Monthly Archives: October 2013

Study: Cannabis Compounds Can Kill Cancer Cells – US News & World Report

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“Researcher says cannabinoids might treat cancer as well as billion-dollar drugs.”

A medical marijuana activist holds a sign during a rally Jan. 4, 2010, in Oakland, Calif. Research suggests marijuana may fight cancer itself, not just side-effects.“A British researcher has found that cannabinoids, a term for chemicals derived from marijuana, can kill leukemia cells, and he expects clinical trials for new medications to begin soon.

The findings, published in the October issue of Anticancer Research: International Journal of Cancer Research and Treatment, show that certain non-psychoactive cannabinoids “resulted in dramatic reductions in cell viability” and “caused a simultaneous arrest at all phases of the cell cycle,” according to an abstract posted online. 

The study tested six cannabinoids, together and independently, on leukemia cells. Study author Wai Liu, an oncologist at the University of London’s St. George’s medical school, told U.S. News the chemicals displayed “potent anti-cancer activity” and, significantly, “target and switch off” pathways that allow cancers to grow.”

More: http://www.usnews.com/news/articles/2013/10/24/study-cannabis-compounds-can-kill-cancer-cells

The endocannabinoid system mediates aerobic exercise-induced antinociception in rats.

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“These results indicate that exercise could activate the endocannabinoid system, producing antinociception.

Supporting this hypothesis, liquid-chromatography/mass-spectrometry measurements demonstrated that plasma levels of endocannabinoids (anandamide and 2-arachidonoylglycerol) and of anandamide-related mediators (palmitoylethanolamide and oleoylethanolamide) were increased after AE.

Therefore, these results suggest that the endocannabinoid system mediates aerobic exercise-induced antinociception at peripheral and central levels.”

http://www.ncbi.nlm.nih.gov/pubmed/24148812

Endocannabinoid system and pain: an introduction.

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“The endocannabinoid (EC) system consists of two main receptors: cannabinoid type 1 receptor cannabinoid receptors are found in both the central nervous system (CNS) and periphery, whereas the cannabinoid type 2 receptor cannabinoid receptor is found principally in the immune system and to a lesser extent in the CNS.

 The EC family consists of two classes of well characterised ligands; the N-acyl ethanolamines, such as N-arachidonoyl ethanolamide or anandamide (AEA), and the monoacylglycerols, such as 2-arachidonoyl glycerol. The various synthetic and catabolic pathways for these enzymes have been (with the exception of AEA synthesis) elucidated.

 To date, much work has examined the role of EC in nociceptive processing and the potential of targeting the EC system to produce analgesia.

Cannabinoid receptors and ligands are found at almost every level of the pain pathway from peripheral sites, such as peripheral nerves and immune cells, to central integration sites such as the spinal cord, and higher brain regions such as the periaqueductal grey and the rostral ventrolateral medulla associated with descending control of pain. EC have been shown to induce analgesia in preclinical models of acute nociception and chronic pain states.

 The purpose of this review is to critically evaluate the evidence for the role of EC in the pain pathway and the therapeutic potential of EC to produce analgesia. We also review the present clinical work conducted with EC, and examine whether targeting the EC system might offer a novel target for analgesics, and also potentially disease-modifying interventions for pathophysiological pain states.”

http://www.ncbi.nlm.nih.gov/pubmed/24148358

Systematic review of the literature on clinical and experimental trials on the antitumor effects of cannabinoids in gliomas.

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“To evaluate, through a systematic review of the literature, the antitumoral effects of cannabinoids on gliomas…

  In all experimental studies included, cannabinoids exerted antitumoral activity in vitro and/or antitumoral evidence in vivo in several models of tumor cells and tumors.

The antitumor activity included: antiproliferative effects (cell cycle arrest), decreased viability and cell death by toxicity, apoptosis, necrosis, autophagy, as well as antiangiogenic and antimigratory effects.

 Antitumoral evidence included: reduction in tumor size, antiangiogenic, and antimetastatic effects.

 Additionally, most of the studies described that the canabinnoids exercised selective antitumoral action in several distinct tumor models. Thereby, normal cells used as controls were not affected.

The safety factor in the cannabinoids’ administration has also been demonstrated in vivo.

 The various cannabinoids tested in multiple tumor models showed antitumoral effects both in vitro and in vivo.

 These findings indicate that cannabinoids are promising compounds for the treatment of gliomas.”

http://www.ncbi.nlm.nih.gov/pubmed/24142199

Cannabidiol, a non-psychoactive cannabinoid compound, affects metalloproteinases and pro-survival intracellular pathways in u87-mg human glioma cell line

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“Malignant gliomas are the most common primary brain tumors… Recently, we have shown that the non-psychoactive cannabinoid compound cannabidiol (CBD) induced apoptosis of human glioma cells in vitro and tumor regression in vivo…the present study was to investigate the anti-migratory action of CBD…

 In conclusion, the present investigation adds further insights into the antitumoral action of the non-psychoactive CBD, showing multiple mechanisms through which the cannabinoid inhibits glioma cell growth and motility.

As CBD is a natural compound without psychotropic and side effects, these data lead us to consider CBD as a new potential anticancer drug useful in the management of gliomas.”

http://air.unimi.it/handle/2434/142533

Study: Marijuana’s Active Ingredient May Shrink Cancerous Tumors – FoxNews

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“The active ingredient in marijuana appears to reduce tumor growth…

The researchers showed giving THC to mice with cancer decreased tumor growth and killed cells off in a process called autophagy.

“Our findings support that safe, therapeutically efficacious doses of THC may be reached in cancer patients,” Guillermo Velasco of Complutense University in Madrid and colleagues reported in the Journal of Clinical Investigation…

Other research has shown benefits, such as staving off Alzheimer’s, and many doctors view THC as a valuable way to treat weight loss associated with AIDS, and nausea and vomiting associated with chemotherapy in cancer patients.

Velasco and his team’s study included an analysis of two tumors from two people with a highly aggressive brain cancer which showed signs of autophagy after receiving THC.

The researchers said the findings could pave the way for cannabinoid-based drugs to treat cancer…”

More: http://www.foxnews.com/story/2009/04/02/study-marijuana-active-ingredient-may-shrink-cancerous-tumors/

“Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells… These findings describe a mechanism by which THC can promote the autophagic death of human and mouse cancer cells and provide evidence that cannabinoid administration may be an effective therapeutic strategy for targeting human cancers.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2673842/

The endocannabinoid system and multiple sclerosis.

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“Multiple sclerosis (MS) is a neurodegenerative disease that is characterised by repeated inflammatory/demyelinating events within the central nervous system (CNS). In addition to relapsing-remitting neurological insults, leading to loss of function, patients are often left with residual, troublesome symptoms such as spasticity and pain. These greatly diminish “quality of life” and have prompted some patients to self-medicate with and perceive benefit from cannabis.

Recent advances in cannabinoid biology are beginning to support these anecdotal observations, notably the demonstration that spasticity is tonically regulated by the endogenous cannabinoid system.

Recent clinical trials may indeed suggest that cannabis has some potential to relieve, pain, spasms and spasticity in MS. However, because the CB(1) cannabinoid receptor mediates both the positive and adverse effects of cannabis, therapy will invariably be associated with some unwanted, psychoactive effects.

In an experimental model of MS, and in MS tissue, there are local perturbations of the endocannabinoid system in lesional areas. Stimulation of endocannabinoid activity in these areas either through increase of synthesis or inhibition of endocannabinoid degradation offers the positive therapeutic potential of the cannabinoid system whilst limiting adverse events by locally targeting the lesion.

 In addition, CB(1) and CB(2) cannabinoid receptor stimulation may also have anti-inflammatory and neuroprotective potential as the endocannabinoid system controls the level of neurodegeneration that occurs as a result of the inflammatory insults.

Therefore cannabinoids may not only offer symptom control but may also slow the neurodegenerative disease progression that ultimately leads to the accumulation of disability.”

http://www.ncbi.nlm.nih.gov/pubmed/18781983

Cannabinoids ameliorate disease progression in a model of multiple sclerosis in mice, acting preferentially through CB1 receptor-mediated anti-inflammatory effects

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“Cannabinoids have been proposed as promising therapeutic agents in MS given their capability to alleviate specific MS symptoms (e.g., spasticity, pain).

Although MS has been considered mainly an inflammatory disorder, recent evidence, however, revealed the importance of neurodegenerative events, opening the possibility that cannabinoid agonists, given their cytoprotective properties, may also serve to reduce oligodendrocyte death and axonal damage in MS.

Thus, the treatment with WIN55,512-2, a potent CB1 and CB2 agonist, was reported to be effective to ameliorate tremor and spasticity in mice with chronic relapsing experimental autoimmune encephalomyelitis, a murine model of MS, but also to delay disease progression in this and other murine models of MS….”

http://www.sciencedirect.com/science/article/pii/S0028390812000500

Control of Spasticity in a Multiple Sclerosis Model is mediated by CB1, not CB2, Cannabinoid Receptors

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Figure 1

“There is increasing evidence to suggest that cannabis can ameliorate muscle-spasticity in multiple sclerosis, as was objectively shown in experimental autoimmune encephalomyelitis models. The purpose of this study was to investigate further the involvement of CB1 and CB2 cannabinoid receptors in the control of experimental spasticity…

Conclusions and Implications:

The CB1 receptor controls spasticity and cross-reactivity to this receptor appears to account for the therapeutic action of some CB2 agonists.

 As cannabinoid-induced psychoactivity is also mediated by the CB1 receptor, it will be difficult to truly dissociate the therapeutic effects from the well-known, adverse effects of cannabinoids when using cannabis as a medicine.

The lack of knowledge on the true diversity of the cannabinoid system coupled with the lack of total specificity of current cannabinoid reagents makes interpretation of in vivo results difficult, if using a purely pharmacological approach.

Gene knockout technology provides an important tool in target validation and indicates that the CB1 receptor is the main cannabinoid target for an anti-spastic effect.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2189718/

Control of spasticity in a multiple sclerosis model using central nervous system-excluded CB1 cannabinoid receptor agonists.

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“The purpose of this study was the generation of central nervous system (CNS)-excluded cannabinoid receptor agonists to test the hypothesis that inhibition of spasticity, due to CNS autoimmunity, could be controlled by affecting neurotransmission within the periphery…

In summary, CNS-excluded CB1 receptor agonists are a novel class of therapeutic agent for spasticity.”

http://www.ncbi.nlm.nih.gov/pubmed/24121462