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But effective anti-cancer agents must be able to selectively kill cancer cells in the human body while sparing healthy ones. The reality is that cannabis simply cannot do this. Arsenic, plutonium and cyanide are also natural, yet it would be a poor strategy to binge on these substances.
The active compounds of many drugs are themselves discovered in plants, synthesised to control the dose and maximise efficacy. We already have THC-derived medicines, but these do not cure cancer, and neither does cannabis.
This is abject nonsense. Such a conspiracy would be massive and would rapidly collapse. The idea that researchers would be callous enough to suppress a cancer cure, and the rewards that would go with it, is ludicrous. The reality is that cancer is a complex family of disease, and it is unlikely that there will ever be a single cure.
Three reasons why scientific advice on drugs is ignored. An ingredient in cannabis may be useful for treating psychosis — new study. Should we be worried about indoor air pollution? Offences against the person? The poetics of retreat: Meditation and space at the shrine in Mahan — York, York.
Available editions United Kingdom. More on evidence-based articles about cannabis: Three reasons why scientific advice on drugs is ignored An ingredient in cannabis may be useful for treating psychosis — new study. Cancer Cannabis Medical marijuana Is it true?
Your donation helps deliver fact-based journalism. Role of cannabis in medicine does not strengthen argument for legalisation. In view of the fair safety profile of.
If this could be established, then one can. Nat Rev Cancer ;3: Cannabinoid receptor-mediated apoptosis induced by. Cannabinoid receptor agonist-induced apoptosis of. J Biol Chem ; J Pharmacol Exp Ther ; Cannabinoids induce apoptosis of pancreatic tumor. D 9 -T etrahydro-. Mol Life Sci ; Proc Am Assoc Cancer Res. Anti-proliferative and apoptotic effects.
Enh ancement of androg en receptor expres-. FEB S Lett ; Exp Cell Res ; Cannabinoid receptor ligand s mediate growth. Pre- clinical studies have shown that certain synthetic cannabi- noids also have antiangiogenic and antitumor effects.
Cannabinoid extracts may have anticancer properties, which can improve cancer treatment outcomes. The aim of this review is to determine the potentially utility of cannabinoids in the treatment of pancreatic cancer. A literature review focused on the biological effects of cannabinoids in cancer treatment, with a focus on pancreatic cancer, was conducted.
In vitro and in vivo studies that investigated the effects of cannabinoids in pancreatic cancer were identified and potential mechanisms of action were assessed. Cannabinol receptors have been identified in pancreatic cancer with several studies showing in vitro antiproliferative and proapoptotic effects. There effects are predominately mediated through, but not limited to cannabinoid receptor-1, cannabinoid receptor-2, and G-protein-coupled receptor 55 pathways.
There are, however, no clinical studies to date showing treatment benefits in patients with pancreatic cancer. Cannabinoids may be an effective adjunct for the treatment of pancreatic cancer. Data on the anticancer effectiveness of various cannabinoid formulations, treatment dosing, precise mode of action, and clinical studies are lacking. Cannabinoids have been revealed to have anti-tumor- ogenic activity for inhibiting tumor cell proliferation and promoting apoptosis  .
Thence, cannabinoids has been forced as a potential chemotherapeutic agent for the therapy of cancer. The function of cannabinoids is carried out through cannabinoid receptor 1 CB1 and CB2, G pro- tein-coupled receptors. CB1 is primarily expressed in the brain, while CB2 is exclusively expressed in immune cells [10, 11].
CB1 and CB2 have been found to express in some tumor cells, including melanoma . Objective To investigate the effect of MDA on progression of melanoma, and explore the relevant mechanism. Methods The melanoma cell lines, M14 and UACC, were treated with different concentrations of MDA, then CCK8, clone formation assay, Transwell and flow cytometry assays were performed to examine cell proliferation, migration, invasion and apoptosis, respectively.
The expression of apoptosis-related proteins Bcl-2, Bax and caspase 3 P17 , EMT and signaling pathway-related proteins were also detected by Western blot. Results MDA inhibited melanoma cells in a dose-dependent manner. Moreover, MDA was observed to up-regulate the expression of E-cad and down-regulate the expression of N-cad, Vimentin and Slug in melanoma cells in vitro. The biological role of the ECS in cancer pathophysiology is not completely clear  but most studies suggest that CB receptors and their endogenous ligands are upregulated in tumor tissue [28,29,31,  41,48] and that the overexpres- sion of ECS components i.
However, a tumor-suppressive role of ECS was also indicated by some studies, e. Moreover, experimental studies showed that the activation of CB receptors by cannabinoids is antitumor- igenic in most cases, i.
The effects of CB receptor over expression in selected human tumor cell lines are described in more detail in Table 1. Cannabinoids in cancer treatment: Therapeutic potential and legislation. The plant Cannabis sativa L. The endocannabinoid system ECS consists of receptors, endogenous ligands endocannabinoids and metabolizing enzymes, and plays an important role in different physiological and pathological processes.
In cancer patients, cannabinoids have primarily been used as a part of palliative care to alleviate pain, relieve nausea and stimulate appetite. In addition, numerous cell culture and animal studies showed antitumor effects of cannabinoids in various cancer types. Here we reviewed the literature on anticancer effects of plant-derived and synthetic cannabinoids, to better understand their mechanisms of action and role in cancer treatment.
We also reviewed the current legislative updates on the use of cannabinoids for medical and therapeutic purposes, primarily in the EU countries. Understanding how cannabinoids are able to regulate essential cellular processes involved in tumorigenesis, such as progression through the cell cycle, cell proliferation and cell death, as well as the interactions between cannabinoids and the immune system, are crucial for improving existing and developing new therapeutic approaches for cancer patients.
The national legislation of the EU Member States defines the legal boundaries of permissible use of cannabinoids for medical and therapeutic purposes, however, these legislative guidelines may not be aligned with the current scientific knowledge. Dec J Canc Res Therapeut.
Cannabinoid is a family of complex chemicals molecules. CB1 and CB2 have been synthesized from mammalian tissues, the main difference between them being their tissue expression . Reporting of three cases. Among different CBRs, CB2R is almost exclusively expressed in peripheral cells and tissues, derived from the immune system , and is unrelated to cannabinoid psychoactivity.
In particular, CB1R and CB2R levels are exclusively upregulated in different cancer cells without necessarily being expressed in the tissue type of origin   .
Several studies demonstrated that cannabinoids reduce tumor growth, inhibit angiogenesis, and decrease cancer cell migration. As these molecules are well tolerated, it would be interesting to investigate the potential benefit of newly synthesized compounds, binding cannabinoid receptors CBRs.
In this study, we describe the synthesis and biological effect of 2-oxo-1,8-naphthyridinecarboxamide derivative LV50, a new compound with high CB2 receptor CB2R affinity. We demonstrated that it decreases viability of Jurkat leukemia cells, evaluated by Trypan Blue and 3- 4,5-dimethylthiazolyl -2,5-diphenyltetrazolium bromide MTT , but mainly induces a proapoptotic effect. We observed an increase of a hypodiploid peak by propidium iodide staining and changes in nuclear morphology by Hoechst In addition, in order to exclude that LV50 non-specifically triggers death of all normal leukocytes, we tested the new compound on normal peripheral blood lymphocytes, excluding the idea of general cytotoxicity.
To characterize the involvement of CB2R in the anti-proliferative and proapoptotic effect of LV50, cells were pretreated with a specific CB2R antagonist and the obtained data showed reverse results. Thus, we suggest a link between inhibition of cell survival and proapoptotic activity of the new compound that elicits this effect as selective CB2R agonist.
Several studies support a role for Cannabis extracts and cannabinoids in growth inhibition of tumor cells or tumor cell death. Further investigation is required to find whether these effects of C.
Effects of standardized Cannabis sativa extract and ionizing radiation in melanoma cells in vitro. Jan J Canc Res Therapeut. Cells were also treated with 6. The inhibition of melanoma cell viability was paralleled by an increase in necrosis but not apoptosis when melanoma cells were treated with the extract alone.
Radiation alone did not have any antiproliferative effects, and radiation also did not synergize antiproliferative effects of the extract when the extract and radiation were combined. Our data suggest that C. The results of this study also indicate that B16F10 mouse melanoma cells are radioresistant. Taken together, these findings may lead to the identification of new therapeutic strategy for the management of melanoma.
Feb Future Oncol. Modulation of gastric acid secretion by cannabinoids in rats: The current study aimed to evaluate the role of cannabinoid receptors in the regulation of gastric acid secretion and oxidative stress in gastric mucosa. Current natural therapies in the treatment against glioblastoma. Glioblastoma GBM is the most common and aggressive brain tumor, which causes the highest number of deaths worldwide.
It is a highly vascularized tumor, infiltrative, and its tumorigenic capacity is exacerbated. All these hallmarks are therapeutic targets in GBM treatment, including surgical removal followed by radiotherapy and chemotherapy. Current therapies have not been sufficient for the effective patient's management, so the classic therapies have had to expand and incorporate new alternative treatments, including natural compounds.
The most important aspects of natural products and their derivatives were described in relation to its antitumoral effects. Natural compounds emerge as promising therapies to attack the progress of GBM. Cannabinoids, the active components of Cannabis sativa L. Cannabi- noids exert palliative effects in cancer patients. For example, they inhibit chemotherapy-induced nausea and vomiting, stimulate appetite and inhibit pain. In addition, cannabinoids inhibit tumor growth in laboratory animals.
They do so by modulating key cell signaling pathways, thereby in- ducing antitumoral actions such as the apoptotic death of tumor cells as well as the inhibition of tumor angiogenesis. Of interest, cannabinoids seem to be selective antitumoral compounds as they can kill tumor cells without significantly affecting the viability of their non-transformed counter- parts. The fair safety profile of THC, together with its possible growth-inhibiting action on tumor cells, may set the ba- sis for future trials aimed at evaluating the potential antitumoral activity of cannabinoids.
Nat Rev Cancer 3: Cannabinoids - the active components of Cannabis sativa and their derivatives - exert palliative effects in cancer patients by preventing nausea, vomiting and pain and by stimulating appetite.
In addition, these compounds have been shown to inhibit the growth of tumour cells in culture and animal models by modulating key cell-signalling pathways. Cannabinoids are usually well tolerated, and do not produce the generalized toxic effects of conventional chemotherapies. So, could cannabinoids be used to develop new anticancer therapies?
Delta 9 -Tetrahydrocannabinol induces apoptosis in human prostate PC-3 cells via a receptor-independent mechanism. The effect of delta9-tetrahydrocannabinol THC , the major psycho-active component of marijuana, in human prostate cancer cells PC-3 was investigated.
THC caused apoptosis in a dose-dependent manner. Morphological and biochemical changes induced by THC in prostate PC-3 cells shared the characteristics of an apoptotic phenomenon.
First, loss of plasma membrane asymmetry determined by fluorescent anexin V binding. Third, presence of typical 'ladder-patterned' DNA fragmentation. Central cannabinoid receptor expression was observed in PC-3 cells by immunofluorescence studies. However, several results indicated that the apoptotic effect was cannabinoid receptor-independent, such as lack of an effect of the potent cannabinoid agonist WIN 55,, inability of cannabinoid antagonist AM to prevent cellular death caused by THC and absence of an effect of pertussis toxin pre-treatment.
Anti-proliferative and apoptotic effects of anandamide in human prostatic cancer cell lines: Implication of epidermal growth factor receptor down-regulation and ceramide production.
Anandamide ANA is an endogenous lipid which acts as a cannabinoid receptor ligand and with potent anticarcinogenic activity in several cancer cell types.
The anti-proliferative and cytotoxic effects of ANA were also evaluated on these human prostatic cancer cell lines by growth tests, flow cytometric analyses, trypan blue dye exclusion assays combined with the Papanicolaou cytological staining method. The potent anti-proliferative and cytotoxic effects of ANA on metastatic prostatic cancer cells might provide basis for the design of new therapeutic agents for effective treatment of recurrent and invasive prostatic cancers.
Cannabinoids were shown to induce apoptosis of glioma cells in vitro and tumor regression in vivo, but mechanisms of their antiproliferative action remain elusive. In the present studies, C6 cells were exposed to a synthetic cannabinoid, WIN 55,, which produced down-regulation of the Akt and Erk signalling pathways prior to appearance of any sign of apoptosis.
We hypothesized that cannabinoid-induced cell death may be mediated by a Bcl-2 family member--Bad, whose function is hampered by these kinases due to control of its phosphorylation state. Using Western blot analysis, we found that levels of phosphorylated Bad, but not total Bad protein, decreased under exposure to WIN 55, WIN 55, treatment further resulted in mitochondrial depolarization and activation of caspase cascade.
Thus, we suggest that the increase of proapoptotic Bad activity is an important link between the inhibition of survival pathways and an onset of execution phase of cannabinoid-induced glioma cell death. Endocannabinoids have been implicated in cancer.
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research articles and other educational resources about cancer and CBD The Influence of Biomechanical Properties and Cannabinoids on Tumor Invasion . Can CBD OIl derived from Hemp or Cannabis be used as a Cancer Treatment? Find out in this comprehensive article. Including where to buy. Whole or crude marijuana (including marijuana oil or hemp oil) is not . for more scientific research on cannabinoids for cancer patients, and.