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Cannabis curesCancerPosted by Dr Sircushttp://drsircus.com/medicine/cannabis-cures-cancerThere should be no more confusion about whether or not marijuana is effective for cancer patients. Medical marijuana is chemotherapy, natural style, for all cancer patients. The two forms of hemp oil, one with THC and CBD and the other CBD alone (which is pretty much legal everywhere) provide the body with chemo therapeutics without the danger and staggering side effects. There are many chapters in this book about cancer patients using marijuana but in this one we present a quick overview of the science that backs up the assertion that every cancer patient and every oncologist should put medical marijuana on their treatment maps.What you will see in this chapter is reference to many scientific studies that are all viewable on governmental sites. The United States government is pathetic in its dishonesty about medical marijuana both believing in it and holding patents for its medical use and claiming at the same time that it has no medical use. The federal government and still many states would rather throw innocent people in jail for using medical marijuana than be honest about how much it can help people recover from cancer and other diseases.Below are summaries to just some of the scientific research out there that sustains the belief that medical marijuana will help people cure their cancer.One of the most exciting areas of current research in the cannabinoid field is the study of the potential application of these compounds as antitumor drugs. CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.[1],[2] The CBD concentrations effective at inhibiting Id-1 expression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. Of the five cannabinoids tested: cannabidiol, cannabigerol, cannnabichromene; cannabidiol-acid and THC-acid, it was found that cannabidiol is the most potent inhibitor of cancer cell growth. Taken together, these data might set the bases for a cannabinoid therapy for the management of breast cancer.[3]http://cannabissativa.com/wp-content/uploads/1/2012/03/marijuana_oil_cures_cancer.jpgResults show that Δ9-tetrahydrocannabinol reduces tumor growth, tumor number, and the amount/severity of lung metastases in MMTV-neu mice.[4] Cannabinoids induce ICAM-1, thereby conferring TIMP-1 induction and subsequent decreased cancer cell invasiveness thus inhibits lung cancer invasion and metastasis.[5]Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide. Researchers have observed expression of CB1 (24%) and CB2 (55%) in NSCLC patients. They have also shown that the treatment of NSCLC cell lines (A549 and SW-1573) with CB1/CB2- and CB2-specific agonists Win55,212-2 and JWH-015, respectively, significantly attenuated random as well as growth factor-directed in vitro chemotaxis and chemoinvasion in these cells.[6]Researchers in lung cancers also reported that they observed significant reduction in focal adhesion complex, which plays an important role in cancer migration. Medical marijuana significantly inhibited in vivo tumor growth and lung metastasis (∼50%).[7]In research on pancreatic cancer it was found that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB2 receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress–related genes ATF-4 and TRB3. These findings may contribute to set the basis for a new therapeutic approach for the treatment of pancreatic cancer as reported by the National Cancer Institute.Prostate cancer cells possess increased expression of both cannabinoid 1 and 2 receptors, and stimulation of these results in decrease in cell viability, increased apoptosis, and decreased androgen receptor expression and prostate-specific antigen excretion.[8]In colorectal carcinoma cell lines, cannabidiol protected DNA from oxidative damage, increased endocannabinoid levels and reduced cell proliferation in a CB(1)-, TRPV1- and PPARγ-antagonists sensitive manner. It is concluded that cannabidiol exerts chemopreventive effect in vivo and reduces cell proliferation through multiple mechanisms.[9]Ovarian cancer represents one of the leading cause of cancer-related deaths for women and is the most common gynecologic malignancy. Results with medical marijuana support a new therapeutic approach for the treatment of ovarian cancer. It is also conceivable that with available cannabinoids as lead compounds, non-habit forming agents that have higher biological effects could be developed.[10]Examination of a number of human leukaemia and lymphoma cell lines demonstrate that CB2 cannabinoid receptors expressed on malignancies of the immune system may serve as potential targets for the induction of apoptosis. Also, because CB2 agonists lack psychotropic effects, they may serve as novel anticancer agents to selectively target and kill tumors of immune origin.[11] Plant-derived cannabinoids, including Delta9-tetrahydrocannabinol (THC), induce apoptosis in leukemic cells.[12]Cannabinoid-treated tumors showed an increased number of apoptotic cells. This was accompanied by impairment of tumor vascularization, as determined by altered blood vessel morphology and decreased expression of proangiogenic factors (VEGF, placental growth factor, and angiopoietin. Abrogation of EGF-R function was also observed in cannabinoid-treated tumors.[13] These results support a new therapeutic approach for the treatment of skin tumors.Hepatocellular carcinoma (HCC) is the third cause of cancer-related death worldwide. When these tumors are in advanced stages, few therapeutic options are available. In this study, the effects of cannabinoids–a novel family of potential anticancer agents–on the growth of HCC was investigated. It was found that Δ(9)-tetrahydrocannabinol (Δ(9)-THC, the main active component of Cannabis sativa) and JWH-015 (a cannabinoid receptor 2 (CB(2)) cannabinoid receptor-selective agonist) reduced the viability of the human HCC cell lines Cannabinoids were able to inhibit tumor growth and ascites in an orthotopic model of HCC xenograft.[14] These findings may contribute to the design of new therapeutic strategies for the management of HCC.Both cholangiocarcinoma cell lines and surgical specimens from cholangiocarcinoma patients expressed cannabinoid receptors. THC inhibited cell proliferation, migration and invasion, and induced cell apoptosis. THC also decreased actin polymerization and reduced tumor cell survival in anoikis assay. pMEK1/2 and pAkt demonstrated the lower extent than untreated cells. Consequently, THC is potentially used to fool cholangiocarcinoma cell growth and metastasis.[15]Smoking marijuana might decrease the smoker’s risk for bladder cancer, a new study shows. Retrospectively analyzing a large database of patients, researchers at Kaiser Permanente in California found that patients who reported cannabis use were 45% less likely to be diagnosed with bladder cancer than patients who did not smoke at all.THC is a potent inducer of apoptosis, even at 1 x IC(50) (inhibitory concentration 50%) concentrations and as early as 6 hours after exposure to the drug. These effects were seen in leukemic cell lines (CEM, HEL-92, and HL60) as well as in peripheral blood mononuclear cells.[16] Cannabinoids represent a novel class of drugs active in increasing the life span in mice carrying Lewis lung tumors and decreasing primary tumor size.[17]http://media-cache-ec0.pinimg.com/236x/49/26/64/49266473e0602a94e12041c2814c9499.jpgResearch has also found a cannabidiol-driven impaired invasion of human cervical cancer (HeLa, C33A) and human lung cancer cells (A549) that was reversed by antagonists to both CB(1) and CB(2) receptorrs as well as to transient receptor potential vanilloid 1 (TRPV1). The decrease of invasion by cannabidiol appeared concomitantly with up regulation of tissue inhibitor of matrix metalloproteinases-1 (TIMP the findings provide a novel mechanism underlying the anti-invasive action of cannabidiol and imply its use as a therapeutic option for the treatment of highly invasive cancers.[18]A new anticancer quinone (HU-331) was synthesized from cannabidiol. It shows significant high efficacy against human cancer cell lines in vitro and against in vivo tumor grafts in nude mice. Two non-psychotropic cannabinoids, cannabidiol (CBD) and cannabidiol-dimethylheptyl (CBD-DMH), induced apoptosis in a human acute myeloid leukemia (AML) HL-60 cell line.[19]Other studies show a synthetic and potent cannabinoid receptor agonist, investigated in hepatoma HepG2 cells and a possible signal transduction pathway that is proposed, indicates a potential positive role in liver cancer.[20] Cannabinoids have been found to counteract intestinal inflammation and colon cancer.[21]The control of the cellular proliferation has become a focus of major attention as opening new therapeutic possibilities for the use of cannabinoids as potential antitumor agents.[22] Cannabinoid treatment inhibits angiogenesis of gliomas in vivo.[23] Remarkably, cannabinoids kill glioma cells selectively and can protect non-transformed glial cells from death. These and other findings reviewed here might set the basis for a potential use of cannabinoids in the management of gliomas. Other confirming studies may provide the basis for a new therapeutic approach for the treatment of malignant gliomas.[24]In summaryCannabinoids are found to exert their anti-cancer effects in a number of ways and in a variety of tissues.Triggering cell death, through a mechanism called apoptosisStopping cells from dividingPreventing new blood vessels from growing into tumoursReducing the chances of cancer cells spreading through the body, by stopping cells from moving or invading neighbouring tissueSpeeding up the cell’s internal ‘waste disposal machine’ – a process known as autophagy – which can lead to cell deathAll these effects are thought to be caused by cannabinoids locking onto the CB1 and CB2 cannabinoid receptors. Almost daily we are seeing new or confirming evidence that Cannibinoids can be used to great benefit in cancer treatment of many types.Buy the new Medical Marijuana 2nd Edition eBook![1] Crosstalk between chemokine receptor CXCR4 and cannabinoid receptor CB2 in modulating breast cancer growth and invasion. Nasser MW; et al; PLoS One. 2011;6(9):e23901. doi: 10.1371/journal.pone.0023901. Epub 2011 Sep 7; http://www.ncbi.nlm.nih.gov/pubmed/21915267 .[2] Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells; McAllister SDet al; Mol Cancer Ther. 2007 Nov;6(11):2921-7; http://www.ncbi.nlm.nih.gov/pubmed/18025276.[3] Delta9-tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation; Caffarel MM et al; Cancer Res; 2006 Jul 1;66(13):6615-21; http://www.ncbi.nlm.nih.gov/pubmed/16818634[4] Cannabinoids: a new hope for breast cancer therapy?Caffarel MM et al; Cancer Treat Rev.: 2012 Nov; 38(7):911-8. doi: 10.1016/j.ctrv.2012.06.005. Epub 2012 Jul 7; http://www.ncbi.nlm.nih.gov/pubmed/22776349[5] Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1.Ramer R et al; FASEB J.; 2012 Apr;26(4):1535-48. doi: 10.1096/fj.11-198184. Epub 2011 Dec 23; http://www.ncbi.nlm.nih.gov/pubmed/22198381?dopt=Abstract[6] Cannabinoid receptors, CB1 and CB2, as novel targets for inhibition of non-small cell lung cancer growth and metastasis; Preet A, et al; Cancer Prev Res (Phila). 2011 Jan;4(1):65-75. doi: 10.1158/1940-6207.CAPR-10-0181. Epub 2010 Nov 19; http://www.ncbi.nlm.nih.gov/pubmed/21097714?dopt=Abstract[7] Δ9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo; A Preetet al; Oncogene; (2008) 27, 339–346; doi:10.1038/sj.onc.1210641; published online 9 July 2007; http://www.nature.com/onc/journal/v27/n3/abs/1210641a.html[8] The role of cannabinoids in prostate cancer: Basic science perspective and potential clinical applications;Juan A. Ramos and Fernando J. Bianco; Indian J Urol. 2012 Jan-Mar; 28(1): 9–14;.doi:10.4103/0970-1591.94942; http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3339795/?report=classic[9] Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer.Aviello G et al; ;J Mol Med (Berl);2012 Aug;90(:925-34. doi: 10.1007/s00109-011-0856-x. Epub 2012; Jan 10.; http://www.ncbi.nlm.nih.gov/pubmed/22231745[10] Cannabinoid receptors as a target for therapy of ovarian cancerFarrukh Afaq; et al;, Proc Amer Assoc Cancer Res, Volume 47, 2006; http://www.aacrmeetingabstracts.org/cgi/content/abstract/2006/1/1084[11] Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease.McKallip RJ et al; Blood. 2002 Jul 15;100(2):627-34.; http://www.ncbi.nlm.nih.gov/pubmed/12091357[12] Delta9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemia T cells is regulated by translocation of Bad to mitochondria.Jia W et al; Mol Cancer Res.; 2006 Aug;4(:549-62; http://www.ncbi.nlm.nih.gov/pubmed/16908594 .[13] Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors.Casanova ML et al: J Clin Invest. 2003 Jan;111(1):43-50; http://www.ncbi.nlm.nih.gov/pubmed/12511587[14] Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy. Vara D et al; Cell Death Differ; 2011 Jul;18(7):1099-111. doi: 10.1038/cdd.2011.32. Epub 2011 Apr 8.; http://www.ncbi.nlm.nih.gov/pubmed/21475304[15] The dual effects of delta(9)-tetrahydrocannabinol on cholangiocarcinoma cells: anti-invasion activity at low concentration and apoptosis induction at high concentration. Leelawat Set al; Cancer Invest. 2010 May;28(4):357-63. doi: 10.3109/07357900903405934; http://www.ncbi.nlm.nih.gov/pubmed/19916793.[16] Cannabis-induced cytotoxicity in leukemic cell lines: the role of the cannabinoid receptors and the MAPK pathway;Powles T et al; Blood;.2005 Feb 1;105(3):1214-21; Epub 2004 Sep 28.; http://www.ncbi.nlm.nih.gov/pubmed/15454482[17] In vivo effects of cannabinoids on macromolecular biosynthesis in Lewis lung carcinomas; Friedman MA; Cancer Biochem Biophys. 1977;2(2):51-4.; http://www.ncbi.nlm.nih.gov/pubmed/616322[18] Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1; Ramer Ret al; Biochem Pharmacol; 2010 Apr 1;79(7):955-66. doi: 10.1016/j.bcp.2009.11.007. Epub 2009 Nov 13; http://www.ncbi.nlm.nih.gov/pubmed/19914218[19] Gamma-irradiation enhances apoptosis induced by cannabidiol, a non-psychotropic cannabinoid, in cultured HL-60 myeloblastic leukemia cells. Gallily R et al; Leuk Lymphoma.: 2003 Oct;44(10):1767-73; http://www.ncbi.nlm.nih.gov/pubmed/14692532.[20] Apoptosis induced in HepG2 cells by the synthetic cannabinoid WIN: involvement of the transcription factor PPARgamma. Giuliano Met et al; Biochimie;. 2009 Apr;91(4):457-65. doi: 10.1016/j.biochi.2008.11.003. Epub 2008 Nov 27. http://www.ncbi.nlm.nih.gov/pubmed/19059457[21] Cannabinoids in intestinal inflammation and cancer. Izzo AA1, Camilleri M.; Pharmacol Res; 2009 Aug;60(2):117-25. doi: 10.1016/j.phrs.2009.03.008. Epub 2009 Mar 18; http://www.ncbi.nlm.nih.gov/pubmed/19442536[22] Involvement of cannabinoids in cellular proliferation;López-Rodríguez ML et al; ;Mini Rev Med Chem; 2005 Jan;5(1):97-106 http://www.ncbi.nlm.nih.gov/pubmed/15638794[23] Hypothesis: cannabinoid therapy for the treatment of gliomas? Velasco G et al; Neuropharmacology;.2004 Sep;47(3):315-23; http://www.ncbi.nlm.nih.gov/pubmed/15275820[24] Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation; Galve-Roperh; Nat Med.; 2000 Mar;6(3):313-9; http://www.ncbi.nlm.nih.gov/pubmed/10700234
Cannabinoid CBG shows a potential pathway for promoting cell-death of colon cancer cells as well as inhibiting tumor growth: "CBG should be considered translationally in colorectal cancer prevention and cure. "Medicine (ncbi.nlm.nih.gov)http://www.ncbi.nlm.nih.gov/pubmed/25269802Colon carcinogenesis is inhibited by the TRPM8 antagonist cannabigerol, a Cannabis-derived non-psychotropic cannabinoid.Borrelli F1, Pagano E2, Romano B2, Panzera S3, Maiello F4, Coppola D4, De Petrocellis L5, Buono L5, Orlando P6, Izzo AA7.Author informationAbstractCannabigerol (CBG) is a safe non-psychotropic Cannabis-derived cannabinoid which interacts with specific targets involved in carcinogenesis. Specifically, CBG potently blocks transient receptor potential (TRP) M8 (TRPM8), activates TRPA1, TRPV1 and TRPV2 channels, blocks 5-HT1A receptors and inhibits the reuptake of endocannabinoids. Here, we investigated whether CBG protects against colon tumorigenesis. Cell growth was evaluated in colorectal cancer cells using the MTT and NR assays; apoptosis was examined by histology and by assessing caspase 3/7 activity; ROS production by a fluorescent probe; cannabinoid (CB) receptors, TRP and CHOP mRNA expression were quantified by RT-PCR; shRNA-vector silencing of TRPM8 was performed by electroporation. The in vivo antineoplastic effect of CBG was assessed using mouse models of colon cancer. Colorectal cancer cells expressed TRPM8, CB1, CB2, 5HT1A receptors, TRPA1, TRPV1 and TRPV2 mRNA. CBG promoted apoptosis, stimulated ROS production, up-regulated CHOP mRNA and reduced cell growth in colorectal cancer cells. CBG effect on cell growth was independent from TRPA1, TRPV1 and TRPV2 channels activation, was further increased by a CB2 receptor antagonist, and mimicked by other TRPM8 channel blockers but not by a 5-HT1Aantagonist. Furthermore, the effect of CBG on cell growth and on CHOP mRNA expression was reduced in TRPM8 silenced cells. In vivo, CBG inhibited the growth of xenograft tumors as well as chemically-induced colon carcinogenesis. CBG hampers colon cancer progression in vivo and selectively inhibits the growth of colorectal cancer cells, an effect shared by other TRPM8 antagonists. CBG should be considered translationally in colorectal cancer prevention and cure.© The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.co
Drugs are for the weak-willed and stupid.Not surprising the left are such enthusiastic supporters.
