Medical cannabis (MC) is increasingly used for chronic pain, but it is unclear how it aids in pain management. Previous literature suggests that MC could holistically alter the pain experience instead of only targeting pain intensity. However, this hypothesis has not been previously systematically tested.
Cancer-related pain management in advanced stages presents a significant challenge that often requires a multidisciplinary approach. Although advancements in pharmacological and interventional therapies, a considerable number of patients still suffer from refractory pain, leading to unmet clinical needs. This study shares our experience with medical cannabis (MC) as a potential therapy for this specific population of patients with cancer-related refractory pain.
Phytocannabinoids and synthetic cannabinoids have been explored as the lead due to their anti-proliferative nature and can be anti-cancer agents. These were found to activate numerous pharmacological targets to generate new therapies in alleviating specic symptoms or delaying the disease of Cancer. However, the comprehensive anti-cancer activities of cannabinoid acids and non-cannabinoids are not fully explored. Herein we report simple extraction, faster bioassay-guided fractionation, and HPLC-assisted purication of bioactive secondary metabolite and their identication.
A minority of oncologists feel qualified to advise adults with can- cer on issues pertaining to medicinal cannabis. Adults with cancer frequently ac- cess medicinal cannabis information from non-medical sources such as cannabis dispensaries. We explored dispensary personnel’s views and experiences regard- ing oncologic cannabis and the counsel they extend individuals with cancer. Methods: Snowball sampling in this qualitative study facilitated recruitment across 13 states (N = 26). Semi-structured phone interviews ceased with thematic saturation. A multi-stage thematic analysis combined inductive and deductive codes.
Glioblastoma multiforme (GBM), also called grade IV astrocytoma, is an aggressive, malignant brain tumor with a low treatment success rate, particularly in patients with immune checkpoint-active tumors. These types of tumors are associated with a 5-year survival rate of <3%. Targeted treatments specifically designed for GBM are urgently needed. The aim of this study was to evaluate the effects of chemovar-specific cannabis extractions (CSCEs) in patients with GBM using liquid chromatography-mass spectrometry (LC-MS).
Breast cancer is the leading cancer among females worldwide. Disease outcome depends on the hormonal status of the cancer and whether or not it is metastatic, but there is a need for more efficacious therapeutic strategies where first line treatment fails. In this study, Fatty Acid Amide Hydrolase (FAAH) inhibition and endocannabinoids were examined as therapeutic alternatives. FAAH is an integral membrane enzyme that hydrolyzes endocannabinoids, rendering them inactive, and FAAH inhibition is predicted to increase cancer cell death. To test this, breast cancer cells were probed for FAAH expression using Western blot analysis, treated with FAAH inhibitors, exogenous endocannabinoids, and combinations of the two treatments, and assessed for viability.
The side effects of cancer therapy continue to cause significant health and cost burden to the patient, their friends and family, and governments. A major barrier in the way in which these side effects are managed is the highly siloed mentality that results in a fragmented approach to symptom control. Increasingly, it is appreciated that many symptoms are manifestations of common underlying pathobiology, with changes in the gastrointestinal environment a key driver for many symptom sequelae. Breakdown of the mucosal barrier (mucositis) is a common and early side effect of many anti-cancer agents, known to contribute (in part) to a range of highly burdensome symptoms such as diarrhoea, nausea, vomiting, infection, malnutrition, fatigue, depression, and insomnia. Here, we outline a rationale for how, based on its already documented effects on the gastrointestinal microenvironment, medicinal cannabis could be used to control mucositis and prevent the constellation of symptoms with which it is associated. We will provide a brief update on the current state of evidence on medicinal cannabis in cancer care and outline the potential benefits (and challenges) of using medicinal cannabis during active cancer therapy.
Chemotherapy-induced peripheral neuropathy (CIPN) is experienced by 37–84% of patients during and/or after end-of-treatment and often results in discontinuation of anti-neoplastic treatment and impairment of health-related quality of life. Cannabidiol (CBD) has shown preventive effects in CIPN animal models without compromising chemotherapy efficacy.
Cannabis roots have been used in folk medicine for millennia and as nutrient storage systems, contain compounds that may have medicinal value. Despite this, cannabis roots have generally received little attention compared to cannabis flowers, leaves and seeds and were for a long time considered just a waste product. In this paper, for the first time, the extracts of dried roots and in- florescences of Cannabis sativa L. cv Eletta Campana, were chemically investigated in order to compare their metabolite content. The obtained results highlighted a profile rich in fatty acids in the roots and cannabinoids in the inflorescences. Other components such as monoterpenes, sesquiterpenes, diterpenes and triterpenes were also detected. The extracts were also evaluated in terms of cytotoxic activity by using a panel of cancer cell lines derived from different histotypes including melanoma (A375, M14), colon (HCT116, HT29), breast (MDAMB231, MCF7) and non- small cell lung cancer (H1299, A549). Although both extracts significantly reduced the cancer cell viability, the inflorescence extract was more potent. Furthermore, the latter induced a comparable response in all tested cancer cell lines, while melanoma and non-small cell lung cancer were the most sensitive histotypes to the root extract treatment.
Δ9-Tetrahydrocannabinol (Δ9-THC) is a principal psychoactive extract of Cannabis sativa and has been traditionally used as palliative medicine for neuropathic pain. Cannabidiol (CBD), an extract of hemp species, has recently attracted increased attention as a cancer treatment, but Δ9-THC is also requiring explored pharmacological application. This study evaluated the pharmacological effects of Δ9-THC in two human colorectal cancer cell lines. We inves-tigated whether Δ9-THC treatment induces cell death in human colorectal cancer cells.
Prostate cancer is the second most frequent cancer diagnosed in men in the world today. Almost all prostate cancers are adenocarcinomas and develop from gland cells. We used the PC3 prostate cancer cell line, which is well studied and derived from a bone metastasis of a grade IV prostatic adenocarcinoma. Cannabidiol (CBD), a major non-psychoactive constituent of cannabis, is a cannabinoid with anti-tumor properties but its effects on prostate cancer cells are not studied in detail. Here, we found cannabidiol decreased prostate cancer cell (PC3) viability up to 37.25% and induced apoptotic cell death in a time and dose-dependent manner. We found that CBD activated the caspases 3/7 pathways and increased DNA fragmentation. Furthermore, we observed an increase of pro-apoptotic genes Bax, an increased level of reactive oxygen species, lower reduced glutathione level, and altered mitochondrial potential in response to CBD treatment leading to lower cellular ATP. Overall, our results suggest that CBD may be effective against prostate cancer cells.
In spite of the huge advancements in both diagnosis and interventions, hormone refractory prostate cancer (HRPC) remains a major hurdle in prostate cancer (PCa). Metabolic reprogramming plays a key role in PCa oncogenesis and resistance. However, the dynamics between metabolism and oncogenesis are not fully understood. Here, we demonstrate that two multi-target natural products, cannabidiol (CBD) and cannabigerol (CBG), suppress HRPC development in the TRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model by reprogramming metabolic and oncogenic signaling. Mechanistically, CBD increases glycolytic capacity and inhibits oxidative phosphorylation in enzalutamide-resistant HRPC cells. This action of CBD originates from its effect on metabolic plasticity via modulation of VDAC1 and hexokinase II (HKII) coupling on the outer mitochondrial membrane, which leads to strong shifts of mitochondrial functions and oncogenic signaling pathways. The effect of CBG on enzalutamide-resistant HRPC cells was less pronounced than CBD and only partially attributable to its action on mitochondria. However, when optimally combined, these two cannabinoids exhibited strong anti-tumor effects in TRAMP mice, even when these had become refractory to enzalutamide, thus pointing to their therapeutical potential against PCa.