# Extra Sources For Medicinal Cannabis
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- This report shows that the reducing power in the environment influences oxidation of glutamate in a neuronal tissue. Glutamate is a neurotransmitter, and it is especially important as a metabolite because it is required for synthesis of glutathione, other amino acids, and proteins. Glutamate also is a key intermediate in glutamine-dependent anaplerosis, now considered to be a principal source of citric acid cycle intermediates in cancer cells. Our analyses also show that the reducing power in the environmental can influence glutamate oxidation in cancer cells
- Cannabidiol protected neurons to a greater degree than either of the dietary antioxidants, α-tocopherol or ascorbate. As in the Fenton reaction system, cannabidiol protected neurons with comparable efficacy to the potent antioxidant BHT. The similar antioxidant abilities of cannabidiol and BHT in this chemical system and their comparable protection in neuronal cultures implies that cannabidiol neuroprotection is caused by an antioxidant effect. The antioxidative properties of cannabinoids suggest a therapeutic use as neuroprotective agents, and the particular properties of cannabidiol make it a good candidate for such development. Although cannabidiol was similar in neuroprotective capacity to BHT, cannabidiol has no known tumor-promoting effects [unlike BHT (25, 26)]
- [5-8]Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis. [9-12] Two reviews summarize the molecular mechanisms of action of cannabinoids as antitumor agents. [13,14] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. For example, these compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats, while they protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor. [9]The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC
- Although CBD enhances the interaction between beclin1 and Vps34, it inhibits the association between beclin1 and Bcl-2. In addition, we showed that CBD reduces mitochondrial membrane potential, triggers the translocation of BID to the mitochondria, the release of cytochrome c to the cytosol, and, ultimately, the activation of the intrinsic apoptotic pathway in breast cancer cells. CBD increased the generation of reactive oxygen species (ROS), and ROS inhibition blocked the induction of apoptosis and autophagy. Our study revealed an intricate interplay between apoptosis and autophagy in CBD-treated breast cancer cells and highlighted the value of continued investigation into the potential use of CBD as an antineoplastic agent
- This study investigates the role of COX-2 and PPAR-γ in cannabidiol's proapoptotic and tumor-regressive action. In lung cancer cell lines (A549, H460) and primary cells from a patient with lung cancer, cannabidiol elicited decreased viability associated with apoptosis. Apoptotic cell death by cannabidiol was suppressed by NS-398 (COX-2 inhibitor), GW9662 (PPAR-γ antagonist), and siRNA targeting COX-2 and PPAR-γ. Cannabidiol-induced apoptosis was paralleled by upregulation of COX-2 and PPAR-γ mRNA and protein expression with a maximum induction of COX-2 mRNA after 8 hours and continuous increases of PPAR-γ mRNA when compared with vehicle. In response to cannabidiol, tumor cell lines exhibited increased levels of COX-2–dependent prostaglandins (PG) among which PGD2 and 15-deoxy-Δ12,14-PGJ2 (15d-PGJ2) caused a translocation of PPAR-γ to the nucleus and induced a PPAR-γ–dependent apoptotic cell death. Moreover, in A549-xenografted nude mice, cannabidiol caused upregulation of COX-2 and PPAR-γ in tumor tissue and tumor regression that was reversible by GW9662. Together, our data show a novel proapoptotic mechanism of cannabidiol involving initial upregulation of COX-2 and PPAR-γ and a subsequent nuclear translocation of PPAR-γ by COX-2–dependent PGs
- Antineoplastic: Acting to prevent, inhibit or halt the development of a neoplasm (a tumor). An agent with antineoplastic properties. For example, oxaliplatin (Eloxatin) is an antineoplastic used in the treatment of metastatic colon cancer. The term is applicable to dozens of other chemotherapy agents used to treat this an other forms of cancer
- Cannabinoids exhibit their action by a modulation of the signaling pathways crucial in the control of cell proliferation and survival. Many in vitro and in vivo experiments have shown that cannabinoids inhibit proliferation of cancer cells, stimulate autophagy and apoptosis, and have also a potential to inhibit angiogenesis and metastasis. In this review, we present an actual state of knowledge regarding molecular mechanisms of cannabinoids’ anticancer action, but we discuss also aspects that are still not fully understood such as the role of the endocannabinoid system in a carcinogenesis, the impact of cannabinoids on the immune system in the context of cancer development, or the cases of a stimulation of cancer cells’ proliferation by cannabinoids. The review includes also a summary of currently ongoing clinical trials evaluating the safety and efficacy of cannabinoids as anticancer agents
- Cannabinoids were used in two forms, pure (P) and as a botanical drug substance (BDS). Results demonstrated a duration- and dose-dependent reduction in cell viability with each cannabinoid and suggested that THC-BDS was more efficacious than THC-P, whereas, conversely, CBD-P was more efficacious than CBD-BDS. Median effect analysis revealed all combinations to be hyperadditive [T98G 48-hour combination index (CI) at FU 50 , 0.77–1.09]. Similarly, pretreating cells with THC-P and CBD- P together for 4 hours before irradiation increased their radiosensitivity when compared with pretreating with either of the cannabinoids individually. The increase in radiosensitivity was associated with an increase in markers of autophagy and apoptosis
- CBD BDS attenuates colon carcinogenesis and inhibits colorectal cancer cell proliferation via CB1 and CB2 receptor activation. The results may have some clinical relevance for the use of Cannabis-based medicines in cancer patients. CBD BDS and CBD reduced cell proliferation in tumoral, but not in healthy, cells. The effect of CBD BDS was counteracted by selective CB1 and CB2 receptor antagonists. Pure CBD reduced cell proliferation in a CB1-sensitive antagonist manner only. In binding assays, CBD BDS showed greater affinity than pure CBD for both CB1 and CB2 receptors, with pure CBD having very little affinity. In vivo, CBD BDS reduced AOM-induced preneoplastic lesions and polyps as well as tumour growth in the xenograft model of colon cancer
- The antiproliferative effect of CBD was partially prevented by the CB2 receptor antagonist N-[(1 S)-endo-1,3,3-trimethylbicyclo[2,2,1]heptan-2-yl]-5-(4-chloro-3-methylphenyl)-1-(4-methylbenzyl)-pyrazole-3-carboxamide (SR144528; SR2) and α-tocopherol. By contrast, the CB1 cannabinoid receptor antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1 H-pyrazole-3-carboximide hydrochloride (SR141716; SR1), capsazepine (vanilloid receptor antagonist), the inhibitors of ceramide generation, or pertussis toxin did not counteract CBD effects. We also show, for the first time, that the antiproliferative effect of CBD was correlated to induction of apoptosis, as determined by cytofluorimetric analysis and single-strand DNA staining, which was not reverted by cannabinoid antagonists. Finally, CBD, administered s.c. to nude mice at the dose of 0.5 mg/mouse, significantly inhibited the growth of subcutaneously implanted U87 human glioma cells. In conclusion, the nonpsychoactive CBD was able to produce a significant antitumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an antineoplastic agent
- To analyze the combined antitumoral action of TMZ and THC in gliomas, we first characterized the ability of the 2 individual agents to promote glioma cell death. In agreement with the results obtained by other groups (29, 30), we observed that TMZ treatment produced a dose-dependent reduction in cell viability that reached a value of 40% to 50% of viable cells even when high concentrations of this agent (up to 400 μmol/L) were used (Supplementary Fig. 2A). Likewise, THC reduced in a dose-dependent manner the viability of glioma cells (Supplementary Fig. 2B). We therefore selected submaximal doses of TMZ and THC to evaluate whether the combined administration of the 2 agents enhanced their ability to induce glioma cell death. In line with this possibility, combined treatment with low doses of THC and TMZ reduced in a synergic fashion the viability of several human glioma cell lines and of 2 primary cultures of glioma cells derived from human GBM biopsies (Fig. 1A and Supplementary Fig. 2B). Use of higher doses of THC or TMZ also enhanced glioma cell death, although at these concentrations, the synergistic action of the 2 agents was not evident (Supplementary Fig. 2C and Supplementary Table 1)
- Increasing lines of evidence support an antitumourigenic effect of cannabinoids, including the cannabidiol (CBD) which does not posses the psychotropic effects of D9-tetrahydrocannabinol (THC). These include anti-proliferative and pro-apoptotic effects and they are known to interfere with several mechanisms in the tumorgenesis. Yet, evidence from clinical trials among cancer patients is needed. The aim of the current study is to evaluate the impact of CBD as single treatment among cancer patients. Conditions Solid TumorIntervention / Treatment Drug: cannabidiol (CBD)Drug: cannabidiol (CBD)Other Study ID Numbers CBD- HMO-CTILStudy Start 2014-11Primary Completion (Estimated) 2015-07Study Completion (Estimated) 2015-07Enrollment (Estimated) 60Study Type InterventionalPhase Phase 2 Resource links provided by the National Library of Medicine Drug Information(https://dailymed
- TRPV2 mRNA was abundantly expressed in T24 cells. The expression level in UC cells was correlated with high-grade disease. The administration of CBD increased intracellular calcium concentrations in T24 cells. In addition, the viability of T24 cells progressively decreased with increasing concentrations of CBD, whereas RT4 cells were mostly unaffected. Cell death occurred via apoptosis caused by continuous influx of calcium through TRPV2
- A total of 73 patients were surveyed. The majority of participants were aware that MM was legal in the state, and most reported learning of this through the media. Over 70% of participants reported having considered using MM, and a third reported using marijuana products after their diagnosis. Most received recommendations from friends/family rather than a medical provider, and only half of the users had obtained a physician's recommendation. Users generally reported benefits
- The designation “brain tumors” is commonly applied to a wide variety of intracranial mass lesions that are distinct in their location, biology, treatment, and prognosis. Since many of these lesions do not arise from brain parenchyma, the more appropriate term would be “intracranial tumors.” The term “tumor” is used to include both neoplastic and non-neoplastic mass lesions, and should be considered in its broadest sense to simply indicate a space-occupying mass. This review describes an imaging-based approach for evaluating intracranial tumors. Conventional MRI is discussed in the setting of a regional classification system. This system provides a framework for analysis, and imaging clues can then be applied to narrow the differential possibilities. Emphasis is placed on advanced MRI techniques and their utility for deciphering common diagnostic problems
- The main psychoactive cannabinoid in Cannabis is delta-9-THC. Another active cannabinoid is cannabidiol (CBD). Cannabinoids may help treat the side effects of cancer and cancer treatment. If Cannabis is illegal, how do some patients with cancer in the United States use it?Although federal law prohibits the use of Cannabis, the map below shows the states and territories that have legalized Cannabis for medical use. Some other states have legalized only one ingredient in Cannabis, such as cannabidiol (CBD), and these states are not included in the map
- We found that these cells express the cannabinoid receptors CB(1) and CB(2), known targets for THC action, and that THC inhibited EGF-induced growth, chemotaxis and chemoinvasion. Moreover, signaling studies indicated that THC may act by inhibiting the EGF-induced phosphorylation of ERK1/2, JNK1/2 and AKT. THC also induced the phosphorylation of focal adhesion kinase at tyrosine 397. Additionally, in in vivo studies in severe combined immunodeficient mice, there was significant inhibition of the subcutaneous tumor growth and lung metastasis of A549 cells in THC-treated animals as compared to vehicle-treated controls. Tumor samples from THC-treated animals revealed antiproliferative and antiangiogenic effects of THC. Our study suggests that cannabinoids like THC should be explored as novel therapeutic molecules in controlling the growth and metastasis of certain lung cancers
- [5-8]Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis. [9-12] Two reviews summarize the molecular mechanisms of action of cannabinoids as antitumor agents. [13,14] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. For example, these compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats, while they protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor. [9]The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC
- This overview on glutamine and cancer discusses the importance of glutamine for tumor growth, summarizes the alterations in interorgan glutamine metabolism that develop in the tumor-bearing host, and reviews the potential benefits of glutamine nutrition in the patient with cancer. SUMMARY BACKGROUND DATA: Glutamine is the most abundant amino acid in the blood and tissues. It is essential for tumor growth and marked changes in organ glutamine metabolism are characteristic of the host with cancer. Because host glutamine depletion has adverse effects, it is important to study the regulation of glutamine metabolism in cancer and to evaluate the impact of glutamine nutrition in the tumor-bearing state
- Someday, everyone will know the name ‘Rick Simpson’. Why? Because, according to sources, the man rediscovered the cure for cancer. After being diagnosed with basal cell carcinoma skin cancer in 2003, Rick underwent conventional treatment and surgery. The Western method of ‘treating’ the issue, however, did little to benefit his condition. Getting desperate, Rick decided to do something drastic – at least in the eyes of the mainstream. Rick remembered that thirty years prior, the University of Virginia discovered that cannabinoid in cannabis THC could kill cancer in mice. He figured, “If it works for mice, why not for me?” Therefore, began applying cannabis oil to his skin cancer. He figured that if the oil didn’t help within four days, he would give up the practice. Amazingly, in just that short period of time, his cancer disappeared. That’s when Simpson knew he was onto something
- 7. Cannabidiol Absorption Cannabidiol (CBD) is a natural, non-psychoactive [49][50] constituent of Cannabis sativa, but possesses pharmacological activity, which is explored for therapeutic applications. CBD has been reported to be neuroprotective [51], analgesic [37][38][52], sedating [37][38][53][54], anti-emetic [54], anti-spasmodic [55], and anti-inflammatory [56]. In addition, it has been reported that CBD blocks anxiety produced by THC [57], and may be useful in the treatment of autoimmune diseases [53]
- Rick Simpson Oil, RSO, Recipie. Cannabis that kills cancer | 1 gallon of everclear, ~1-4 Oz. Cannabis, a rice cooker, these instructions, and a hot plate/oven
- Explore a detailed compilation of scientific and anecdotal sources on medicinal cannabis, focusing on its potential therapeutic benefits for cancer treatment. This page highlights research on cannabinoids like THC and CBD, their antitumor properties, including apoptosis induction and tumor growth inhibition, and their role in supporting cancer patients. Backed by peer-reviewed studies, government reports, and practical guides like Rick Simpsons cannabis oil recipe, this resource offers valuable insights into cannabis as a complementary therapy
- Cannabinoids are good for much more than providing appetite, pain management, and mental laxity. have shown an ability to cause tumor anti-genesis of cancerous tumors as well as apoptosis, or programmed cell death, of various cancer cells. At times, it is necessary to separate the 2 molecules entirely, however, THC and CBD go hand in hand for the most part. Imagine a world where CBD, Cannabidiol, could not be found naturally and could only be created synthetically in a lab. I'm sure that you would surmise that these articles would be no surprise; that clinical trials would have already come to a close; that this would be available over the counter or via easy pharmacy pick up. Even merino has been a pharmaceutical remedy far before the natural herb was allowed to be considered