Inhibition of adenylate cyclase by delta 9-tetrahydrocannabinol in mouse spleen cells: a potential mechanism for cannabinoid-mediated immunosuppression.

“The ability of delta 9-Tetrahydrocannabinol (delta 9-THC) to modulate adenylate cyclase activity in mouse spleen cells was investigated…

delta 9-THC treated spleen cells demonstrated a 33% inhibition and a 66% inhibition in intracellular cAMP… respectively…

These studies suggest that inhibition of immune function by delta 9-THC may be mediated through the inhibition of intracellular cAMP early after antigen stimulation.”

http://www.ncbi.nlm.nih.gov/pubmed/1321935

Anandamide, a naturally-occurring agonist of the cannabinoid receptor, blocks adenylate cyclase at the frog neuromuscular junction.

“Anandamide (arachydonylethanolamide) is a naturally-occurring ligand of the canabinoid receptor. When anandamide binds to its receptor, adenylate cyclase is inhibited…

The conclusions are that the motor nerve terminal has a cannabinoid receptor.

The binding of anandamide to this receptor seems to block adenylate cyclase.”

http://www.ncbi.nlm.nih.gov/pubmed/7953630

The peripheral cannabinoid receptor: adenylate cyclase inhibition and G protein coupling.

“Two cannabinoid receptors, designated neuronal (or CB1) and peripheral (or CB2), have recently been cloned. Activation of CB1 receptors leads to inhibition of adenylate cyclase and N-type voltage-dependent Ca2+ channels.

Here we show, using a CB2 transfected Chinese hamster ovary cell line, that this receptor binds a variety of tricyclic cannabinoid ligands as well as the endogenous ligand anandamide.

Activation of the CB2 receptor by various tricyclic cannabinoids inhibits adenylate cyclase activity and this inhibition is pertussis toxin sensitive indicating that this receptor is coupled to the Gi/G(o) GTP-binding proteins…

These results characterize the CB2 receptor as a functional and distinctive member of the cannabinoid receptor family.”

http://www.ncbi.nlm.nih.gov/pubmed/7498464

 

Nonclassical cannabinoid analgetics inhibit adenylate cyclase: development of a cannabinoid receptor model.

“Extensive structure-activity relationship studies have demonstrated that specific requirements within the cannabinoid structure are necessary to produce potent analgesia.

A three-point association between the agonist and the receptor mediating analgesia consists of: 1) the C ring hydroxyl, 2) the phenolic A ring hydroxyl, and 3) the A ring alkyl hydrophobic side chain. Potent tricyclic and bicyclic structures were synthesized as “nonclassical” cannabinoid analgetics that conform to this agonist-receptor three-point interaction model.

At the cellular level, centrally active cannabinoid drugs inhibit adenylate cyclase activity in a neuroblastoma cell line. The structure-activity relationship profile for inhibition of adenylate cyclase in vitro was consistent with this same three-point association of agonists with the receptor.

A correlation exists between the potency of drugs to produce analgesia in vivo and to inhibit adenylate cyclase in vitro.

Based on the parallels in structure-activity relationships and the enantioselective effects, it is postulated that the receptor that is associated with the regulation of adenylate cyclase in vitro may be the same receptor as that mediating analgesia in vivo.

A conceptualization of the cannabinoid analgetic receptor is presented.”

http://www.ncbi.nlm.nih.gov/pubmed/3352594

Anandamide, a brain endogenous compound, interacts specifically with cannabinoid receptors and inhibits adenylate cyclase.

“A putative endogenous cannabinoid ligand, arachidonylethanolamide (termed “anandamide”), was isolated recently from porcine brain.

Here we demonstrate that this compound is a specific cannabinoid agonist and exerts its action directly via the cannabinoid receptors.

Anandamide specifically binds to membranes from cells transiently (COS) or stably (Chinese hamster ovary) transfected with an expression plasmid carrying the cannabinoid receptor DNA but not to membranes from control nontransfected cells.

Moreover, anandamide inhibited the forskolin-stimulated adenylate cyclase in the transfected cells and in cells that naturally express cannabinoid receptors (N18TG2 neuroblastoma) but not in control nontransfected cells. As with exogenous cannabinoids…

These data indicate that anandamide is an endogenous agonist that may serve as a genuine neurotransmitter for the cannabinoid receptor.”

http://www.ncbi.nlm.nih.gov/pubmed/8515284

Regulation of adenylate cyclase by cannabinoid drugs. Insights based on thermodynamic studies.

“The abilities of lipophilic cannabinoid drugs to regulate adenylate cyclase activity in neuroblastoma cell membranes were analyzed by thermodynamic studies…

These data suggest that, for the entropy-driven hormone-stimulated adenylate cyclase enzyme, less disorder of the system occurs in the presence of regulators that inhibit the enzyme via Gi.

In summary, thermodynamic data suggest that cannabidiol can influence adenylate cyclase by increasing membrane fluidity, but that the inhibition of adenylate cyclase by delta 9-tetrahydrocannabinol is not related to membrane fluidization.”

http://www.ncbi.nlm.nih.gov/pubmed/2554920

“Regulation of adenylate cyclase in a cultured neuronal cell line by marijuana constituents, metabolites of delta-9-tetrahydrocannabinol, and synthetic analogs having psychoactivity.” http://www.ncbi.nlm.nih.gov/pubmed/2830535

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

“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

It’s Lung Cancer Awareness Month. Please, BE AWARE:

A tourist looks over the city's skyline over a thin haze of pollution on a clear day in Hong Kong on February 1, 2013. Emissions from factories in southern China, which seep over Hong Kong's border, combined with local emissions from power plants and transport, generate an almost daily thick blanket of haze over the teeming metropolis.

“Air pollution causes lung cancer, World Health Organization confirms” http://www.cbsnews.com/8301-204_162-57607955/air-pollution-causes-lung-cancer-world-health-organization-confirms/

“Marijuana May Fight Lung Tumors… active ingredient in marijuana may help combat lung cancer… In lab and mouse studies, the compound, known as THC, cut lung tumor growth in half and helped prevent the cancer from spreading…” http://www.cbsnews.com/2100-500368_162-2696726.html

“Lung cancer leads all cancer deaths”  http://www.thespectrum.com/story/life/features/mesquite/2014/10/20/lung-cancer-leads-cancer-deaths/17640075/

“Air Pollution a Leading Cause of Cancer. The United Nation’s World Health Organization (WHO) has classified air pollution as a prime cause of cancer worldwide, especially in the case of lung cancer.” http://www.webmd.com/cancer/news/20131018/air-pollution-cancer

“Pot Smoking Not Linked to Lung Cancer. Study Shows No Increased Risk for Even the Heaviest Marijuana Smokers.” http://www.webmd.com/lung-cancer/news/20060523/pot-smoking-not-linked-to-lung-cancer

“Marijuana May Fight Lung Tumors… the active ingredient in marijuana may help combat lung cancer…”http://www.webmd.com/lung-cancer/news/20070417/marijuana-may-fight-lung-tumors

“WHO agency: Air pollution causes cancer. What many commuters choking on smog have long suspected has finally been scientifically validated: air pollution causes lung cancer.” http://www.abclocal.go.com/ktrk/story?section=news%2Fhealth&id=9290406

“Marijuana Compound May Fight Lung Cancer… Harvard University researchers have found that, in both laboratory and mouse studies, delta-tetrahydrocannabinol (THC) cuts tumor growth in half in common lung cancer while impeding the cancer’s ability to spread.”
http://abcnews.go.com/Health/Healthday/story?id=4506595&page=1

“Don’t Smoke? You Could Still Get Lung Cancer”  http://health.clevelandclinic.org/2014/10/dont-smoke-you-could-still-get-lung-cancer/

“Radon No. 1 lung cancer cause in nonsmokers”  http://www.rgj.com/story/life/wellness/2014/10/24/radon-lung-cancer-cause-nonsmokers/17866569/

“Air pollution causes lung cancer, World Health Organization says”  http://articles.latimes.com/2013/oct/17/science/la-sci-sn-air-pollution-causes-lung-cancer-20131017

“Smog Tied to Higher Risk of Lung Cancer, Heart Failure” http://health.usnews.com/health-news/news/articles/2013/07/10/smog-tied-to-higher-risk-of-lung-cancer-heart-failure

“Mountaintop Removal Mining Dust Linked To Increased Risk Of Lung Cancer, According to Study”  http://lungcancernewstoday.com/2014/10/20/mountaintop-removal-mining-dust-linked-increased-risk-lung-cancer-according-study/

“Study Shows Direct Connections Between Mountaintop Removal Dust Exposure and Lung Cancer”  http://wfpl.org/post/study-shows-direct-connections-between-mountaintop-removal-dust-exposure-and-lung-cancer

“Compound in chili pepper slows lung cancer tumor growth. New laboratory research shows capsaicin decrease growth of an aggressive form of lung cancer.”  http://www.teatronaturale.com/food-and-fun/health/4983-compound-in-chili-pepper-slows-lung-cancer-tumor-growth.htm

“Drinking alcohol may boost lung cancer risk” http://www.foodconsumer.org/newsite/Nutrition/Food/drinking_alcohol_and_lung_cancer_risk_1024110625.html

“Link Between Alcohol And Cancer Explained: Alcohol Activates Cellular Changes That Make Tumor Cells Spread” http://www.sciencedaily.com/releases/2009/10/091026172052.htm

“Groups seek to curb tobacco use in cancer patients… Tobacco use plays a role in 18 different cancers… Patients who use tobacco have worse outcomes and more difficult treatment… tobacco use decreases the effectiveness of chemotherapies and interferes with drug metabolism… data also shows that it decreases survival… we call on the oncology community… to provide cessation support to all cancer patients,” http://www.oncologypractice.com/oncologyreport/news/top-news/single-view/groups-seek-to-curb-tobacco-use-in-cancer-patients/1a87bf57bcccdadf01ae769c48eadce4.html

“Marijuana habit not linked to lung cancer” http://www.oncologypractice.com/oncologyreport/news/top-news/single-view/marijuana-habit-not-linked-to-lung-cancer/73840afd2cca226b9e6a9ddc7cb0d039.html

“Cannabis and tobacco smoke are not equally carcinogenic… Available scientific data, that examines the carcinogenic properties of inhaling smoke and its biological consequences, suggests reasons why tobacco smoke, but not cannabis smoke, may result in lung cancer… Furthermore, compounds found in cannabis have been shown to kill numerous cancer types including: lung cancer…”  http://www.harmreductionjournal.com/content/2/1/21

“Tobacco Smoke Causes Lung Inflammation, Promotes Lung Cancer Growth” http://www.sciencedaily.com/releases/2010/01/100119121206.htm

“Marijuana Cuts Lung Cancer Tumor Growth In Half, Study Shows”
http://www.sciencedaily.com/releases/2007/04/070417193338.htm

“Delta–9 Tetrahydrocannabinol inhibits growth and metastasis of lung cancer” http://www.thctotalhealthcare.com/delta-9-tetrahydrocannabinol-inhibits-growth-and-metastasis-of-lung-cancer-harvard-university/

“Δ-9 Tetrahydrocannabinol inhibits growth and metastasis of lung cancer.”  http://cancerres.aacrjournals.org/content/67/9_Supplement/4749.short

“Antineoplastic activity of cannabinoids. Lewis lung adenocarcinoma growth was retarded by the oral administration of delta-9-tetrahydrocannabinol, delta-8-tetrahydrocannabinol, and cannabinol (CBN)… Delta-9-THC, delta-8-THC, and cannabinol (CBN) all inhibited primary Lewis lung tumor growth….. All occur naturally in marihuana… these compounds readily cross the blood-brain barrier and do not possess many of the toxic manifestations of presently used cytotoxic agents…” http://www.ukcia.org/research/AntineoplasticActivityOfCannabinoids/index.php

“Antineoplastic activity of cannabinoids.”  http://www.ncbi.nlm.nih.gov/pubmed/1159836

“Antineoplastic: A drug used to inhibit the growth and spread of cancerous cells.. a chemotherapeutic agent that controls or kills cancer cells…” http://medical-dictionary.thefreedictionary.com/antineoplastic

“The Inhibition of DNA Synthesis by Cannabinoids. Several of the cannabinoids found in marihuana have been shown to inhibit tumor growth and increase the life-span… our in vitro observations with these cannabinoids are supported by in vivo tumor inhibition studies… Δ9-trans-tetrahydrocannabinol demonstrated the least toxicity of all inhibitory cannabinoids in vivo…” http://cancerres.aacrjournals.org/content/36/1/95.short

“Inhibition: “arrest or restraint of a process… Something that restrains, blocks, or suppresses… (in chemistry) the stopping or slowing of the rate of a chemical reaction.” http://medical-dictionary.thefreedictionary.com/inhibition

“Effects of delta9-tetrahydrocannabinol in Lewis lung adenocarcinoma cells in tissue culture… We found a dose-related decrease in DNA synthesis in transformed cell cultures treated with delta9-tetrahydrocannabinol (delta9-THC)… delta9-THC inhibited DNA synthesis…” http://www.ncbi.nlm.nih.gov/pubmed/943561

“In vivo effects of cannabinoids on macromolecular biosynthesis in Lewis lung carcinomas. Cannabinoids represent a novel class of drugs active in increasing the life span mice carrying Lewis lung tumors and decreasing primary tumor size…” http://www.ncbi.nlm.nih.gov/pubmed/616322

“Anti-emetic efficacy and toxicity of nabilone, a synthetic cannabinoid, in lung cancer chemotherapy… Symptom scores were significantly better for patients on nabilone for nausea, retching and vomiting. Fewer subjects vomited with nabilone and the number of vomiting episodes was lower; no patients on nabilone required additional parenteral anti-emetic. More patients preferred nabilone for anti-emetic control… Nabilone is an effective oral anti-emetic drug for moderately toxic chemotherapy, but the range and unpredictability of its side-effects warrant caution in its use.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2011510/

Antiemetic: “preventing or alleviating nausea and vomiting…” http://medical-dictionary.thefreedictionary.com/antiemetic
“Double-blind comparison of the antiemetic effects of nabilone and prochlorperazine on chemotherapy-induced emesis. The antiemetic effect of oral nabilone, a synthetic cannabinoid, was compared to oral slow-release capsules of prochlorperazine… Nabilone appeared to be the more effective antiemetic…” http://www.ncbi.nlm.nih.gov/pubmed/6250699
“Superiority of nabilone over prochlorperazine as an antiemetic in patients receiving cancer chemotherapy. Two double-blind, crossover trials comparing the antiemetic effectiveness of nabilone, a new synthetic cannabinoid, with that of prochlorperazine were conducted in patients with severe nausea and vomiting associated with anticancer chemotherapy… patients clearly favored nabilone…” http://www.ncbi.nlm.nih.gov/pubmed/375088
“Nabilone versus prochlorperazine for control of cancer chemotherapy-induced emesis in children: a double-blind, crossover trial… Nabilone appears to be a safe, effective, and well-tolerated antiemetic drug for children receiving cancer chemotherapy. Although major side effects may occur at higher dosages, nabilone is preferable to prochlorperazine because of improved efficacy.” http://www.ncbi.nlm.nih.gov/pubmed/3035479
“Nabilone: an effective antiemetic in patients receiving cancer chemotherapy… Eighty evaluable patients receiving chemotherapy were entered on a random prospective double-blind study to evaluate the effecti…veness of nabilone, a synthetic cannabinoid, compared to prochlorperazine… Sixty patients (75 per cent) reported nabilone to be more effective than prochlorperazine for relief of nausea and vomiting.” http://www.ncbi.nlm.nih.gov/pubmed/6271844
“Antiemetic effect of delta-9-tetrahydrocannabinol in patients receiving cancer chemotherapy. Anecdotal accounts suggested that smoking marihuana decreases the nausea and vomiting associated with cancer chemotherapeutic agents. Oral delta-9-tetrahydrocannabinol was compared with placebo in a controlled, randomized, “double-blind” experiment… For all patients an antiemetic effect was observed… No patient vomited while experiencing a subjective “high”. Oral tetrahydrocannabinol has antiemetic properties and is significantly better than a placebo in reducting vomiting caused by chemotherapeutic agents.” http://www.ncbi.nlm.nih.gov/pubmed/1099449
“… a randomized, double-blind, placebo-controlled trial of oral and smoked delta-9-tetrahydrocannabinol (THC) as an antiemetic… Delta-9-tetrahydrocannabinol was significantly more effective than placebo in reducing the number of vomiting and retching episodes, degree of nausea, duration of nausea, and volume of emesis… Delta-9-tetrahydrocannabinol appears to have significant antiemetic properties…” http://www.ncbi.nlm.nih.gov/pubmed/293141
“Antiemetic effect of tetrahydrocannabinol. Compared with placebo and prochlorperazine in chemotherapy-associated nausea and emesis… The antiemetic effect of THC appeared to be more efficacious… Tetrahydrocannabinol appears to offer significant control of nausea in most patients and exceeding by far that provided by prochlorperazine.”
http://www.ncbi.nlm.nih.gov/pubmed/6254456
“Antiemetic effect of delta 9-tetrahydrocannabinol in chemotherapy-associated nausea and emesis as compared to placebo and compazine… THC appeared to be more efficacious in controlling the emesis… THC appears to offer significant control of nausea in most patients…” http://www.ncbi.nlm.nih.gov/pubmed/6271846
“Delta-9-tetrahydrocannabinol as an antiemetic… THC appears to be an effective antiemetic in cancer patients undergoing chemotherapy… THC has been found consistently more effective than placebo and at least as effective as prochlorperazine… THC’s effectiveness has exceeded that of the phenothiazines.” http://www.ncbi.nlm.nih.gov/pubmed/6269423
“Efficacy of tetrahydrocannabinol in patients refractory to standard antiemetic therapy… This study confirms the usefulness of THC in patients whose chemotherapy-induced nausea and vomiting is refractory to other standard antiemetics.” http://www.ncbi.nlm.nih.gov/pubmed/2847994

“Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1.”  http://www.ncbi.nlm.nih.gov/pubmed/22198381

“Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1.” http://www.ncbi.nlm.nih.gov/pubmed/19914218

“Decrease of plasminogen activator inhibitor-1 may contribute to the anti-invasive action of cannabidiol on human lung cancer cells” http://www.ncbi.nlm.nih.gov/pubmed/20668920

“CYCLOOXYGENASE-2 AND PEROXISOME PROLIFERATOR ACTIVATED RECEPTOR γ CONFER CANNABIDIOL-INDUCED APOPTOSIS OF HUMAN LUNG CANCER CELLS.” http://www.ncbi.nlm.nih.gov/pubmed/23220503 

“Apoptosis: programmed cell death at a molecular level.” http://www.ncbi.nlm.nih.gov/pubmed/12833244

“WHO agency says air pollution causes lung cancer” http://www.foxnews.com/health/2013/10/17/who-agency-says-air-pollution-causes-lung-cancer/

“Marijuana Does Not Raise Lung Cancer Risk” http://www.foxnews.com/story/0,2933,196678,00.html

“Marijuana May Fight Lung Tumors… marijuana may help combat lung cancer… In lab and mouse studies, the compound, known as THC, cut lung tumor growth in half and helped prevent the cancer from spreading, says Anju Preet, PhD, a Harvard University researcher in Boston…”http://www.foxnews.com/story/2007/04/18/marijuana-may-fight-lung-tumors/

“Air pollution causes lung cancer, WHO agency announces. Experts at the International Agency for Research on Cancer, an agency of the World Health Organization, have concluded that exposure to outdoor air pollution.causes lung cancer and increases the risk for bladder cancer.” http://www.nbcnews.com/video/nightly-news/53309399/#53309399

“Marijuana Compound Fights Cancer; Human Trials Next.
Research shows component in medical cannabis fights cancer.” http://www.nbcbayarea.com/news/local/Marijuana-Compound-Fights-Cancer-Human-Trials-Next-170406116.html

“The endocannabinoid system and cancer: therapeutic implication… Identification of safe and effective treatments to manage and improve cancer therapy is critical to improve quality of life and reduce unnecessary suffering in cancer patients. In this regard, cannabis-like compounds offer therapeutic potential for the treatment of… cancer… anti-cancer properties of cannabinoids…” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165955/

“The endocannabinoid system in the cancer therapy: an overview.” http://www.ncbi.nlm.nih.gov/pubmed/21428888

“The endocannabinoid signaling system in cancer.”  http://www.ncbi.nlm.nih.gov/pubmed/23602129

“Changes in the Endocannabinoid System May Give Insight into new and Effective Treatments for Cancer” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2791688/

“Endocannabinoid system modulation in cancer biology and therapy.” http://www.ncbi.nlm.nih.gov/pubmed/19559362

“The endocannabinoid system in cancer-potential therapeutic target?” http://www.ncbi.nlm.nih.gov/pubmed/18249558

“Targeting the endocannabinoid system for the treatment of cancer–a practical view.” http://www.ncbi.nlm.nih.gov/pubmed/20370711

“The endocannabinoid system and its therapeutic exploitation… since the discovery of cannabinoid receptors, the endocannabinoid system seems to hold even more promise for the future development of therapeutic drugs.” http://www.ncbi.nlm.nih.gov/pubmed/15340387

“The endocannabinoid system as a target for the development of new drugs for cancer therapy… evidence has accumulated indicating that stimulation of cannabinoid receptors by either THC or the endocannabinoids influence the intracellular events controlling the proliferation and apoptosis of numerous types of cancer cells, thereby leading to anti-tumour effects both in vitro and in vivo. This evidence is reviewed here and suggests that future anti-cancer therapy might be developed from our knowledge of how the endocannabinoid system controls the growth and metastasis of malignant cells.”
http://www.ncbi.nlm.nih.gov/pubmed/12723496

“Cannabinoid receptor systems: therapeutic targets for tumour intervention… there is now a genuine expectation that the manipulation of cannabinoid receptor systems may have therapeutic potential for a diverse range of human diseases… demonstrated antitumour actions of cannabinoids indicates possible avenues for the future development of cannabinoids as antitumour agents.”
http://www.ncbi.nlm.nih.gov/pubmed/14640910

“Cannabinoid-associated cell death mechanisms in tumor models… cannabinoids (the active components of Cannabis sativa)… in addition to their inhibitory effects on tumor growth and migration, angiogenesis and metastasis… these compounds induce different pathways of cell death… death mechanisms induced by cannabinoids… we analyze the pathways triggered by cannabinoids to induce apoptosis or autophagy… 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.” http://www.ncbi.nlm.nih.gov/pubmed/22614735

“Towards the use of cannabinoids as antitumour agents.. cannabinoids (the active components of marijuana and their derivatives) can reduce tumour growth and progression in animal models of cancer, in addition to their well-known palliative effects on some cancer-associated symptoms.”
http://www.ncbi.nlm.nih.gov/pubmed/22555283

“Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide…only limited therapeutic treatments are available. Hence, we investigated the role of cannabinoid receptors, CB1 and CB2, as novel therapeutic targets against NSCLC…. Overall, our results indicate a novel role for cannabinoid receptors CB1 and CB2 in NSCLC growth and metastasis… These results suggest that CB1 and CB2 could be used as novel therapeutic targets against NSCLC.”
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3025486/

“Cannabinoid receptors as therapeutic targets.”
http://www.ncbi.nlm.nih.gov/pubmed/16402900

“Inhibitory effects of cannabinoid CB1 receptor stimulation on tumor growth and metastatic spreading: actions on signals involved in angiogenesis and metastasis… Our findings indicate that CB1 receptor agonists might be used therapeutically to retard tumor growth in vivo by inhibiting at once tumor growth, angiogenesis, and metastasis.” http://www.ncbi.nlm.nih.gov/pubmed/12958205

“Targeting the endocannabinoid system with cannabinoid receptor agonists: pharmacological strategies and therapeutic possibilities. Human tissues express cannabinoid CB(1) and CB(2) receptors that can be activated by endogenously released ‘endocannabinoids’ or exogenously administered compounds in a manner that reduces the symptoms or opposes the underlying causes of several disorders in need of effective therapy. Three medicines that activate cannabinoid CB(1)/CB(2) receptors are now in the clinic: Cesamet (nabilone), Marinol (dronabinol; Δ(9)-tetrahydrocannabinol (Δ(9)-THC)) and Sativex (Δ(9)-THC with cannabidiol)… several possible additional therapeutic targets for cannabinoid receptor agonists. These include other kinds of pain, epilepsy, anxiety, depression, Parkinson’s and Huntington’s diseases, amyotrophic lateral sclerosis, stroke, CANCER, drug dependence, glaucoma, autoimmune uveitis, osteoporosis, sepsis, and hepatic, renal, intestinal and cardiovascular disorders.”
http://www.ncbi.nlm.nih.gov/pubmed/23108552

“Cannabinoid receptor agonists are mitochondrial inhibitors: a unified hypothesis of how cannabinoids modulate mitochondrial function and induce cell death. Time-lapse microscopy of human lung cancer cells showed t…hat the endogenous cannabinoid anandamide (AEA), the phyto-cannabinoid Delta-9-tetrahydrocannabinol (THC) and a synthetic cannabinoid HU 210 all caused morphological changes characteristic of apoptosis.” http://www.ncbi.nlm.nih.gov/pubmed/17931597

“Programmed Cell Death (Apoptosis)” http://www.ncbi.nlm.nih.gov/books/NBK26873/

“Δ9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo…Tumor samples from THC-treated animals revealed antiproliferative and antiangiogenic effects of THC. Our study suggests that cannabinoids like THC should be explored as novel therapeutic molecules in controlling the growth and metastasis of certain lung cancers.” http://www.nature.com/onc/journal/v27/n3/abs/1210641a.html

“Use of cannabinoid receptor agonists in cancer therapy as palliative and curative agents. Cannabinoids (the active components of Cannabis sativa)… evidence suggests that agonists of cannabinoid receptors expressed by tumour cells may offer a novel strategy to treat cancer… use of cannabinoid agonists for cancer therapy, not only as palliative but also as curative drugs.” http://www.ncbi.nlm.nih.gov/pubmed/19285265

http://www.thctotalhealthcare.com/category/lung-cancer/

Pot Slows Cancer in Test Tube – WebMD

“THC and another marijuana-derived compound slow the spread of cervical and lung cancers, test-tube studies suggest.

The new findings add to the fast-growing number of animal and cell-culture studies showing different anticancer effects for cannabinoids, chemical compounds derived from marijuana.

Cannabinoids, and sometimes marijuana itself, are currently used to lessen the nausea and pain experienced by many cancer patients. The new findings — suggest that cannabinoids may have a direct anticancer effect.

“Cannabinoids’ … potential therapeutic benefit in the treatment of highly invasive cancers should be addressed in clinical trials,” conclude Robert Ramer, PhD, and Burkhard Hinz, PhD, of the University of Rostock, Germany…

Doses of THC that reduce pain in cancer patients yield blood concentrations much higher than the concentrations needed to inhibit cancer invasion.

“Thus the effects of THC on cell invasion occurred at therapeutically relevant concentrations,” Ramer and Hinz note…

Ramer and Hinz report the findings in the Jan. 2, 2008 issue of the Journal of the National Cancer Institute.”

More: http://www.webmd.com/cancer/news/20071226/pot-slows-cancer-in-test-tube

“Inhibition of Cancer Cell Invasion by Cannabinoids via Increased Expression of Tissue Inhibitor of Matrix Metalloproteinases-1”: http://jnci.oxfordjournals.org/content/100/1/59.long

Marijuana Inhibits Tumors