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Int J Oncol. 2012 May 14. doi: 10.3892/ijo.2012.1476. [Epub ahead of print]

Cannabinoid-associated cell death mechanisms in tumor models (Review).

Calvaruso G, Pellerito O, Notaro A, Giuliano M.

Source

Department of Experimental Biomedicine and Clinical Neuroscience, Section of Biochemical Sciences, University of Palermo, 90129 Palermo, Italy.

 

 

Abstract

In recent years, cannabinoids (the active components of Cannabis sativa) and their derivatives have received considerable interest due to findings that they can affect the viability and invasiveness of a variety of different cancer cells. Moreover, in addition to their inhibitory effects on tumor growth and migration, angiogenesis and metastasis, the ability of these compounds to induce different pathways of cell death has been highlighted. Here, we review the most recent results generating interest in the field of death mechanisms induced by cannabinoids in cancer cells. In particular, we analyze the pathways triggered by cannabinoids to induce apoptosis or autophagy and investigate the interplay between the two processes. Overall, the results reported here suggest that the exploration of molecular mechanisms induced by cannabinoids in cancer cells can contribute to the development of safe and effective treatments in cancer therapy.

 

PMID:22614735 [PubMed - as supplied by publisher] My link

 

 

 

 

 

 

 

Anti-tumoral action of cannabinoids: Involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation

 

 

 

Δ9-Tetrahydrocannabinol, the main active component of marijuana, induces apoptosis of transformed neural cells in culture. Here, we show that intratumoral administration of Δ9-tetrahydrocannabinol and the synthetic cannabinoid agonist WIN-55,212-2 induced a considerable regression of malignant gliomas in Wistar rats and in mice deficient in recombination activating gene 2. Cannabinoid treatment did not produce any substantial neurotoxic effect in the conditions used. Experiments with two subclones of C6 glioma cells in culture showed that cannabinoids signal apoptosis by a pathway involving cannabinoid receptors, sustained ceramide accumulation and Raf1/extracellular signal-regulated kinase activation. These results may provide the basis for a new therapeutic approach for the treatment of malignant gliomas.

 

 

 

My link

 

15 Rats with "incurable" brain tumors treated with THC infusions:3 die, 9 live up to twice as long as untreated Rats, 3 had tumors completely eliminated.Effective treatment: 60%

Complete cure: 20%

 

Cancer Killed by Cannabis - Weed - Pot - Marijuana finds UCLA research and others Full-length Doc

 

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NEOPLASIA

 

Cannabis-induced cytotoxicity in leukemic cell lines: the role of the cannabinoid receptors and the MAPK pathway

Thomas Powles, Robert te Poele, Jonathan Shamash, Tracy Chaplin, David Propper, Simon Joel, Tim Oliver, and Wai Man Liu

From the New Drug Study Group, St Bartholomew's Hospital (SBH), London, United Kingdom; the Department of Medical Oncology, SBH, London, United Kingdom; the Centre for Cancer Therapeutics, Institute of Cancer Research, Surrey, United Kingdom; the Department of Medical Oncology, Charterhouse Square, London, United Kingdom; and the Barry Reed Oncology Laboratory, SBH, London, United Kingdom.

 

 

9-Tetrahydrocannabinol (THC) is the active metabolite of cannabis. THC causes cell death in vitro through the activation of complex signal transduction pathways. However, the role that the cannabinoid 1 and 2 receptors (CB1-R and CB2-R) play in this process is less clear. We therefore investigated the role of the CB-Rs in mediating apoptosis in 3 leukemic cell lines and performed microarray and immunoblot analyses to establish further the mechanism of cell death. We developed a novel flow cytometric technique of measuring the expression of functional receptors and used combinations of selective CB1-R and CB2-R antagonists and agonists to determine their individual roles in this process. We have shown that THC is a potent inducer of apoptosis, even at 1 x IC50 (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. Additionally, THC did not appear to act synergistically with cytotoxic agents such as cisplatin. One of the most intriguing findings was that THC-induced cell death was preceded by significant changes in the expression of genes involved in the mitogen-activated protein kinase (MAPK) signal transduction pathways. Both apoptosis and gene expression changes were altered independent of p53 and the CB-Rs.

 

source: http://bloodjournal.hematologylibrary.org/...ract/105/3/1214

 

Title Cannabinoids induce incomplete maturation of cultured human leukemia cells

Creator/Author Murison, G. ; Chubb, C.B.H. ; Maeda, S. ; Gemmell, M.A. ; Huberman, E.

Publication Date 1987 Aug 01

OSTI Identifier OSTI ID: 5164483

DOE Contract Number W-31-109-ENG-38

Other Number(s) CODEN: PNASA

Resource Type Journal Article

Resource Relation Proc. Natl. Acad. Sci. U.S.A. ; Vol/Issue: 84:15

Research Org Argonne National Lab., IL (USA)

Subject 560300 -- Chemicals Metabolism & Toxicology; MARIHUANA-- BIOLOGICAL EFFECTS;TUMOR CELLS-- AUTORADIOGRAPHY;TUMOR CELLS-- CELL DIFFERENTIATION; BIOLOGICAL MARKERS;CARCINOGENESIS;DOSE-RESPONSE RELATIONSHIPS;HALLUCINOGENS;LEUKEMIA;MAN;METHIONINE;MONOCLONAL ANTIBODIES;MONOCYTES;PHORBOL ESTERS;SULFUR 35;TWO-DIMENSIONAL ELECTROPHORESIS

Related Subject AMINO ACIDS;ANIMAL CELLS;ANIMALS;ANTIBODIES;BETA DECAY RADIOISOTOPES;BETA-MINUS DECAY RADIOISOTOPES;BIOLOGICAL MATERIALS;BLOOD;BLOOD CELLS;BODY FLUIDS;CARBOXYLIC ACIDS;CARCINOGENS;CENTRAL NERVOUS SYSTEM AGENTS;DAYS LIVING RADIOISOTOPES;DISEASES;DRUGS;ELECTROPHORESIS;ESTERS;EVEN-ODD NUCLEI;HEMIC DISEASES;HERBS;ISOTOPES;LEUKOCYTES;LIGHT NUCLEI;LIPOTROPIC FACTORS;MAMMALS;MATERIALS;NEOPLASMS;NUCLEI;ORGANIC ACIDS;ORGANIC COMPOUNDS;ORGANIC SULFUR COMPOUNDS;PATHOGENESIS;PLANTS;PRIMATES;PSYCHOTROPIC DRUGS;RADIOISOTOPES;SULFUR ISOTOPES;VERTEBRATES

Description/Abstract Monocyte maturation markers were induced in cultured human myeloblastic ML-2 leukemia cells after treatment for 1-6 days with 0.03-30 ..mu..M ..delta../sup 9/-tetrahydrocannabinol (THC), the major psychoactive component of marijuana.^After a 2-day or longer treatment, 2- to 5-fold increases were found in the percentages of cells exhibiting reactivity with either the murine OKM1 monoclonal antibody of the Leu-M5 monoclonal antibody, staining positively for nonspecific esterase activity, and displaying a promonocyte morphology.^The increases in these differentiation markers after treatment with 0.03-1 ..mu..M THC were dose dependent.^At this dose range, THC did not cause an inhibition of cell growth.^The THC-induced cell maturation was also characterized by specific changes in the patterns of newly synthesized proteins.^The THC-induced differentiation did not, however, result in cells with a highly developed mature monocyte phenotype.^However, treatment of these incompletely matured cells with either phorbol 12-myristate 13-acetate of 1..cap alpha..,25-dihydroxycholecalciferol, which are inducers of differentiation in myeloid leukemia cells (including ML-2 cells), produced cells with a mature monocyte morphology.^The ML-2 cell system described here may be a useful tool for deciphering critical biochemical events that lead to the cannabinoid-induced incomplete cell differentiation of ML-2 cells and other related cell types.^Findings obtained from this system may have important implications for studies of cannabinoid effects on normal human bone-marrow progenitor cells.

 

source: http://www.osti.gov/energycitations/produc...osti_id=5164483

 

PDF CB1 CB2 Receptors

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More Evidence That Marijuana Prevents Cancer

By Bruce Mirken, Marijuana Policy Project.

 

Among the more interesting pieces of news that came out while I was on vacation the first half of August was a new study in the journal Cancer Prevention Research, which found that marijuana smokers have a lower risk of head and neck cancers than people who don't smoke marijuana. Alas, this important research has been largely ignored by the news media.

 

While this type of study cannot conclusively prove cause and effect, the combination of this new study and existing research -- which for decades has shown that cannabinoids are fairly potent anticancer drugs -- raises a significant possibility that marijuana use is in fact protective against certain types of cancer.

 

A team of researchers from several major universities conducted what is known as a "case-control" study, comparing patients who had squamous cell carcinoma of the mouth, larynx, and pharynx with control patients matched for age, gender, and residence location who did not have cancer. By looking at matched groups with and without cancer, researchers hope to find patterns indicating risk or protective factors. In this case they focused on marijuana use, but also took into account known risk factors for this type of cancer, including tobacco and alcohol use.

 

After adjusting for those confounding factors, current marijuana users had a 48% reduced risk of head and neck cancer, and the reduction was statistically significant. Former users also had a lower risk, though it fell short of being significant. The investigators crunched the numbers several different ways -- for example, by amount of marijuana used or the frequency of use -- and the findings stayed the same nearly across the board, with moderate users showing the strongest and most consistent reduction in cancer risk.

 

The scientists write, "We found that moderate marijuana use was significantly associated with reduced risk HNSCC [head and neck squamous cell carcinoma]. The association was consistent across different measures of marijuana use (marijuana use status, duration, and frequency of use)."

 

Strikingly, among drinkers and cigarette smokers, those who also used marijuana reduced their cancer risk compared to those who only drank and smoked cigarettes. So marijuana may actually have been countering the known bad effects of booze and cigarettes.

 

 

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Cannabinoids Kill Cancer Cells: "Publius" Deciphers Update from National Cancer Institute

 

In June the National Cancer Institute added text to its online resource "Cannabis and Cannabinoids" highlighting the role of herbal cannabinoids in killing cancer cells (apoptosis). Authors of The Cannabis Papers: a citizen's guide to cannabinoids, cite the 2003 US Cannabinoid Patent and 37 years of US evidence showing how the Cannabinoid System kills cancer.

 

Chicago, IL (PRWEB) August 17, 2012

In June the National Cancer Institute added text to its online resource "Cannabis and Cannabinoids" highlighting the role of herbal cannabinoids in killing cancer cells (apoptosis).

“We’ve known for quite some time the Cannabinoid System (CS) fights cancer,” noted Steve Young, member of Publius and author of Maximizing Harm: Winners and Losers in the Drug War (2000). “We’re happy to see NCI publicize this profound information 37 years after NCI first noted the anticancer properties of cannabis and the CS.”

 

http://www.prweb.com/releases/prweb2012/8/prweb9767752.htm

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They are just gearing up to support big pharma's takeover the medical marijuana industry.

In typical pharmaceutical fashion, of course.... more pills, inhalers, and such.

 

Never forget that pharmaceuticals only list the "active ingredients". They don't tell you what other crap they put in it ....or what sort of nasty toxic chemicals they used to extract it. Ever weigh a pill? It doesn't add up.


 

                                                                                                                                                   

 

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CANNABIDIOL INHIBITS ANGIOGENESIS BY MULTIPLE MECHANISMS.

Solinas M, Massi P, Cantelmo A, Cattaneo M, Cammarota R, Bartolini D, Cinquina V, Valenti M, Vicentini L, Noonan D, Albini A, Parolaro D.

Source

Department of Biomedical, Computer and Communication Sciences, University of Insubria, Busto Arsizio (VA), Italy, Department of Pharmacology, Chemotherapy and Toxicology, University of Milan, 20129 Milan, Italy, Oncology Research Laboratory, Science and Technology Park, IRCCS MultiMedica, 20138 Milan, Italy, Department of Biotechnology and Life Sciences, University of Insubria, 21100 Varese, Italy.

 

 

Abstract

Background and purpose: Several studies demonstrated anti-proliferative and pro-apoptotic actions of cannabinoids on several tumours, together with their anti-angiogenic properties. The non-psychoactive cannabinoid cannabidiol (CBD) effectively inhibits in vitro and in vivo the growth of different types of tumours and down-regulates some pro-angiogenic signal produced by glioma cells. As its anti-angiogenic properties have not been thoroughly investigated to date, and given its very favorable pharmacological and toxicological profile, here we evaluated CBD ability to modulate tumour angiogenesis. Experimental approach: We firstly evaluated CBD effect on human umbilical vein endothelial cell (HUVEC) proliferation and viability- through MTT assay and FACS analysis-and in vitro motility-both in a classical Boyden chamber test and in a wound-healing assay. We next investigated CBD effects on different angiogenesis-related proteins released by HUVECs, using an angiogenic Array Kit and an enzyme-linked immunosorbent assay (ELISA) directed at MMP2. Afterwards we evaluated in vitro angiogenesis in treated HUVECs invading a Matrigel layer and in HUVEC spheroids embedded into collagen gels. We further characterized CBD effects using a Matrigel sponge model of in vivo angiogenesis. Key results: CBD induced HUVEC cytostasis without inducing apoptosis, inhibited HUVEC migration, invasion, and sprouting in vitro, and angiogenesis in vivo in matrigel sponges. These effects were associated with down-modulation of several angiogenesis-related molecules. Conclusions and Implications: This study reveals that CBD inhibits angiogenesis by multiple mechanisms. Its dual effect on both tumour and endothelial cells reinforces the hypothesis that CBD could represent a potential effective agent in cancer therapy. © 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.

 

© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.

 

 

 

 

 

Source: http://www.ncbi.nlm....pubmed/22624859

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