information, Section 5.3; the manufacturer's studies, only summarized in the label; no peer-reviewed publications were found in this search | Number of animals not stated in the label Mice and rats (not human data) | Pure CBD (approved oral solution, Epidiolex) | Mice 30, 100 and 300 mg/kg/day; rats 15, 50 and 150 mg/kg/day, by mouth (animal study dose; not a personal recommendation) | 2 years | According to the US label, in mice, oral CBD for 2 years increased the incidence of benign liver tumors (hepatocellular adenoma) in males at the highest dose (300 mg/kg/day); at the middle dose (100 mg/kg/day), blood exposure was about 1–2 times that at the highest recommended human doses of the medicine. In rats, there was no significant increase in tumor incidence over 2 years (exposure at the highest dose about 10–12.5 times the human dose). The European product information reports the same studies differently: in mice, benign liver tumors increased in males at all doses and in females at the highest dose (exposure at the highest dose about 3 times the human dose); in the 104-week rat study, focal Leydig cell hyperplasia and Leydig cell adenoma increased in males at all doses (exposure at the lowest dose below the human dose), and at the highest dose (exposure about 10 times) a Leydig cell carcinoma was seen in one male rat; the document states that Leydig tumors in rats are generally considered of limited relevance to humans. Neither document explains the reason for the difference. CBD and its two main metabolites were negative in genotoxicity tests (bacterial mutation, rat Comet and bone marrow micronucleus). The label contains no information on cancer risk in humans | DailyMed setid 8bf27097-4870-43fb-94f0-f3d0871d1eec (version 35, June 15, 2026), Section 13.1 Carcinogenesis and Mutagenesis, European product information: EMA, Epidyolex EPAR product information, Section 5.3 Preclinical safety data (read on October 29, 2026, server date October 8, 2026, revision date in Section 10 is blank) |
| NTP 1996 (THC, animal study) Animal: 2-year carcinogenicity study (US National Toxicology Program, Technical Report 446; oral, by gavage) | 60–70 rats and 60–62 mice per dose group per sex F344/N rats and B6C3F1 mice | THC (97% pure), in corn oil | Rats 12.5, 25 and 50 mg/kg; mice 125, 250 and 500 mg/kg; 5 days a week (animal study dose; not a personal recommendation) | 2 years (104–106 weeks); plus 13-week studies | No evidence of carcinogenic activity of THC in rats. 'Equivocal' evidence in mice: thyroid follicular adenomas increased at the lowest dose (125 mg/kg), but the increase was not dose-related. Mammary gland, uterine, pituitary, pancreatic, testicular interstitial cell and liver tumors were less common in the THC groups; the report attributed this decrease most likely to the animals' lower body weight. THC did not cause mutations in bacteria and did not increase micronucleus frequency in mice Side effects: Convulsions and seizures after dosing or handling; lower body weight; in the 13-week study, testicular shrinkage and reduced uterine and ovarian development at high doses | PMID 12594529, PMID 8812248, Section 13.1) |
Reported side effects
- Cannabis use and low birth weight in pregnancy (equivalent OR 1.43) and small-for-gestational-age babies (1.61), crashes among drivers (1.27) and psychosis with use in adolescence in the general population (1.71): the strongest evidence class in the umbrella review; the pregnancy estimates were not adjusted for confounders, and for psychosis this class was reached only with cohorts (Solmi 2023)
- In randomized trials of cannabis-based medicines, an increase in nervous system (equivalent OR 2.84) and psychiatric side effects (3.07) (Solmi 2023)
- Pure CBD: consistent liver effects in animals; in people, a possibility of liver harm, especially together with other medicines (EFSA 2026)
- Pure CBD, animals: an increase in benign liver tumors (hepatocellular adenoma) in mice in 2-year studies (according to the US label, in males at the highest dose; according to the European product information, in males at all doses and in females at the highest dose); in rats, no significant increase in tumors according to the US label, but according to the European product information, an increase in Leydig cell overgrowth and benign tumors in the testis in males (relevance to humans generally considered limited)
- THC, animals: no carcinogenic effect in rats over 2 years, an equivocal finding in the thyroid in mice that was not dose-related; convulsions and seizures at high doses, testicular shrinkage at 13 weeks (NTP 1996)
- In chronic pancreatitis, a slight increase in acute pancreatitis attacks with cannabis use disorder (HR 1.10; Maan 2026)
Monitoring done in studies
- No ongoing or planned study measuring the cancer risk of cannabis or CBD use was found on ClinicalTrials.gov (October 2026)
- It has been suggested that routine oral exams may be useful in people with cannabis use disorder (Cuomo 2025)
- The European Food Safety Authority wants genetic damage in CBD products to be assessed product by product; data gaps for long-term use remain (EFSA 2026)
Who should be careful
- Almost all of the cancer findings on this page come from smoked marijuana; they cannot be carried over to CBD oil as evidence of either harm or benefit
- Smoking marijuana mixed with tobacco: in the North African study, the odds of lung cancer were highest in people who smoked both tobacco and cannabis (a single pooled analysis entangled with tobacco; Berthiller 2008)
- Pregnancy and breastfeeding: avoiding cannabis is recommended (Solmi 2023); the safety of CBD in people who are pregnant or breastfeeding could not be established (EFSA 2026)
- Young men: the link with testicular cancer was seen in young men with long-term, frequent or heavy use (weak evidence; Gurney 2015; Callaghan 2017; Coste 2026)
- If you have been diagnosed with cancer: the effect of cannabis and CBD on the course of cancer is covered on the 'Cancer Treatment and CBD' page; talk to your oncologist before using them during treatment
- People who take medicines regularly: CBD interacts with the liver enzymes that break down medicines (EFSA 2026)
Drug interactions
- The studies on this page did not examine drug interactions; details are in the site's drug interactions section
- CBD interacts with the enzymes in the liver that break down medicines; people being treated for cancer should consult their oncologist before starting (EFSA 2026)
Abbreviations: RCT, randomized controlled trial (a study in which participants are assigned to groups by chance); placebo, an inactive substance; SMD, OR and RR, effect measures used in analyses that pool studies; CYP, liver enzymes that break down medicines.
If you are considering CBD
- Tobacco is one of the habits that most affects cancer risk: in the North African study, the odds of lung cancer were very high in cigarette smokers, and even higher in those who smoked both cigarettes and cannabis. Smoking marijuana mixed with tobacco means breathing in both kinds of smoke together; you can talk with your doctor about getting support to quit.
- CBD oil and smoked marijuana are not the same thing: almost all of the cancer findings on this page come from smoked marijuana; there are no human data for CBD oil.
- Check the label and certificate of analysis (COA) to see whether the product you use contains THC.
- Avoiding cannabis products during pregnancy and breastfeeding is recommended; the safety of CBD during these periods has not been established either.
- If you have used cannabis frequently for a long time, tell your doctor; some researchers suggest that an oral exam could be added to routine checkups for people with cannabis use disorder.
- If you have been diagnosed with cancer or are being treated, talk with your oncologist before using CBD or cannabis.
Choose your age group, medicines and situation to prepare a short summary you can take to your doctor. Nothing you enter is sent anywhere.
Bottom line
Whether pure CBD raises cancer risk is not known: there are no studies looking at this in people; in two-year animal studies, benign liver tumors increased in mice and, according to the European product information, benign tumors of the testis also increased in male rats, and what this means for people is not known. For smoked cannabis, the most consistent finding is a link with testicular cancer after long-term or frequent use; results for lung and head and neck cancers are mixed and hard to separate from the effect of tobacco; and for some cancers there are findings in the opposite direction. The strength of evidence is weak. Cannabis smoke contains many of the harmful substances in tobacco smoke, and the highest risk was seen in people who breathe in both kinds of smoke together; talking through your questions with your doctor is the safest path.
Frequently asked questions
Does CBD oil cause cancer?
There is no human study showing this, and no study has looked at this question directly. In two-year animal studies of the approved pure CBD medicine, benign liver tumors increased in mice; in rats, the US label reports no significant increase in tumors, while the European product information reports an increase in benign tumors of the testis in male rats and adds that the relevance of these rat tumors to humans is generally considered limited; CBD was negative in genotoxicity (genetic damage) tests. The European Food Safety Authority stresses that the effects of long-term use are unknown and that the way a product is made matters. In short, it has not been shown that CBD either raises or lowers cancer risk; the evidence is insufficient.
Does smoking marijuana cause cancer?
It depends on the type of cancer, and the evidence is weak. The most consistent link was seen with testicular cancer after long-term or frequent use. For lung cancer, large combined analyses found no increase (the 2017 report of the US National Academies also saw no association), while some cohort and registry studies found an increase with heavy use; results for head and neck cancers are also conflicting. These studies are observational, and because most people who smoke cannabis also smoke cigarettes, it is hard to separate the effects.
Is cannabis smoke as harmful as cigarette smoke?
Laboratory comparisons found that cannabis smoke contains many of the harmful substances in tobacco smoke, and some of them (e.g., ammonia and hydrogen cyanide) at higher levels. In human studies, however, the lung cancer risk seen with cannabis remained small or unclear next to the very high risk seen with tobacco; but because cannabis is often used together with tobacco, this comparison is not easy. The highest risk was seen in people who breathe in both kinds of smoke together.
Does cannabis raise the risk of testicular cancer?
This is the most consistent link seen in research. In analyses that combined three US case-control studies, long-term (more than 10 years) or frequent use was linked to about a 1.4–1.9-fold increase in testicular tumors; an increase with heavy use was also seen in young Swedish men followed for 42 years. However, all of these analyses are based on the same three studies, the tumor type affected differed between studies, and no link was found in a large UK cohort with older participants; the strength of evidence is low. Because testicular cancer is rare, the absolute risk is small: in the Swedish study it occurred in 119 of 45,000 men over 42 years.
Some studies say cannabis lowers cancer risk; is that true?
There are studies reporting fewer bladder, prostate, kidney, oral and pancreatic cancers in cannabis users; a 2021 meta-analysis also found a lower overall risk when some studies were excluded. But these findings are also observational and not consistent: there are also registry studies reporting an increase in the same cancers; factors such as limited adjustment for confounders, short follow-up and starting use after diagnosis can affect the results. It has not been shown that cannabis or CBD prevents cancer; the role of CBD in cancer treatment is covered on a separate page.
Does cannabis use during pregnancy cause cancer in the child?
Some small case-control studies carried out between 1989 and 2006 linked the mother's (and in one, also the father's) use of marijuana or other recreational drugs to leukemia, rhabdomyosarcoma and neuroblastoma in the child (the increase seen for brain tumors was not significant); however, the largest leukemia study did not confirm this link, and use was reported from memory years later. The evidence is insufficient. That said, cannabis use during pregnancy was more consistently linked to other outcomes such as low birth weight; for this reason, avoiding cannabis during pregnancy and breastfeeding is recommended. The safety of CBD during these periods could not be established either.
Is THC that is eaten, vaporized or taken as a medicine safer?
This search found no human study of cancer risk from edible or vaporized cannabis products or from THC taken by mouth as a medicine. THC given by mouth did not cause cancer in a two-year rat study; this suggests that the main concern for lung and head and neck cancers may be the products of burning, but it is not evidence in people. Whether the link seen with testicular cancer is due only to smoke is also not known. The non-cancer side effects of THC-containing products, however, apply in every form: in randomized trials of cannabis-based medicines, nervous system and psychiatric side effects also increased.
Do CBD oils sold in Turkey contain THC?
In Turkey, products obtained from cannabis are regulated by the Kenevirden Elde Edilen Ürünlere Dair Yönetmelik (Regulation on Products Derived from Hemp) dated January 31, 2026. These products, including CBD, can be sold only in pharmacies. Those classified as medicines or health products are dispensed with a prescription; for supplement products and cosmetics with a THC content of at most 0.3%, the regulation does not state a prescription requirement. So these products may contain a very small amount of THC; it is a good idea to check the label and certificate of analysis (COA). The cancer findings on this page come from smoked marijuana; cancer risk has not been studied with oils this low in THC.
References
Show 41 references
- Nargis 2025. Umbrella review (review of the global epidemiological evidence on cannabis and cancer risk). PMID 39427677, doi:10.1016/S2468-2667(24)00223-8, PMID 40921170, 10:e814, its content could not be read)
- Solmi 2023. Umbrella review (101 meta-analyses: 50 observational, 51 of RCTs; evidence classes for observational evidence, GRADE for RCTs). PMID 37648266, doi:10.1136/bmj-2022-072348, PROSPERO CRD42018093045, PMID 37722728
- Ghasemiesfe 2019. Systematic review and meta-analysis (observational studies; strength-of-evidence grading). PMID 31774524, doi:10.1001/jamanetworkopen.2019.16318, PMID 31940033, does not change the results). PROSPERO CRD42018102457
- Clark 2021. Scoping review and meta-analysis (observational studies; US-focused). PMID 33998861, doi:10.1089/can.2019.0095
- NASEM 2017 (US National Academies report). Expert committee report (US National Academies of Sciences, Engineering, and Medicine; assessment based on good- and fair-quality systematic reviews and selected primary studies; five-level evidence grading). PMID 28182367, doi:10.17226/24625, National Academies Press, chapter 5 'Cancer' (nationalacademies.org/read/24625/chapter/7, read on October 28, 2026), the NCBI Bookshelf copy (NBK425767) could not be opened because of bot verification. The same report also appears in the Glaucoma and Irritable Bowel and Stomach Problems tables
- Mehra 2006. Systematic review (no meta-analysis). PMID 16832000, doi:10.1001/archinte.166.13.1359
- de Carvalho 2015. Systematic review and meta-analysis (matched case-control studies). PMID 26433192, doi:10.1016/j.archoralbio.2015.09.009, PMID 27449844, title 'insufficient evidence to support or refute the association')
- Ibrahim Mohammad 2025. Systematic review and meta-analysis (case-control studies; random effects). PMID 41236922, doi:10.1080/15332640.2025.2581692
- Song 2020. Systematic review and meta-analysis (epidemiological studies; random effects). PMID 32409200, doi:10.1016/j.urolonc.2020.03.013
- Gurney 2015. Systematic review and meta-analysis (case-control studies; random effects). PMID 26560314, doi:10.1186/s12885-015-1905-6, PMID 19204904, PMID 20925043, PMID 22965656, PMID 23233189, PMID 41188200, which re-pooled the same studies, was not given a separate row: its current-use result (OR 1.62, 1.13–2.31) is identical to this meta-analysis and its nonseminoma result (1.71, 1.12–2.60) is identical to Song 2020
- Mehrnoush 2022. Systematic review (qualitative synthesis; Newcastle-Ottawa scale). PMID 35775355, doi:10.4081/aiua.2022.2.248
- Baumeister 2021. Two-sample Mendelian randomization (a 'natural experiment' using genetic liability). PMID 33852959, doi:10.1016/j.jtho.2021.03.025
- Niu 2024. Two-sample Mendelian randomization. PMID 37947877, doi:10.1007/s00508-023-02303-3
- Huang 2023 (Mendelian randomization). Two-sample Mendelian randomization. PMID 37099198, doi:10.1007/s00432-023-04807-x
- Su 2025. Two-sample Mendelian randomization (FinnGen and UK Biobank). PMID 40178608, doi:10.1007/s00213-025-06781-3
- Gallagher 2026. Retrospective matched cohort (US electronic health records, 67 health care organizations, 20 years; propensity score matching). PMID 42044619, doi:10.1016/j.lungcan.2026.109421, PMID 42172736, PMID 42442866, PMID 42372382
- Gallagher 2024. Retrospective multicenter cohort (US electronic health records, 64 health care organizations; propensity score matching). PMID 39115834, doi:10.1001/jamaoto.2024.2419, PMID 40014339, PMID 39636626, PMID 39636627, PMID 39636616, the texts of the commentary and letters could not be read
- Davis 2025. Retrospective matched cohort (US, TriNetX health records, 2004–2024; separate propensity score matching for each cancer). PMID 40484779, doi:10.1016/j.urolonc.2025.05.010
- Maan 2026. Retrospective multicenter matched cohort (TriNetX; propensity score matching). PMID 41533288, doi:10.1007/s12029-025-01383-w, PMID 41779300
- Cuomo 2025. Retrospective cohort (health records of 6 academic centers of the University of California). PMID 40746396, doi:10.1016/j.pmedr.2025.103185
- Katz 2026. Retrospective hospital database study (i2b2, ICD-10 codes; logistic regression). PMID 40935384, doi:10.1111/jop.70055
- Huang 2023 (UK Biobank). Prospective population cohort (UK Biobank) and Mendelian randomization. PMID 35975633, doi:10.1002/cam4.5132
- Callaghan 2017. Prospective population cohort (Swedish military conscription, 42-year follow-up; linkage with national registries). PMID 29093004, doi:10.1158/1055-9965.EPI-17-0428
- Callaghan 2013. Prospective population cohort (Swedish military conscription, 40-year follow-up; linkage with national registries). PMID 23846283, doi:10.1007/s10552-013-0259-0
- Thomas 2015. Prospective cohort (California Men's Health Study; questionnaire and electronic health records). PMID 25623697, doi:10.1016/j.urology.2014.08.060, PMID 25623698, PMID 25623699, PMID 26292856, their texts could not be read
- Efird 2004. Prospective cohort (Kaiser Permanente, Northern California). PMID 15174522, doi:10.1023/b:neon.0000024746.87666.ed
- Sidney 1997. Retrospective cohort (Kaiser Permanente health checkups, San Francisco and Oakland). PMID 9328194, doi:10.1023/a:1018427320658, PMID 31940033
- Zhang 2015. Pooled case-control analysis (International Lung Cancer Consortium; individual data from 6 studies). PMID 24947688, doi:10.1002/ijc.29036, Studies in the pool include the Los Angeles (Hashibe 2006, PMID 17035389, PMID 18238947, PMID 18238942, PMID 18591344, 18757709) studies
- Marks 2014. Pooled case-control analysis (INHANCE consortium; individual data from 9 studies). PMID 24351902, doi:10.1158/1055-9965.EPI-13-0181
- Berthiller 2009. Pooled case-control analysis (INHANCE consortium; individual data from 5 studies). PMID 19423532, doi:10.1158/1055-9965.EPI-08-0845, Studies in the pool include Los Angeles (Hashibe 2006, PMID 17035389, PMID 15173020
- Berthiller 2008. Pooled case-control analysis (Tunisia, Morocco, Algeria; 3 hospital-based studies). PMID 19057263, doi:10.1097/JTO.0b013e31818ddcde, PMID 17409920, OR 4.1, PMID 19057257
- Coste 2026 (TESTIS). Nationwide hospital-based case-control study (France). PMID 42447513, doi:10.1016/j.ejca.2026.116939
- Feng 2009. Multicenter case-control study (Algeria, Morocco, Tunisia). PMID 19724280, doi:10.1038/sj.bjc.6605281
- Bluhm 2006. Case-control study (US, Children's Oncology Group). PMID 16633913, doi:10.1007/s10552-005-0580-3
- Trivers 2006. Matched case-control study (US and Canada, Children's Cancer Group). PMID 16466429, doi:10.1111/j.1365-3016.2006.00700.x
- Grufferman 1993. Matched case-control study (US, national). PMID 8318638, doi:10.1007/BF00051316
- Kuijten 1990. Matched case-control study (US; Pennsylvania, New Jersey, Delaware). PMID 2328486
- Robison 1989. Matched case-control study (US, Children's Cancer Study Group). PMID 2649219
- EFSA 2026 (European Food Safety Authority statement). Agency assessment (safety of CBD as a novel food; animal and human literature and application dossiers from the 2022 statement through June 2024). PMID 41668771, doi:10.2903/j.efsa.2026.9862, EFSA Journal 2026, 24(2):e9862, previous statement: EFSA NDA Panel 2022
- Epidiolex US label 2026 (animal studies). Animal: 2-year carcinogenicity studies (mouse and rat) and genotoxicity (genetic damage) tests; US label of the approved pure CBD medicine, Section 13.1, and European product information, Section 5.3; the manufacturer's studies, only summarized in the label; no peer-reviewed publications were found in this search. DailyMed setid 8bf27097-4870-43fb-94f0-f3d0871d1eec (version 35, June 15, 2026), Section 13.1 Carcinogenesis and Mutagenesis, European product information: EMA, Epidyolex EPAR product information, Section 5.3 Preclinical safety data (read on October 29, 2026, server date October 8, 2026, revision date in Section 10 is blank)
- NTP 1996 (THC, animal study). Animal: 2-year carcinogenicity study (US National Toxicology Program, Technical Report 446; oral, by gavage). PMID 12594529, PMID 8812248, Section 13.1)
Points that could not be verified from the full text
- The full text of most studies in the table is not open access; the numbers were taken from the abstracts. Full texts read: Ghasemiesfe 2019, Zhang 2015, Berthiller 2009, Marks 2014, Gurney 2015, Callaghan 2017 (methods), Huang 2023 (UK Biobank), Clark 2021, Solmi 2023, Gallagher 2024, Cuomo 2025, Maan 2026, Feng 2009 and the European Food Safety Authority statement. The cancer chapter of the 2017 report of the US National Academies was read on the publisher's website.
- The content of the commentaries and letters criticizing the 2024 head and neck and 2026 lung registry studies (five texts in total) and of the correction to the 2025 cancer-specific umbrella review could not be read; only their titles are known.
- A 2026 meta-analysis reporting an increase in lung cancer (Karimi 2026) was not included in the table: the relative risks listed in its table for the 1997 cohort (10.3 and 9.8) do not match the cannabis results in that study's own abstract and in the 2019 review (RR 0.9 and 1.1), and when one of these two numbers is removed, the increase in the cohorts is no longer significant.
- One table of the comprehensive 2019 review (Ghasemiesfe 2019) lists 'low' strength of evidence for head and neck cancer and an increase with use of more than 8 joint-years; the text and abstract, however, say no association was found. This page is based on the text and abstract. The review's published correction changes only one table comment.
- A non-peer-reviewed 2026 preprint (Mendelian randomization) was not included in the table.
- The licensing status in Turkey of THC-containing medicines such as dronabinol and nabiximols was not verified in this search.
Research history
Here we record what changed on this page, when and why, with dates. The newest change is at the top.
A note was added that the psychosis rate in the side effects refers to cannabis use in adolescence (Solmi 2023, PMID 37648266, full text). The conclusion and the evidence level did not change.
The number of critical texts in the unverifiable items was corrected: one commentary and four letters were published in response to the registry studies, five texts in total (PMID 39115811, 39636626, 39636627, 42172736, 42442866). The conclusion and the evidence level did not change.
The information on the two-year animal studies of the approved pure CBD medicine was completed with the European product information. The previous text relied only on the US label: in mice, an increase in benign liver tumors in males at the highest dose; in rats, no significant increase in tumors. The European product information writes that, in the same studies, these liver tumors increased in male mice at all doses and in female mice at the highest dose, and that in male rats, overgrowth and benign tumors of the Leydig cells in the testis increased, with a malignant tumor seen in one rat at the highest dose; it adds that the relevance of these rat tumors for humans is generally considered limited. These are animal findings; there is still no study examining cancer risk with pure CBD in humans. The conclusion and the strength of evidence did not change.
Older changes (1)
Page published. This first review examined 41 studies.