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|Cannabis Cures Cancer|
There 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. Results show that ?9-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 PPAR?-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 ?(9)-tetrahydrocannabinol (?(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 retard 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. Research 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 summary Cannabinoids 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 apoptosis
Stopping cells from dividing Preventing new blood vessels from growing into tumours Reducing the chances of cancer cells spreading through the body, by stopping cells from moving or invading neighbouring tissue Speeding up the cell's internal 'waste disposal machine' - a process known as autophagy - which can lead to cell death All 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.
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/?term=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. 9-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(8):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 cancer Farrukh 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(8):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
Marijuana compound may stop deadly cancer metastasis
We've known about medical applications of cannabis (or marijuana) for years, but the research findings of two scientists studying it have the potential to change the deadliness of cancer forever. A cannabis compound known as cannabidiol can stop metastasis in many types of aggressive cancers, found the researchers from California Pacific Medical Center in San Francisco.
Cannabidiol (CBD) is a non-toxic, non-psychoactive chemical found in the cannabis plant, that had already been effective in relieving convulsion, inflammation, anxiety and nausea, and in treating schizophrenia and dystonia. For the 2007 study, Sean McAllister, who was specifically studying the effects of cannabidiol, collaborated with Pierre Desprez, who for the last 10 years has been studying the ID-1 gene in cancer that causes metastasis.
Metastasis is when a cancer spreads from the primary tumor area to other parts of the body, typically using the bloodstream or lymphatic system, and is one of the hallmarks of a tumor becoming malignant.
"What we found was that his Cannabidiol could essentially 'turn off' the ID-1," Desprez told The Huffington Post. "We likely would not have found this on our own," he added.
"That's why collaboration is so essential to scientific discovery."
Since publishing their study, the two went on to study the effect of CBD on other cancers.
"Now we've found that Cannabidiol works with many kinds of aggressive cancers brain, prostate any kind in which these high levels of ID-1 are present." said Desprez.
Since CBD has already been safely used by people for other ailments, the two hope that clinical trials can begin soon. However, treating cancer metastasis in this way requires more than just lighting up.
"We used injections in the animal testing and are also testing pills," he said. "But you could never get enough cannabidiol for it to be effective just from smoking."
The two are now working on synthesizing the cannabidiol in the lab, rather than using samples from the plant, which should not only make it more potent, but also hopefully clear any obstacles at getting the drug approved.
By Scott Sutherland | Geekquinox Thu, 20 Sep, 2012..
Cancer Hope By Paul Armentano
Cannabinoids As Cancer Hope
by Paul Armentano
Senior Policy Analyst
NORML | NORML Foundation
Cannabinoids possess anticancer activity [and may] possibly represent a new class of anti-cancer drugs that retard cancer growth, inhibit angiogenesis (the formation of new blood vessels) and the metastatic spreading of cancer cells." So concludes a comprehensive review published in the October 2005 issue of the scientific journal Mini-Reviews in Medicinal Chemistry.
Not familiar with the emerging body of research touting cannabis' ability to stave the spread of certain types of cancers? You're not alone.
For over 30 years, US politicians and bureaucrats have systematically turned a blind eye to scientific research indicating that marijuana may play a role in cancer prevention -- a finding that was first documented in 1974. That year, a research team at the Medical College of Virginia (acting at the behest of the federal government) discovered that cannabis inhibited malignant tumor cell growth in culture and in mice. According to the study's results, reported nationally in an Aug. 18, 1974, Washington Post newspaper feature, administration of marijuana's primary cannabinoid THC, "slowed the growth of lung cancers, breast cancers and a virus-induced leukemia in laboratory mice, and prolonged their lives by as much as 36 percent."
Despite these favorable preclinical findings, US government officials dismissed the study (which was eventually published in the Journal of the National Cancer Institute in 1975), and refused to fund any follow-up research until conducting a similar - though secret - clinical trial in the mid-1990s. That study, conducted by the US National Toxicology Program to the tune of $2 million concluded that mice and rats administered high doses of THC over long periods experienced greater protection against malignant tumors than untreated controls.
Rather than publicize their findings, government researchers once again shelved the results, which only came to light after a draft copy of its findings were leaked in 1997 to a medical journal, which in turn forwarded the story to the national media.
Nevertheless, in the decade since the completion of the National Toxicology trial, the U.S. government has yet to encourage or fund additional, follow up studies examining the cannabinoids' potential to protect against the spread cancerous tumors.
Fortunately, scientists overseas have generously picked up where US researchers so abruptly left off. In 1998, a research team at Madrid's Complutense University discovered that THC can selectively induce apoptosis (program cell death) in brain tumor cells without negatively impacting the surrounding healthy cells. Then in 2000, they reported in the journal Nature Medicine that injections of synthetic THC eradicated malignant gliomas (brain tumors) in one-third of treated rats, and prolonged life in another third by six weeks.
In 2003, researchers at the University of Milan in Naples, Italy, reported that non-psychoactive compounds in marijuana inhibited the growth of glioma cells in a dose dependent manner and selectively targeted and killed malignant cancer cells.
The following year, researchers reported in the journal of the American Association for Cancer Research that marijuana's constituents inhibited the spread of brain cancer in human tumor biopsies. In a related development, a research team from the University of South Florida further noted that THC can also selectively inhibit the activation and replication of gamma herpes viruses. The viruses, which can lie dormant for years within white blood cells before becoming active and spreading to other cells, are thought to increase one's chances of developing cancers such as Karposis Sarcoma, Burkitts lymphoma, and Hodgkins disease.
More recently, investigators published pre-clinical findings demonstrating that cannabinoids may play a role in inhibiting cell growth of colectoral cancer, skin carcinoma, breast cancer, and prostate cancer, among other conditions. When investigators compared the efficacy of natural cannabinoids to that of a synthetic agonist, THC proved far more beneficial selectively decreasing the proliferation of malignant cells and inducing apoptosis more rapidly than its synthetic alternative while simultaneously leaving healthy cells unscathed.
Nevertheless, US politicians have been little swayed by these results, and remain steadfastly opposed to the notion of sponsoring or even acknowledging this growing body clinical research, preferring instead to promote the unfounded notion that cannabis use causes cancer. Until this bias changes, expect the bulk of research investigating the use of cannabinoids as anticancer agents to remain overseas and, regrettably, overlooked in the public discourse.
Cannabinoids As Cancer Hope
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