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cbd oil follicular lymphoma

Hodgkin lymphoma (HL) is one of the most curable malignancies. Despite its effectiveness, chemotherapy is often associated with adverse events (AEs) such as nausea, anorexia, and impairment of general well-being. Our objective was to assess the extent of medical cannabis use among HL patients and evaluate its efficacy in controlling chemotherapy-related AEs. Patterns of medical cannabis use and efficacy were evaluated using physician-completed application forms, medical files, and patient-completed questionnaires, for all consecutive adult HL patients treated at the Tel-Aviv Medical Center between June 2010 and November 2016. One-hundred and thirty-three patients met the inclusion criteria. The median age of the cohort was 37 years, 53% were male, 46% were diagnosed at an early stage, and 88% achieved a complete response to treatment. Fifty-one patients (38%) used medical cannabis. There were no significant differences in baseline characteristics between cannabis users and nonusers. Cannabis users reported improvement in pain, general well-being, appetite, and nausea in 94, 87, 82, and 79% of cases, respectively. Importantly, 81.5% reported a high overall efficacy of cannabis in relieving symptoms. AEs related to cannabis use itself were mild. Thus, medical cannabis use is prevalent in this HL cohort, and appears to be effective in ameliorating chemotherapy-related AEs.

Keywords: Cannabis; Chemotherapy-related adverse events; Hodgkin lymphoma.

Cbd oil follicular lymphoma

Thyroid cancer is the most common endocrine malignancy and Ligresti et al. [30] demonstrated that CBD exerted anti-proliferative effects on rat thyroid KiMol cells, transformed with the v-K-ras oncogene. This effect of CBD was associated with a cell cycle block at the G1/S phase transition, as well as the induction of apoptosis.

Later on, Lee et al. [55] demonstrated that CBD markedly induced apoptosis in both murine thymocytes and EL-4 thymoma cells, with CBD-mediated apoptosis occurring earlier in EL-4 cells than in thymocytes. The cellular events triggered by CBD were similar in both T cells, ROS generation playing a pivotal role. The presence of N-acetyl-L-cysteine (NAC), a precursor of glutathione, markedly attenuated the induction of apoptosis and restored the diminished levels of cellular thiols.

Colon cancer is a major cause of morbidity and mortality in Western countries. A recent paper from Izzo’s group [57] demonstrated the chemopreventive effect of CBD in a preclinical animal model of colon cancer based on azoxymethane (AOM) administration in mice. AOM treatment was associated with aberrant crypt foci (ACF), polyps and tumour formation, as well as with the upregulation of phospho-Akt, iNOS and COX-2 and the downregulation of caspase-3. CBD was effective in reducting ACF, polyps and tumours and counteracted AOM-induced phospho-Akt and caspase-3 changes. In vitro studies, supported the beneficial effect of CBD. Indeed, in colorectal carcinoma cell lines, CBD protected DNA from oxidative damage, increased endocannabinoid concentrations and reduced cell proliferation in a CB1-, TRPV1- and PPARγ-antagonist sensitive manner.

The endocannabinoid system (eCB) is a recently discovered signalling system comprising the cannabinoid CB1 and CB2 receptors, their intrinsic lipid ligands, endocannabinoids (eCBs), such as the N-arachidonoylethanolamide (anandamide, AEA) and the 2-arachidonoylglycerol (2-AG), and the associated enzymatic machinery (transporters, biosynthetic and degradative enzymes).

CBD and angiogenesis

Schematic representation of the signalling pathways associated with CBD effects on glioma

AEA and 2-AG do not share the same biosynthetic or metabolic pathways. Different pathways can produce AEA from the phospholipid precursor N-arachidonoyl-phosphatidylethanolamine, the most important being a direct conversion catalyzed by an N-acyl-phosphatidylethanolamine-selective phosphodiesterase. 2-AG is mainly synthesized through activation of phospholipase C and subsequent production of diacylglycerol, which is converted to 2-AG by diacylglycerol lipase. After its re-uptake, AEA is hydrolyzed by the enzyme fatty acid amide hydrolase (FAAH), producing arachidonic acid and ethanolamine, while 2-AG is primarily metabolized by monoacylglycerol lipase, leading to the formation of arachidonic acid and glycerol [9]. Apart from their binding to CB1 and CB2 receptors, eCBs may bind to other receptors. For example, AEA may intracellularly activate the potential vanilloid receptor type 1 (TRPV1) [10]. Moreover, other putative cannabinoid receptors are the ‘orphan’ G protein-coupled receptor, GPR55 [11], and the peroxisome proliferator-activated receptor, PPAR [12, 13]. However, CB1 and CB2 receptors are certainly the most known targets for AEA and 2-AG, which activate them with different affinity. AEA has the highest affinity in both cases, whereas 2-AG has the highest efficacy in both cases [14].

In 2006 Ligresti et al. [30] demonstrated for the first time that CBD potently and selectively inhibited the growth of different breast tumour cell lines (MCF7, MDA-MB-231), with an IC50 of about 6 µ m , and exhibited significantly lower potency in non-cancer cells. CBD and CBD-rich extracts (containing approximately 70% CBD together with lesser amounts of other cannabinoids) also inhibited the growth of xenografts, obtained by s.c. injection into athymic mice of human MDA-MB-231 cells, and reduced infiltration of lung metastases derived from intrapaw injection of breast carcinoma cells. Among the possible cellular and molecular mechanisms underlying these effects, CBD seemed to involve direct TRPV1 activation and/or CB2 indirect activation (via FAAH), as well as induction of oxidative stress. Later on, McAllister’s group [31] demonstrated that, besides proliferation, CBD also interfered with two other crucial steps of breast cancer cell progression, invasion and metastasization. Among the three different groups of cannabinoid compounds tested (phytocannabinoids with affinity for CB1 and CB2 receptors, phytocannabinoids with no appreciable affinity for CB1 and CB2 receptors and synthetic compounds with affinity for CB1 and CB2 receptors), CBD was shown to be one of the most effective inhibitors of human breast cancer cell proliferation, being equipotent to Δ 9 -THC and CP55940 in inhibiting, respectively, MDA-MB-231 and MDA-MB-436 cell growth, and being the most potent inhibitor of the MDA-MB-231 cell migration. Interestingly, CBD regulated the expression of key genes involved in the control of cell proliferation and invasion through the downregulation of Id-1 expression, an inhibitor of basic helix-loop-helix transcription factors, whose overexpression in breast cancer cells is responsible for proliferation, migration and invasion. Therefore, the ability of CBD to decrease significantly Id-1 expression in breast cancer cells was associated with its efficacy in reducing tumour aggressiveness.

CBD and colon cancer

CBD also possesses anti-tumoural properties in gliomas, tumours of glial origin characterized by a high morphological and genetic heterogeneity and considered one of the most devastating neoplasms, showing high proliferative rate, aggressive invasiveness and insensitivity to radio- and chemotherapy.

The anti-proliferative effect of CBD was cannabinoid and vanilloid receptors independent. The CB2 receptor antagonist SR144528 reverted the effect of CBD, but in a weak and transient manner [37]. More importantly, this paper demonstrated for the first time that the anti-tumour effect of CBD involved the induction of oxidative stress, through increased early production of ROS, depletion of intracellular glutathione and increased GSH-associated enzymatic activity. Accordingly, the CBD anti-proliferative effect was reversed by the anti-oxidant, tocopherol. Importantly, CBD did not induce ROS production in non-transformed primary glial cells [38].

Non-Hodgkin lymphoma can begin in B lymphocytes, T lymphocytes, or natural killer cells. Lymphocytes can also be found in the blood and also collect in the lymph nodes, spleen, and thymus. — National Cancer Institute

Non-Hodgkin lymphoma is a type of cancer that forms in the lymph system, which is part of the body’s immune system. The immune system protects the body from foreign substances, infection, and diseases. The lymph system is made up of the following lymphocytes: B lymphocytes, T lymphocytes, and Natural Killer Cells.

Below is a Library of Cannabis Research Study for Non-Hodgkin’s Lymphoma.

Cannabinoids as Anticancer Drugs

Over 1000 studies covering over 130 topics compiled for easy browsing.

Short-Term Medical Cannabis Treatment Regimens Produced Beneficial Effects among Palliative Cancer Patients