What will save cannabis from its embrace with legality is raw consumable cannabis. The most die hard non user can get over consuming this stuff as a beverage or tablet. The benefits are now becoming well known and if it ends up as the go to for all cancer victims as it should then opposition will become ludicrous.
I do not expect cannabis to be a cure all but i expect to see superior outcomes across the board. That itself will be a huge blessing. Just dying comfortably is a positive outcome against the alternative. what matters is ending the present barbarous protocols that neither alleviate distress nor cure and often give a worse death in exchange for a speculative pause in the death march.
Cannabis promises to do much better. I think it is high time that we do an extensive clinical trial that confirms this across the whole spectrum of clinical cancer care. This will mean merely prescribing all new victims with a cannabis protocol along with the usual recommendations not necessarily enforced either because enough participants will provide us ample numbers and ample variation to observe and measure. Those that decline will provide the natural comparison if anyone is so stupid:-).
Cannabis Cures Cancer
Posted by on September 27, 2014
http://drsircus.com/medicine/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 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
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.
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
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(8):925-34. doi: 10.1007/s00109-011-0856-x. Epub 2012; Jan 10.; http://www.ncbi.nlm.nih.gov/pubmed/22231745
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
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
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 .
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
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
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