Category Archives: Cancer

Cannabinoid inhibition of adenylate cyclase. Biochemistry of the response in neuroblastoma cell membranes.

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“The inhibition of adenylate cyclase activity by cannabimimetic compounds in a membrane fraction from cultured neuroblastoma cells has been examined. The inhibition was shown to be concentration-dependent over a nanomolar range for both delta 9-tetrahydrocannabinol and its synthetic analog…

This study points to the similarities between the enzyme inhibition by cannabimimetic compounds and by muscarinic cholinergic compounds. It is inferred that the cannabimimetic compounds must act via regulatory mechanisms similar to those operating for receptor-mediated inhibition of adenylate cyclase.”

http://www.ncbi.nlm.nih.gov/pubmed/2984538

Cannabinoid inhibition of adenylate cyclase. Pharmacology of the response in neuroblastoma cell membranes.

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“Adenylate cyclase in plasma membranes was inhibited by micromolar concentrations of delta 8-tetrahydrocannabinol and delta 9-tetrahydrocannabinol…

The inhibition of adenylate cyclase was specific for psychoactive cannabinoids, since cannabinol and cannabidiol produced minimal or no response…

Possible mechanisms for the effects of cannabinoid drugs on adenylate cyclase activity…”

http://www.ncbi.nlm.nih.gov/pubmed/6092901

Cannabinoid inhibition of adenylate cyclase: relative activity of constituents and metabolites of marihuana.

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“delta 9Tetrahydrocannabinol (THC) has been shown to inhibit the activity of adenylate cyclase in the N18TG2 clone of murine neuroblastoma cells. The concentration of delta 9THC exhibiting half-maximal inhibition was 500 nM. delta 8Tetrahydrocannabinol was less active, and cannabinol was only partially active. Cannabidiol, cannabigerol, cannabichromene, olivetol and compounds having a reduced length of the C3 alkyl side chain were inactive. The metabolites of delta 8THC and delta 9THC hydroxylated at the C11 position were more potent than the parent drugs. However, hydroxylation at the C8 position of the terpenoid ring resulted in loss of activity. Compounds hydroxylated along the C3 alkyl side chain were equally efficacious but less potent than delta 9THC. These findings are compared to the pharmacology of cannabinoids reported for psychological effects in humans and behavioral effects in a variety of animal models.”

http://www.ncbi.nlm.nih.gov/pubmed/3601007

Plant-derived cannabinoids modulate the activity of transient receptor potential channels of ankyrin type-1 and melastatin type-8.

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“… we have reported here for the first time the potent and efficacious modulatory effects by some phytocannabinoids on TRPA1- and TRPM8-mediated [Ca2+]ielevation…

Our findings suggest that phytocannabinoids and cannabis extracts exert some of their pharmacological actions also by interacting with TRPA1 and TRPM8 channels, with potential implications for the treatment of pain and cancer.”

http://jpet.aspetjournals.org/content/325/3/1007.long

Cannabis extract treatment for terminal acute lymphoblastic leukemia with a Philadelphia chromosome mutation.

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” This case study is on a 14-year-old patient diagnosed with a very aggressive form of ALL (positive for the Philadelphia chromosome mutation). A standard bone marrow transplant, aggressive chemotherapy and radiation therapy were revoked, with treatment being deemed a failure after 34 months.

Without any other solutions provided by conventional approaches aside from palliation, the family administered cannabinoid extracts orally to the patient.

Cannabinoid resin extract is used as an effective treatment for ALL with a positive Philadelphia chromosome mutation and indications of dose-dependent disease control.

The clinical observation in this study revealed a rapid dose-dependent correlation.”

http://www.ncbi.nlm.nih.gov/pubmed/24474921

Inhibition of colon carcinogenesis by a standardized Cannabis sativa extract with high content of cannabidiol.

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“Colon cancer is a major public health problem. Cannabis-based medicines are useful adjunctive treatments in cancer patients. Here, we have investigated the effect of a standardized Cannabis sativa extract with high content of cannabidiol (CBD), here named CBD BDS, i.e. CBD botanical drug substance, on colorectal cancer cell proliferation and in experimental models of colon cancer in vivo.

RESULTS:

CBD BDS and CBD reduced cell proliferation in tumoral, but not in healthy, cells… In vivo, CBD BDS reduced AOM-induced preneoplastic lesions and polyps as well as tumour growth in the xenograft model of colon cancer.

CONCLUSIONS:

CBD BDS attenuates colon carcinogenesis and inhibits colorectal cancer cell proliferation via CB1 and CB2 receptor activation. The results may have some clinical relevance for the use of Cannabis-based medicines in cancer patients.”

http://www.ncbi.nlm.nih.gov/pubmed/24373545

The Endocannabinoid System and Sex Steroid Hormone-Dependent Cancers.

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“The “endocannabinoid system (ECS)” comprises the endocannabinoids, the enzymes that regulate their synthesis and degradation, the prototypicalcannabinoid receptors (CB1 and CB2), some noncannabinoid receptors, and an, as yet, uncharacterised transport system.

Recent evidence suggests that both cannabinoid receptors are present in sex steroid hormone-dependent cancer tissues and potentially play an important role in those malignancies.

Sex steroid hormones regulate the endocannabinoid system and the endocannabinoids prevent tumour development through putative protective mechanisms that prevent cell growth and migration, suggesting an important role for endocannabinoids in the regulation of sex hormone-dependent tumours and metastasis.

Here, the role of the endocannabinoid system in sex steroid hormone-dependent cancers is described and the potential for novel therapies assessed.”

http://www.ncbi.nlm.nih.gov/pubmed/24369462

Direct modulation of the outer mitochondrial membrane channel, voltage-dependent anion channel 1 (VDAC1) by cannabidiol: a novel mechanism for cannabinoid-induced cell death.

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“Cannabidiol (CBD) is a non-psychoactive plant cannabinoid that inhibits cell proliferation and induces cell death of cancer cells and activated immune cells. It is not an agonist of the classical CB1/CB2 cannabinoid receptors and the mechanism by which it functions is unknown.

…using microscale thermophoresis, we showed a direct interaction between purified fluorescently labeled VDAC1 and CBD.

Thus, VDAC1 seems to serve as a novel mitochondrial target for CBD.

The inhibition of VDAC1 by CBD may be responsible for the immunosuppressive and anticancer effects of CBD.”

http://www.ncbi.nlm.nih.gov/pubmed/24309936

Research Shows that Marijuana Kills Cancer Cells

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The marijuana molecula cannabidiol. Cell studies show it to be an anti-cancer agent.

“New research published this month in the journal Anticancer Research concludes that certain non-psychoactive cannabinoids “resulted in dramatic reductions in [leukemia] cell viability” and “caused a simultaneous arrest at all phases of the [leukemia] cell cycle,” according to an abstract posted online.

Study author Wai Liu, a University of London – St. George’s medical school oncologist, tested six cannabinoids, together and independently, on leukemia cells.

Liu told US News the molecules had “potent anti-cancer activity” and, significantly, “target and switch off” chemical signals that promote cancer growth.

Liu’s research builds on what is now at least a decade of startling research showing marijuana molecules’ effects on cancer cells…

Drug law reform advocates note that the United States all but ceased medical research into the benefits of marijuana during the decades-long and ongoing drug war. Research, however, continues overseas.”

http://www.eastbayexpress.com/LegalizationNation/archives/2013/10/25/research-shows-that-marijuana-kills-cancer-cells

Marijuana Might Kill Cancer – Newsweek

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“A new study suggests that several components of the cannabis plant slow or kill malignant cells.”
Pot

 “Recent research gives new hope and meaning to the phrase “medical marijuana.”

In a paper published in October’s Anticancer Research, Wai Liu, a senior research fellow at St. George’s University of London, reports that he found six cannabinoids – active components of the cannabis plant – that can slow or outright kill cancer cells.

Though THC is the main cannabinoid associated with marijuana and has been recognized to have a “really strong anti-cancer effect,” Liu says, “it’s not a good candidate for therapeutic use because of its psychoactive properties.”

He examined whether several lesser-known cannabinoids would impact the growth of leukemia cells both individually and in combination.

The result?

“They’re good at killing cancer cells,” he says. And “because they’re not psychoactive, you can actually have the benefits associated with anti-cancer technology but not have the feelings of high, which are associated with THC.””

More: http://www.newsweek.com/marijuana-might-kill-cancer-1289