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In spite of the increasing scientific interest to understand how cannabinoids can help to treat cancer disease, symptoms and the associated chemotherapy side effects, the existing scientific evidence is not enough to satisfy the clinical criteria to consider cannabinoids as a part of the treatment. One of the main caveats of cancer research is that we do not face just one type of cancer, but as many cancers as types of cells exist in the body. The underlying mechanisms of cancer development can be different for each type of cancer cell, and therefore specific treatments should be applied to treat them. We created a different entry for each of the most known cancer types in order to collect the scientific evidence indicating therapeutic potential of cannabinoids.

When we summarize all these scientific studies and try to come up with a general rule to use cannabinoids to treat cancer, we have to be aware of the limitations of cancer research.

Treatment of cancer symptoms and chemotherapy related side effects

Scientific studies and general patient experiences show that THC and CBD can help to treat cancer symptoms and chemotherapy side effects as pain or nausea (Maida & Daeninck, 2016; Turgeman & Bar-Sela, 2017). The route of administration for these cannabinoids can be smoked, vaporized, oral or topical. The main limitation for this type of treatment is the lack of research about the interactions between cannabinoids and chemotherapy drugs.

Treatment of cancer disease

Regarding the treatment of the disease, preclinical scientific evidence shows that several cannabinoids like THC and CBD can reduce tumors, cancer cell development and metastasis (Velasco, Sánchez, & Guzmán, 2016). However, one of the most important limitations is how cannabinoids can reach the cancer cells inside the body. The most common routes of administration and dosages used in humans could not reach the minimum concentration of cannabinoids around the cancer cells to produce an anti-cancer effect, therefore missing their therapeutic potential to treat the disease (Fowler, 2015).

Dosage of cannabinoids is not only important to reach the desired therapeutic effect, but also because different dosages could have opposite effects. In fact, few studies reported cancerogenic effects of THC and other cannabinoids in cancer cells when it was administered in low doses (Caffarel et al., 2010; Carracedo et al., 2006; Hall & MacPhee, 2002; Hart, Fischer, & Ullrich, 2004; Marselos & Karamanakos, 1999; McAllister et al., 2005; McKallip, Nagarkatti, & Nagarkatti, 2005; Sánchez, Ruiz-Llorente, Sánchez, & Díaz-Laviada, 2003; Sánchez, Sánchez, Ruiz-Llorente, & Díaz-Laviada, 2003; Zhu et al., 2000). Since we do not know the exact concentration of THC that targets cancer cells, we should be cautious when we decide to treat cancer with THC.

For more information, please, select a specific type of cancer in the list of diseases in this website.

Alternative Names

malignant tumor



Wiki Entry

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Prescription Advice

In general, THC and CBD appear to be effective in the treatment of pain, lack of appetite and general malaise that often accompany cancer or cancer therapy. In addition both THC and CBD show promise in preventing cancer cell division and promoting cancer cell apoptosis. However, for some cancer subtypes THC treatment actually proves counterproductive. Therefore, please also see cancer subtype-specific entries when choosing a treatment regime.

Given the nature of the disease, sublingual application may be beneficial.

Please follow generic prescription advice.

Please note that, while based on preclinical and/or clinical research, this prescription advice is solely intended as a guideline to help physicians determine the right prescription. We intend to continuously update our prescription advice based on patient and/or expert feedback. If you have information that this prescription advice is inaccurate, incomplete or outdated please contact us here.

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Literature Discussion

For an excellent publicly available review on therapeutic cannabinoids in cancer please see:

Chakravarti, B., Ravi, J., and Ganju, R.K. (2014). cannabinoids as therapeutic agents in cancer: current status and future implications. Oncotarget 5, 5852–5872.  


Caffarel, M. M., Andradas, C., Mira, E., Pérez-Gómez, E., Cerutti, C., Moreno-Bueno, G., … Sánchez, C. (2010). cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition. Molecular cancer, 9, 196.

Carracedo, A., Gironella, M., Lorente, M., Garcia, S., Guzmán, M., Velasco, G., & Iovanna, J. L. (2006). cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress-related genes. cancer Research, 66(13), 6748-6755.

Fowler, C. (2015). Delta9-tetrahydrocannabinol and cannabidiol as potential curative agents for cancer: A critical examination of the preclinical literature. Clinical Pharmacology & Therapeutics, 97(6), 587-596.

Hall, W., & MacPhee, D. (2002). Cannabis use and cancer. Addiction (Abingdon, England), 97(3), 243-247.

Hart, S., Fischer, O. M., & Ullrich, A. (2004). cannabinoids induce cancer cell proliferation via tumor necrosis factor alpha-converting enzyme (TACE/ADAM17)-mediated transactivation of the epidermal growth factor receptor. cancer Research, 64(6), 1943-1950.

Maida, V., & Daeninck, P. J. (2016). A user’s guide to cannabinoid therapies in oncology. Current Oncology, 23(6), 398-406.

Marselos, M., & Karamanakos, P. (1999). Mutagenicity, developmental toxicity and carcinogenicity of cannabis. Addiction Biology, 4(1), 5-12.

McAllister, S. D., Chan, C., Taft, R. J., Luu, T., Abood, M. E., Moore, D. H., … Yount, G. (2005). cannabinoids selectively inhibit proliferation and induce death of cultured human glioblastoma multiforme cells. Journal of Neuro-Oncology, 74(1), 31-40.

McKallip, R. J., Nagarkatti, M., & Nagarkatti, P. S. (2005). Δ-9-Tetrahydrocannabinol Enhances breast cancer Growth and Metastasis by Suppression of the Antitumor Immune Response. The Journal of Immunology, 174(6), 3281-3289.

Sánchez, M. G., Ruiz-Llorente, L., Sánchez, A. M., & Díaz-Laviada, I. (2003). Activation of phosphoinositide 3-kinase/PKB pathway by CB(1) and CB(2) cannabinoid receptors expressed in prostate PC-3 cells. Involvement in Raf-1 stimulation and NGF induction. Cellular Signalling, 15(9), 851-859.

Sánchez, M. G., Sánchez, A. M., Ruiz-Llorente, L., & Díaz-Laviada, I. (2003). Enhancement of androgen receptor expression induced by (R)-methAnandamide in prostate LNCaP cells. FEBS Letters, 555(3), 561-566.

Turgeman, I., & Bar-Sela, G. (2017). Cannabis Use in Palliative Oncology: A Review of the Evidence for Popular Indications. The Israel Medical Association Journal: IMAJ, 19(2), 85-88.

Velasco, G., Sánchez, C., & Guzmán, M. (2016). Anticancer mechanisms of cannabinoids. Current Oncology, 23(Suppl 2), S23-S32.

Zhu, L. X., Sharma, S., Stolina, M., Gardner, B., Roth, M. D., Tashkin, D. P., & Dubinett, S. M. (2000). Δ-9-Tetrahydrocannabinol Inhibits Antitumor Immunity by a CB2 Receptor-Mediated, Cytokine-Dependent Pathway. The Journal of Immunology, 165(1), 373-380.

Clinical Trials

Already, 80 clinical trials have shown the potential of cannabinoids in the treatment of cancer and many more are underway. The therapeutic potential of cannabinoids in specific sub-types of cancer are discussed below.