​​​​​​cannabis data.org

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5101100:  The mechanism of action of CBD is multifold.1–3 Two cannabinoid receptors are known to exist in the human body: CB1 and CB2 receptors. The CB1 receptors are located mainly in the brain and modulate neurotransmitter release in a manner that prevents excessive neuronal activity (thus calming and decreasing anxiety), as well as reduces pain, reduces inflammation, regulates movement and posture control, and regulates sensory perception, memory, and cognitive function.a2 An endogenous ligand, anandamide, which occurs naturally in our bodies, binds to the CB1 receptors through the G-protein coupling system. CBD has an indirect effect on the CB1 receptors by stopping the enzymatic breakdown of anandamide, allowing it to stay in the system longer and provide medical benefits.4 CBD has a mild effect on the CB2 receptors, which are located in the periphery in lymphoid tissue. CBD helps to mediate the release of cytokines from the immune cells in a manner that helps to reduce inflammation and pain.2

​Other mechanisms of action of CBD include stimulation of vanilloid pain receptors (TRPV-1 receptor), which are known to mediate pain perception, inflammation, and body temperature.5 In addition, CBD may exert its anti-anxiety effect by activating adenosine receptors which play a significant role in cardiovascular function and cause a broad anti-inflammatory effect throughout the body.5 At high concentrations, CBD directly activates the 5-HT1A serotonin receptor, thereby conferring an antidepressant effect.6 Cannabidiol has been found to be an antagonist at the potentially new third cannabinoid receptor, GPR55, in the caudate nucleus and putamen, which if stimulated may contribute to osteoporosis.7

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2503660:  The anti-inflammatory contributions of THC are also extensive, including inhibition of PGE-2 synthesis (Burstein et al 1973), decreased platelet aggregation (Schaefer et al 1979), and stimulation of lipooxygenase (Fimiani et al 1999). THC has twenty times the anti-inflammatory potency of aspirin and twice that of hydrocortisone (Evans 1991), but in contrast to all nonsteroidal anti-inflammatory drugs (NSAIDs), demonstrates no cyclo-oxygenase (COX) inhibition at physiological concentrations (Stott et al 2005a)​.​

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828614:   The role of inflammation in evolution of certain types of cancer has been strongly suggested, linking the inflammatory response to 15–20% of all deaths from cancer worldwide [84]. The hallmarks of cancer-related inflammation include the presence of inflammatory cells in tumor tissue, and the regulation of tumor growth, metastasis and angiogenesis by inflammatory mediators (e.g., chemokines, cytokines and prostaglandins). The connection between inflammation and cancer is now generally accepted and nonsteroidal anti-inflammatory drugs have been shown to reduce varied cancer risk. Use of these drugs reduces colon cancer risk by 40–50% and is indicated to be preventative for lung, esophagus and stomach cancer [87]. Hence, inflammation can be considered as a therapeutic opportunity in certain types of cancer. Recent applications of cannabinoids have been extended as antitumor agents [1,88], which relies on their ability to inhibit tumor angiogenesis [89] or induce direct apoptosis or cell cycle arrest in neoplastic cells [89–92]. A focus on the antiproliferative effects of these compounds in various tumors, such as breast and prostate cancers, pheochromocytoma and malignant gliomas, has been proposed [1,92–94]. Our laboratory reported that, in vitro, THC and other cannabinoids could induce apoptosis in transformed murine and human T cells [95], including primary acute lymphoblastic human leukemia cells. Furthermore, the treatment of mice bearing a T-cell leukemia with THC could cure approximately 25% of the mice [95]. We further showed that treatment with THC caused interruption of the MAPK/ERK kinase/ERK signaling module that was required for apoptotic lethality [96,97]. The role of endocannabinoids as potential endogenous tumor growth inhibitors has been suggested in a study where it was observed that levels of both AEA and 2-AG were higher in precancerous polyps than in fully developed carcinomas in the colon [98]. Recent in vivo studies proposed that selective targeting of CB2 receptors resulted in colorectal tumor growth inhibition via apoptosis, which was mediated through the stimulation of ceramide [98]. In a xenograft model of thyroid cancer, substances that blocked endocannabinoid degradation also increased the levels of AEA and 2-AG in the tissue and reduced tumor growth [99]. Various attempts have been made to inactivate cannabinoid-degrading enzymes, thereby increasing the local concentration of endocannabinoids at the tumor cell surface. This leads to anti-tumor effects of CB receptor signaling in various cancer types, such as thyroid, brain and prostate cancer [99–103]. Although the majority of the effects of cannabinoids are CB receptor mediated, AEA has been shown to induce its effects on cancerous cells by interacting with TRPV1 receptor [104,105] or cholesterol-rich lipid rafts [106]. Furthermore, it has been reported that signaling pathways are differentially regulated by cannabinoids in normal cells versus cancer cells. In malignancies, such as thyroid cancer, lymphoma, melanoma, pancreas and breast cancer, the levels of cannabinoid receptors are often higher in the tumor compared with normal cells of the same origin, resulting in increased sensitivity to cannabinoids in the malignancies [89,107–110]. Moreover, many animal studies have reported antiproliferative and pro-apoptotic effects of cannabinoids on tumor cells but not on normal tissue [89,91]. Thus, the role of the cannabinoid system in cancer indicates that this system is involved in regulating many of the functions that are essential in cancer development.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2503660:  The endocannabinoid system is tonically active in control of pain, as demonstrated by the ability of SR141716A (rimonabant), a CB1 antagonist, to produce hyperalgesia upon administration to mice (Richardson et al 1997). As mentioned above, the ECS is active throughout the neuraxis, including integrative functions in the periacqueductal gray (Walker et al 1999a; Walker et al 1999b), and in the ventroposterolateral nucleus of the thalamus, in which cannabinoids proved to be 10-fold more potent than morphine in wide dynamic range neurons mediating pain (Martin et al 1996). The ECS also mediates central stress-induced analgesia (Hohmann et al 2005), and is active in nociceptive spinal areas (Hohmann et al 1995; Richardson et al 1998a) including mechanisms of wind-up (Strangman and Walker 1999) and N-methyl-D-aspartate (NMDA) receptors (Richardson et al 1998b). It was recently demonstrated that cannabinoid agonists suppress the maintenance of vincristine-induced allodynia through activation of CB1 and CB2receptors in the spinal cord (Rahn et al 2007). The ECS is also active peripherally (Richardson et al 1998c) where CB1 stimulation reduces pain, inflammation and hyperalgesia. These mechanisms were also proven to include mediation of contact dermatitis via CB1 and CB2 with benefits of THC noted systemically and locally on inflammation and itch (Karsak et al 2007). Recent experiments in mice have even suggested the paramount importance of peripheral over central CB1 receptors in nociception of pain (Agarwal et al 2007)

Cannabis -vs- Inflammation