More than 33 percent used cannabis-infused oil, about 24 percent inhaled or smoked the cannabis, and around 6 percent used vaporization.
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… A variety of doses ranging from 2.7–43.2 mg/day THC and 0–40 mg/day CBD were administered. Higher doses of THC were correlated with increased pain relief in some studies. One study found that significant pain relief was achieved in doses as low as 2.7–10.8 mg THC in combination with 2.5–10.0 mg CBD, but there was conflicting evidence on whether higher doses provide superior pain relief. Some reported side effects include drowsiness, hypotension, mental clouding, and nausea and vomiting. There is evidence suggesting that medical cannabis reduces chronic or neuropathic pain in advanced cancer patients. However, the results of many studies lacked statistical power, in some cases due to the limited number of study subjects. Therefore, there is a need for the conduct of further double-blind, placebo-controlled clinical trials with large sample sizes in order to establish the optimal dosage and efficacy of different cannabis-based therapies…
Patients were eligible to participate in the study if they had active cancer and chronic pain that was moderate to severe despite taking opioids…Results of the study showed that nabiximols have analgesic efficacy when used as an add-on therapy for cancer patients with pain not controlled by an opioid alone. In the low-dose nabiximols group, there was a 25 percent improvement in pain compared with baseline.”
Cannabinoids in the management of difficult to treat pain
” Insufficient management of cancer-associated chronic and neuropathic pain adversely affects patient quality of life. Patients who do not respond well to opioid analgesics, or have severe side effects from the use of traditional analgesics are in need of alternative therapeutic options. Anecdotal evidence suggests that medical cannabis has potential to effectively manage pain in this patient population.
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“Medical cannabis was found to safely and significantly reduce chronic pain in older patients with multiple sclerosis (MS) and a wide range of other conditions, researchers in Israel report…
The solution? Take an integrative approach to managing your multiple myeloma. Enhance the efficacy of chemotherapy and while you reduce the toxicity. I live an anti-MM lifestyle based on nutrition, supplementation, lifestyle, bone health and mind-body therapies.
“Cannabinoids may offer significant “side benefits” beyond analgesia. These include anti-emetic effects, well established with THC, but additionally demonstrated for CBD (Pertwee 2005), the ability of THC and CBD to produce apoptosis in malignant cells and inhibit cancer-induced angiogenesis (Kogan 2005; Ligresti et al 2006), as well as the neuroprotective antioxidant properties of the two substances (Hampson et al 1998), and improvements in symptomatic insomnia (Russo et al 2007)…”
The statistical significance was determined by analysis of variance (ANOVA) or Student’s t test. The statistical analysis of IC50 levels was performed using Prism 5.01 (Graph Pad). Data from untreated cells were omitted because no differences were observed between vehicle-treated and untreated cells.
Over the last twenty years the antitumor benefits afforded by cannabinoids have been proved in different human cancer cell lines and in vivo preclinical models . The main effects of cannabinoids in impairing tumor progression were related to their anti-proliferative, pro-cell death and anti-migratory activities, which were noted in solid and haematological cancers. In GBM both CBD and the THC-CBD combination, were found to reduce cell viability and induce apoptosis in vitro and in GBM xenografts [4, 27]. CBD induces apoptotic cell death in vitro in A549, H460 lung cancer cell lines and in primary cells from patients with lung cancer and causes tumor regression in A549-xenografted nude mice . In breast cancer, THC inhibits cell proliferation by blocking the cell cycle and inducing apoptotic cell death [29, 30], while CBD inhibits AKT and mTOR signaling inducing autophagic-cell death .
A, B. Cell cycle analysis of U266 and RPMI cell lines treated with THC (12.5 μM) alone or in combination with CBD (12.5 μM). Cell cycle was performed using the PI incorporation assay and FACS analysis, after 48 h post-treatments. Histograms are representative of one of three separate experiments. The values represent the percentage of cells in each phase and are expressed as mean ± SD. *p<0.05 vs vehicle treated cells; #p<0.05 vs THC treated cells.
In multiple myeloma, our previous findings demonstrated that CBD reduced cell proliferation and induced necrotic cell death . In the present study, our data on THC and mainly on the THC-CBD combination as stimulatory factors of autophagic-dependent cell death in MM cell lines, support previous data regarding the efficacy of cannabinoids as anti-tumoral drugs, in different human cancer models.
SUPPLEMENTARY MATERIALS FIGURES
A. U266 cells were treated with CBD 12.5 μM, THC 12.5 μM, CFZ 100 nM alone or in combination for 24 h. CXCR4 and CD147 mRNA levels were determined by qRT-PCR. GAPDH was used for normalization. Data are expressed as relative fold with respect to vehicle treated cells used as control. Data are expressed as mean ± SD. *p<0.01 vs vehicle; # p<0.01 vs THC, CBD, CFZ alone and CBD-THC; § p<0.05 vs CBD, THC. B. CXCR4 and CD147 expression was analyzed by fow cytometry on U266 cell line treated as described above. Representative dot plots illustrate the double fluorescence. Numbers represent the percentage of cells in each quadrant. Data are representative of 1 of 4 independent experiments. C-E. Cell migration was analysed by transwell migration assays. Data represent the percentage of migrated U266 cells and are expressed as mean ± SD. In C: *p<0.01 vs vehicle; # p<0.01 vs THC, CBD, CBD-THC. In D: *p<0.01 vs vehicle; # p<0.01 vs THC, CBD, THC-CBD, CFZ. In E: *p<0.01 vs vehicle; # p<0.01 vs THC, CBD, THC-CBD; § p<0.01 vs CFZ.
We evaluated a potential role of THC-CBD in regulating the β5i subunit. So, U266 and RPMI cell lines were treated with CBD and THC, after 24 h exposure to IFN-γ (100 U/ml). Using qRT-PCR, we showed that the THC-CBD combination strongly reduces the β5i increased expression level induced by IFN-γ, while low effects were observed with single CBD and THC treatments respect to IFN-γ alone (Figure (Figure6A). 6A ). At protein levels, the expression of the precursor and mature form of β5i was examined by western blot analysis. Results evidenced that the administration of IFN-γ increases both the precursor and the mature form of β5i in MM-treated compared with MM non-treated cells. Moreover, THC and CBD alone had low efficacy in reducing β5i, while the THC-CBD combination impaired the expression of both forms, in U266 and RPMI cell lines (Figure (Figure6B 6B ).
For cannabinoids, different experimental data suggested that the combined administration of cannabinoids with other anti-cancer drugs, could act synergistically, to reduce tumor growth and chemoresistance. In GBM, temozolomide and carmustine, exert anti-tumor activity and the combination with CBD or THC-CBD synergistically increases GBM cells death both in vitro and in vivo, overpowering resistance mechanisms and lowering the chemotherapeutic doses, thereby leading to few adverse events [4, 32]. In another study it was reported that the combination of THC with cytotoxic agents (cytarabine, doxorubicin, vincristine) increased apoptosis in leukemia cells  and CBD was shown to enhance the ability of triple negative breast cancer subtype cells to uptake doxorubicin and significantly enhance its anti-tumorigenic efficacy . In MM cells, the CBD and BTZ combination was found to be more effective compared with BTZ alone and to act synergistically in inducing cell death . Herein we investigated the effect of CBD and THC in combination with CFZ, showing a synergistic effect between the three drugs, supporting the fact that combining THC-CBD with established cytotoxic agents should result in a higher level of anticancer activity compared with that of cytotoxic agents acting alone.
After treatment with the appropriate drugs for a maximum of 72 h, 4 × 10 4 U266 and RPMI cells/ml, were incubated in a binding buffer containing 20 μg/ml PI for 10 min at room temperature. The cells were then analysed by flow cytometry using CellQuest software.
Pure CBD and THC were supplied from GW Pharmaceuticals (batch CBD/160810; batch THC/CG/1301). CBD and THC were dissolved in ethanol. AM630 and bafilomycin A1 (Tocris Bioscience, Bristol, UK) were dissolved in DMSO. z-VAD, CFZ and IFN-γ (Sigma Aldrich, Sant Luis, MO, USA) were dissolved in distilled water.