THC and Cannabidiol (CBD), are the two major constituent of medical cannabis.  THC is the psychoactive component which creates a "high".  Cannabidiol is non-psychoactive and has extensive medicinal use.

Although the anti-cancer activity of CBD was reported in 1975 in a Lewis Lung Cancer model, further reseach in the US was banned shortly thereafter. 

Two groups outside the US, Guzman and Italy have reported recentkly anticancer activlty of Cannbidiol.

In  November 2007, Maccalister in California was reported that CBD reduces growth of aggressive human breast cancer cells in vitro and reduces their invasiveness. CBD represents the first non-toxic exogenous agent that down-regulates tumor aggressiveness.

Very BEST Review articles in medical literature

http://americanmarijuana.org/Guzman-Cancer.pdf

OCTOBER 2003 | VOLUME 3 www.nature.com/reviews/cancer

CANNABINOIDS: POTENTIAL ANTICANCER AGENTS by Manuel Guzmán

Cannabinoids — the active components of Cannabis sativa and their derivatives — exert palliative effects in cancer patients by preventing nausea, vomiting and pain and by stimulating appetite. In addition, these compounds have been shown to inhibit the growth of tumour cells in culture and animal models by modulating key cell-signalling pathways. Cannabinoids are usually
well tolerated, and do not produce the generalized toxic effects of conventional drugs.

CANNABINOIDS: POTENTIAL ANTICANCER AGENTS

Manuel Guzmán about the author: Manuel Guzmán is Associate Professor of Biochemistry and Molecular Biology at Madrid Complutense University, Spain. He received his Ph.D. from Complutense University in 1990 for his research on lipid metabolism in the liver. Since then, his research has focused on the mechanism of cannabinoid action in unravelling the signalling mechanisms involved in the control of cell fate by cannabinoids and establishing the preclinical basis for clinical trials on cannabinoids and cancer.

Preface Cannabinoids — the active components of Cannabis sativa and their derivatives — exert palliative effects in cancer patients by preventing nausea, vomiting and pain and by stimulating appetite. In addition, these compounds have been shown to inhibit the growth of tumour cells in culture and animal models by modulating key cell-signalling pathways. Cannabinoids are usually well tolerated, and do not produce the generalized toxic effects of conventional chemotherapies. So, could cannabinoids be used to develop new anti-cancer therapies?

Summary:  Cannabinoids, the active components of Cannabis sativa and their derivatives, act in the organism by mimicking endogenous substances, the endocannabinoids, that activate specific cannabinoid receptors.

Cannabinoids exert palliative effects in patients with cancer and inhibit tumour growth in laboratory animals.

The best-established palliative effect of cannabinoids in cancer patients is the inhibition of chemotherapy-induced nausea and vomiting. Today, capsules of 9-tetrahydrocannabinol (dronabinol (Marinol)) and its synthetic analogue nabilone (Cesamet) are approved for this purpose.

Other potential palliative effects of cannabinoids in cancer patients — supported by Phase III clinical trials — include appetite stimulation and pain inhibition. In relation to the former, dronabinol is now prescribed for anorexia associated with weight loss in patients with AIDS.
 
Cannabinoids inhibit tumour growth in laboratory animals. They do so by modulating key cell-signalling pathways, thereby inducing direct growth arrest and death of tumour cells, as well as by inhibiting tumour angiogenesis and metastasis.

Cannabinoids are selective antitumour compounds, as they can kill tumour cells without affecting their non-transformed counterparts. It is probable that cannabinoid receptors regulate cell-survival and cell-death pathways differently in tumour and non-tumour cells.

Cannabinoids have favourable drug-safety profiles and do not produce the generalized toxic effects of conventional chemotherapies.

http://www.brainlife.org/reprint/2008/sarfaraz_s080115.pdf

Cannabinoids for Cancer Treatment: Progress and Promise. Sami Sarfaraz, Vaqar M. Adhami, Deeba N. Syed, Farrukh Afaq, and Hasan Mukhtar. Chemoprevention Program, Paul P. Carbone Comprehensive Cancer Center and Department of Dermatology, School of Medicine and Public Health, University of Wisconsin, Madison, Wisconsin

Cannabinoids are a class of pharmacologic compounds that offer potential applications as antitumor drugs, based on the ability of some members of this class to limit inflammation, cell proliferation, and cell survival. In particular, emerging evidence suggests that agonists of cannabinoid receptors expressed by tumor cells may offer a novel strategy to treat cancer. Here, we review recent work that raises interest in the development and exploration of potent, nontoxic, and nonhabit forming cannabinoids for cancer therapy. [Cancer Res 2008;68(2):339–42] Cannabinoid Receptors:

"there is overwhelming evidence to suggest that cannabinoids can be explored as chemotherapeutic agents for the treatment of cancer. In view of the fair safety profile of most cannabinoids together with their antiproliferative action on tumor cells, clinical trials are required to determine whether cannabinoids could be used for the inhibition of tumor growth in a clinical setting. If this could be established, then one can hope that nontoxic, nonhabit forming cannabinoids could be developed as novel therapeutic agents for the treatment of cancer."

http://www.geocities.com/cannabinoidscience/Cancer.html
Cannabinoids as Anti-Cancer Agents

There is now abundant evidence that cannabinoids can inhibit tumor growth, in a variety of tumor types, both in vitro and in vivo (Guzman, 2003). The primary cannabinoids in cannabis, THC and cannabidiol, have also proven to be potent antioxidants (Hampson et al, 1998), which may reduce some types of cancers. Surprisingly, promising experimental results were first reported by Munson et al (1975) over a quarter or a century ago. Their results showed THC dose-dependent increase in survival time and inhibition of tumor growth in mice with Lewis lung adenocarcinoma, but were little pursued until recently, following the discovery of the cannabinoid receptors.

http://www.ncbi.nlm.nih.gov/pubmed/16250836

Mini Rev Med Chem. 2005 Oct;5(10):941-52. Links
Cannabinoids and cancer.
Kogan NM. Hebrew University, Pharmacy School, Department of Medicinal Chemistry and Natural Products, Israel.

Marijuana has been used in medicine for millennia, but it was not until 1964 that delta9-tetrahydrocannabinol (delta9-THC), its major psychoactive component, was isolated in pure form and its structure was elucidated. Shortly thereafter it was synthesized and became readily available.

However, it took another decade until the first report on its antineoplastic activity appeared. In 1975, Munson discovered that cannabinoids suppress Lewis lung carcinoma cell growth. The mechanism of this action was shown to be inhibition of DNA synthesis. Antiproliferative action on some other cancer cells was also found. In spite of the promising results from these early studies, further investigations in this area were not reported until a few years ago, when almost simultaneously two groups initiated research on the antiproliferative effects of cannabinoids on cancer cells: Di Marzo's group found that cannabinoids inhibit breast cancer cell proliferation, and Guzman's group found that cannabinoids inhibit the growth of C6 glioma cell. Other groups also started work in this field, and today, a wide array of cancer cell lines that are affected is known, and some mechanisms involved have been elucidated.

BEST

http://mct.aacrjournals.org/cgi/content/full/6/11/2921
http://safeaccess.ca/research/cbd_breast_cancer.pdf
Molecular Cancer Therapeutics 6, 2921, November 1, 2007.
Research Articles: Therapeutics, Targets, and Development

Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells. 

Sean D. McAllister, Rigel T. Christian, Maxx P. Horowitz, Amaia Garcia and Pierre-Yves Desprez California Pacific Medical Center, Research Institute, San Francisco, California

http://erc.endocrinology-journals.org/cgi/content/abstract/15/2/391
Endocrine-Related Cancer 15 (2) 391 -408  
Endocannabinoids in endocrine and related tumours
Maurizio Bifulco, Anna Maria Malfitano, Simona Pisanti and Chiara Laezza1
Dipartimento di Scienze Farmaceutiche, Università di Salerno, 84084 Fisciano (Salerno), Italy1 IEOS, CNR Napoli, 80131 Napoli, Italy

The ‘endocannabinoid system’, comprising the cannabinoid CB1 and CB2 receptors, their endogenous ligands, endocannabinoids and the enzymes that regulate their biosynthesis and degradation, has drawn a great deal of scientist attention during the last two decades. The endocannabinoid system is involved in a broad range of functions and in a growing number of physiopathological conditions. Indeed, recent evidence indicates that endocannabinoids influence the intracellular events controlling the proliferation of numerous types of endocrine and related cancer cells, thereby leading to both in vitro and in vivo antitumour effects. In particular, they are able to inhibit cell growth, invasion and metastasis of thyroid, breast and prostate tumours. The chief events of endocannabinoids in cancer cell proliferation are reported highlighting the correspondent signalling involved in tumour processes: regulation of adenylyl cyclase, cyclic AMP-protein kinase-A pathway and MEK-extracellular signal-regulated kinase signalling cascade.

"There is compelling evidence that endo/cannabinoids may regulate the growth and spread of normal and neoplastic tissues."

http://news.bbc.co.uk/1/hi/health/7098340.stm
Cannabis compound 'halts cancer' BBC NEws Nov 2007.
 
The CBD compound found in cannabis is non-toxic.
A compound found in cannabis may stop breast cancer spreading throughout the body, US scientists believe.  The California Pacific Medical Center Research Institute team are hopeful that cannabidiol or CBD could be a non-toxic alternative to chemotherapy. Unlike cannabis, CBD does not have any psychoactive properties so its use would not violate laws, Molecular Cancer Therapeutics reports. CBD works by blocking the activity of a gene called Id-1 which is believed to be responsible for the aggressive spread of cancer cells away from the original tumour site - a process called metastasis.

Cannabidiol is a Schedule I drug in the USA, despite having no psychoactive effects and no known abuse potential.

http://www.thenhf.com/articles/articles_659/articles_659.htm
Hemp Oil and Cancer By Mark Sircus Ac., OMD February 23, 2008 For the astonishing and true story of hemp, as told by Rick Simpson, the man who cured cancer with hemp oil. Please visit www.phoenixtears.ca Still sceptical? Rick Simpson introduces you to the people he has cured of cancer, via his youtube channel . If you never watch another youtube video in your life, you need to watch Rick Simpsons videos.

http://pr.cannazine.co.uk/20090205875/cannabis-news/cannabis-cancer-and-hemp-medicine.html
Cannabis, Cancer and Hemp Medicine by Rick Simpson

http://www.phoenixtearsmovie.com/
Rick  Simpson MOVIE anti cancer effects of hemp cannabis

http://video.google.com/videoplay?docid=-7331006790306000271
run from the cure-rick simpson entire movie

http://en.wikipedia.org/wiki/Removal_of_cannabis_from_Schedule_I_of_the_Controlled_Substances_Act
Cannabis and schedule I COntrolled Substance

http://en.wikipedia.org/wiki/Medicinal_marijuana
Cannabidiol Main article: cannabidiol
 
Cannabidiol structureCannabidiol, also known as "CBD", is a major constituent of medical cannabis. CBD represents up to 40% of extracts of the medical cannabis plant.[27] Cannabidiol relieves convulsion, inflammation, anxiety, nausea, and inhibits cancer cell growth.[28] Recent studies have shown cannabidiol to be as effective as atypical antipsychotics in treating schizophrenia.[29] In November 2007 it was reported that CBD reduces growth of aggressive human breast cancer cells in vitro and reduces their invasiveness. It thus represents the first non-toxic exogenous agent that can lead to down-regulation of tumor aggressiveness.[30][31] It is also a neuroprotective antioxidant.[32]

Feds Raid medical -marijuana distributors

http://www.huffingtonpost.com/2009/02/26/holder-vows-to-end-raids_n_170119.html
Obama's Attorney General, Holder, Vows To End Raids On Medical Marijuana Clubs

Two years before, the medical-marijuana movement had received a significant public-relations boost in the form of an elderly San Francisco General Hospital volunteer, Mary Jane Rathbun, who'd realized that marijuana eased the suffering of AIDS patients and allowed them to eat. Brownie Mary, as she became known, was arrested and charged with drug distribution for baking pot brownies and giving them to AIDS patients. Rathbun refused to take any plea bargain, demanding a jury trial and creating a media disaster for the district attorney. The charges were dropped, and Brownie Mary was free to help Peron open the Cannabis Buyers Club and advocate for Prop 215.

http://www.alternet.org/drugreporter/129383/
marijuana_milestone:_
no_more_raids_on_pot_dispensaries,_says_attorney_general/?page=2
Marijuana Milestone: No More Raids on Pot Dispensaries, Says Attorney General By Phillip S. Smith, Drug War Chronicle. Posted February 28, 2009.

Mainstream Medical Journals

http://jnci.oxfordjournals.org/cgi/content/abstract/djm268v1
 
Journal of the National Cancer Institute Advance Access published online on December 25, 2007 Inhibition of Cancer Cell Invasion by Cannabinoids via Increased Expression of Tissue Inhibitor of Matrix Metalloproteinases-1
Robert Ramer, Burkhard Hinz  Affiliation of authors: Institute of Toxicology and Pharmacology, University of Rostock, Rostock, Germany

http://www.informapharmascience.com/doi/abs/10.1517/13543780802691951
Expert Opinion on Investigational Drugs February 2009, Vol. 18, No. 2, Pages 125-133

Cannabinoids against pain. Efficacy and strategies to reduce psychoactivity: a clinical perspective    Matthias Karst‌† MD PhD & Sonja Wippermann‌

http://www.ncbi.nlm.nih.gov/pubmed/11106791
Chem Phys Lipids. 2000 Nov;108(1-2):191-209. Links
Endocannabinoids and fatty acid amides in cancer, inflammation and related disorders.De Petrocellis L, Melck D, Bisogno T, Di Marzo V.
Istituto di Cibernetica, Consiglio Nazionale delle Ricerche, Via Toiano 6, 80072 Arco Felice, Napoli, Italy.

The long history of the medicinal use of Cannabis sativa and, more recently, of its chemical constituents, the cannabinoids, suggests that also the endogenous ligands of cannabinoid receptors, the endocannabinoids, and, particularly, their derivatives may be used as therapeutic agents. Studies aimed at correlating the tissue and body fluid levels of endogenous cannabinoid-like molecules with pathological conditions have been started and may lead to identify those diseases that can be alleviated by drugs that either mimic or antagonize the action of these substances, or modulate their biosynthesis and degradation. Hints for the therapeutic applications of endocannabinoids, however, can be obtained also from our previous knowledge of marijuana medicinal properties. In this article, we discuss the anti-tumor and anti-inflammatory activity of: (1) the endocannabinoids anandamide (arachidonoylethanolamide) and 2-arachidonoyl glycerol; (2) the bioactive fatty acid amides palmitoylethanolamide and oleamide; and (3) some synthetic derivatives of these compounds, such as the N-acyl-vanillyl-amines. Furthermore, the possible role of cannabimimetic fatty acid derivatives in the pathological consequences of cancer and inflammation, such as cachexia, wasting syndrome, chronic pain and local vasodilation, will be examined.

http://www.ncbi.nlm.nih.gov/pubmed/19229996
Amphiregulin is a factor for resistance of glioma cells to cannabinoid-induced apoptosis.Lorente M, Carracedo A, Torres S, Natali F, Egia A, Hernández-Tiedra S, Salazar M, Blázquez C, Guzmán M, Velasco G. Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Madrid, Spain.

Gliomas, one of the most malignant forms of cancer, exhibit high resistance to conventional therapies. Identification of the molecular mechanisms responsible for this resistance is therefore of great interest to improve the efficacy of the treatments against these tumors. Delta9-Tetrahydrocannabinol (THC), the major active ingredient of marijuana, and other cannabinoids inhibit tumor growth in animal models of cancer, including glioma, an effect that relies, at least in part, on the ability of these compounds to induce apoptosis of tumor cells. By analyzing the gene expression profile of two sub-clones of C6 glioma cells with different sensitivity to cannabinoid-induced apoptosis, we found a subset of genes with a marked differential expression in the two sub-clones. Furthermore, we identified the epidermal growth factor receptor ligand amphiregulin as a candidate factor to mediate the resistance of glioma cells to cannabinoid treatment. Amphiregulin was highly overexpressed in the cannabinoid-resistant cell line, both in culture and in tumor xenografts. Moreover, in vivo silencing of amphiregulin rendered the resistant tumors xenografts sensitive to cannabinoid antitumoral action. Amphiregulin expression was associated with increased extracellular signal-regulated kinase (ERK) activation, which mediated the resistance to THC by blunting the expression of p8 and TRB3-two genes involved in cannabinoid-induced apoptosis of glioma cells. Our findings therefore identify Amphirregulin as a factor for resistance of glioma cells to THC-induced apoptosis and contribute to unraveling the molecular bases underlying the emerging notion that targeted inhibition of the EGFR pathway can improve the efficacy of antitumoral therapies. (c) 2009 Wiley-Liss, Inc.

http://www.ncbi.nlm.nih.gov/pubmed/19059457
Biochimie. 2008 Nov 27. Apoptosis induced in HepG2 cells by the synthetic cannabinoid WIN: Involvement of the transcription factor PPARgamma.Giuliano M, Pellerito O, Portanova P, Calvaruso G, Santulli A, De Blasio A, Vento R, Tesoriere G. Dipartimento di Scienze Biochimiche, Università di Palermo, Via del Vespro 129, 90127 Palermo, Italy.

It has recently been shown that cannabinoids induce growth inhibition and apoptosis in different tumour cell lines. In the current study, the effects of WIN 55,212-2 (WIN), a synthetic and potent cannabinoid receptor agonist, are investigated in hepatoma HepG2 cells and a possible signal transduction pathway is proposed. In these cells, WIN induces a clear apoptotic effect which was accompanied by up-regulation of the death-signalling factors Bax, Bcl-X(S), t-Bid and down-regulation of the survival factors survivin, phospho-AKT, Hsp72 and Bcl-2. Moreover, WIN-induced apoptosis is associated with JNK/p38 MAPK pathway activation and mitochondrial depolarisation demonstrated by a cytofluorimetric assay. The results also show that in HepG2 cells WIN markedly increases the level of the transcription factor PPARgamma in a dose- and time-dependent manner. The addition of the PPARgamma antagonists GW9662 and T0070907 significantly reduces the effects of the drug on both cell viability and the levels of survivin, phospho-AKT and phospho-BAD, suggesting that PPARgamma plays a key role in WIN-induced apoptosis. Altogether, the results seem to indicate a potential therapeutic role of WIN in hepatic cancer treatment.

http://www.ncbi.nlm.nih.gov/pubmed/19047095
Clin Cancer Res. 2008 Dec 1;14(23):7691-700.

Cannabinoid receptor activation induces apoptosis through tumor necrosis factor alpha-mediated ceramide de novo synthesis in colon cancer cells.

Cianchi F, Papucci L, Schiavone N, Lulli M, Magnelli L, Vinci MC, Messerini L, Manera C, Ronconi E, Romagnani P, Donnini M, Perigli G, Trallori G, Tanganelli E, Capaccioli S, Masini E.Department of Medical and Surgical Critical Care, University of Florence, Florence, Italy.

PURPOSE: Cannabinoids have been recently proposed as a new family of potential antitumor agents. The present study was undertaken to investigate the expression of the two cannabinoid receptors, CB1 and CB2, in colorectal cancer and to provide new insight into the molecular pathways underlying the apoptotic activity induced by their activation. EXPERIMENTAL DESIGN: Cannabinoid receptor expression was investigated in both human cancer specimens and in the DLD-1 and HT29 colon cancer cell lines. The effects of the CB1 agonist arachinodyl-2'-chloroethylamide and the CB2 agonist N-cyclopentyl-7-methyl-1-(2-morpholin-4-ylethyl)-1,8-naphthyridin-4(1H)-on-3-carboxamide (CB13) on tumor cell apoptosis and ceramide and tumor necrosis factor (TNF)-alpha production were evaluated. The knockdown of TNF-alpha mRNA was obtained with the use of selective small interfering RNA. RESULTS: We show that the CB1 receptor was mainly expressed in human normal colonic epithelium whereas tumor tissue was strongly positive for the CB2 receptor. The activation of the CB1 and, more efficiently, of the CB2 receptors induced apoptosis and increased ceramide levels in the DLD-1 and HT29 cells. Apoptosis was prevented by the pharmacologic inhibition of ceramide de novo synthesis. The CB2 agonist CB13 also reduced the growth of DLD-1 cells in a mouse model of colon cancer. The knockdown of TNF-alpha mRNA abrogated the ceramide increase and, therefore, the apoptotic effect induced by cannabinoid receptor activation. CONCLUSIONS: The present study shows that either CB1 or CB2 receptor activation induces apoptosis through ceramide de novo synthesis in colon cancer cells. Our data unveiled, for the first time, that TNF-alpha acts as a link between cannabinoid receptor activation and ceramide production.

Full text of both studies,
"Cannabinoids induce apoptosis of pancreatic tumor cells via endoplasmic reticulum stress- related genes" 

"Delta-9-tetrahydrocannabinol inhibits cell cycle progression in human breast
cancer cells through Cdc2 regulation" are available in the

July 1, 2006 issue of Cancer Research, available online at:
http://cancerres.aacrjournals.org/

http://www.ncbi.nlm.nih.gov/pubmed/616322
Cancer Biochem Biophys. 1977;2(2):51-4.Links
In vivo effects of cannabinoids on macromolecular biosynthesis in Lewis lung carcinomas.Friedman MA.

Cannabinoids represent a novel class of drugs active in increasing the life span mice carrying Lewis lung tumors and decreasing primary tumor size. In the present studies, the effects of delta9-THC, delta8-THC, and cannabidiol on tumor macromolecular biosynthesis were studied. These drugs inhibit thymidine-3H incorporation into DNA acutely, but did not inhibit leucine uptake into tumor protein. At 24 h after treatment, cannabinoids did not inhibit thymidine-3H incorporation into DNA, leucine-3H uptake into protein or cytidine-3H into RNA.

http://www.jackherer.com/chapters.html
The emperor wears no clothes, Jack Herer.

http://www.suntimes.com/news/huntley/1456881,CST-EDT-hunt03.article
Legalizing marijuana makes sense, cents March 3, 2009 BY STEVE HUNTLEY Chicago Sun TImes

California Assemblyman Tom Ammiano of San Francisco, says licensing and taxing legal marijuana production and sales would earn California $1.3 billion a year. His bill would legalize marijuana possession and use for adults 21 or older, license commercial farming of it and tax it at $50 an ounce.

A like number of states have humane laws allowing marijuana smoking by people with chronic or terminal diseases to combat pain and nausea. New Jersey could become the 14th since its state senate has approved a medicinal bill.

 the Obama administration says it will not continue the Bush administration's policy of having U.S. Drug Enforcement Administration officers raid medical marijuana dispensaries. That reflects the simple fact a huge part of America thinks a medical ban is cruel and prohibition in general is silly.

A 2005 study endorsed by the late Milton Friedman and 530 other economists found legal regulation would save the nation $7.7 billion in enforcement costs and bring in up to $6.2 billion in taxes

http://www.suntimes.com/news/blogentries/index.html?bbPostId=Cz9ojeT0Jcr1WBD0O7q71iA1vB5TB1K4GpJeRCzE3VN5b4Uruq
&bbParentWidgetId=B8k88rWwXopuz5STgLeVwBLu
Marijuana, fully outlawed in 1970 by the Controlled Substances Act of 1970, has been the largest producer of drug related crimes in the past 40 years. Recently, states such as California, Nevada, and Maryland have legalized medical marijuana if a patient can prevent substantial need

Here is the list of thirteen states that allow the sale, distribution and use of marijuana for limited medical purposes:  Alaska  California  Colorado  Hawaii  Maine  Michigan  Montana  Nevada  New  Mexico  Oregon  Rhode Island  Vermont  Washington

http://www.associatedcontent.com/article/
1524315/california_state_assembly_considering.html?cat=8

California State Assembly Considering Marijuana Legalization
March 03, 2009 by P. Trembeth   P. Trembeth  Published Content: 5 Total Views: 845 Favorited By: 1 CPs Full Profile | Subscribe | Add to Favorites Recommend (2)Single page Font SizeRead comments (3) Could Widespread Marijuana Legalization Be Just Around the Corner?

http://newmexicoindependent.com/20182/feds-make-medical-marijuana-de-facto-legal
Obama administration makes medical marijuana de facto legal
 By Marjorie Childress 3/2/09 9:28 AM  U.S. Attorney General Eric Holder announced last week that the Drug Enforcement Administration would stop shutting down state-approved medical marijuana dispensaries,

http://www.medboardwatch.com/wb/pages/therapeutic-effects.php
Russo and Grotenhermen report:  Review of Therapeutic Effects of cannabis

Relieves Nausea and vomiting, anorexia, and weight loss associated with chemotherapy or HIV/AIDS. Relieves spasticity, neurogenic pain, asthma, glaucoma.

http://en.wikipedia.org/wiki/Cannabis_(drug)#cite_note-60
Humans have been consuming cannabis since prehistory,[5] although in the 20th century there was a rise in its use for recreational, religious or spiritual, and medicinal purposes. It is estimated that about four percent of the world's adult population (162 million) use cannabis annually and 0.6 percent (22.5 million) daily.[6] The possession, use, or sale of psychoactive cannabis products became illegal in most parts of the world in the early 20th century.

http://www.iht.com/articles/2006/10/24/news/dems.php
Barack Obama, asked about drug history, admits he inhaled
By Katharine Q. Seelye  OCTOBER 25, 2006

http://en.wikipedia.org/wiki/Medical_cannabis
the medical use of cannabis is legal only in a limited number of territories, including Canada, Belgium, Austria, the Netherlands, Spain, Israel, Finland, and 14 U.S. states.

Cannabis has been used for medicinal purposes for approximately 4,000 years in Ancient China, Egypt. India, ancient Greeks.

Medical Cannabis was used extensively in the medieval Islamic World 8th century to 18th century.

An advertisement for cannabis americana distributed by a pharmacist in New York in 1917.Cannabis as a medicine became common throughout much of the world by the 19th century. It was used as the primary pain reliever until the invention of aspirin. The United States banned cannabis in a federal law, the 1937 Marijuana Tax Act. Historian Jacob Appel has argued that the medicinal marijuana movement bears striking similarities to the medicinal beer movement of the 1920s. [26] Both efforts attempted to muster medical expertise in the face of a national Prohibition and both pitted the rights of physicians against the authority of the federal government.

Cannabidiol, also known as "CBD", is a major constituent of medical cannabis. CBD represents up to 40% of extracts of the medical cannabis plant.[27] Cannabidiol relieves convulsion, inflammation, anxiety, nausea, and inhibits cancer cell growth.[28] Recent studies have shown cannabidiol to be as effective as atypical antipsychotics in treating schizophrenia.[29] In November 2007 it was reported that CBD reduces growth of aggressive human breast cancer cells in vitro and reduces their invasiveness. It thus represents the first non-toxic exogenous agent that can lead to down-regulation of tumor aggressiveness.[30][31] It is also a neuroprotective antioxidant.[32]

___________________________________

http://www.spandidos-publications.com/or/article.jsp?article_id=or_17_4_813

Endocannabinoids as emerging suppressors of angiogenesis and tumor invasion (Review) MAURIZIO BIFULCO1, CHIARA LAEZZA2, PATRIZIA GAZZERRO1 and FRANCESCA PENTIMALLI3 1Dipartimento di Scienze Farmaceutiche, Università di Salerno, Via Ponte Don Melillo, 84084 Fisciano (SA);

2Istituto di Endocrinologia ed Oncologia Sperimentale I.E.O.S., CNR; 3Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli ‘Federico II’, Via Pansini 5, 80131 Napoli, Italy Received August 7, 2006; Accepted September 25, 2006

The ‘endocannabinoid system’ is involved in a broad range of functions and in a
growing number of pathological conditions. There is increasing evidence that endocannabinoids are able to inhibit cancer cell growth in culture as well as in animal models. Most work has focused on the role of endocannabinoids in regulating tumor cell growth and apoptosis and ongoing research is addressed
to further dissect the precise mechanisms of cannabinoid antitumor action.

However, endocannabinoids are now emerging as suppressors of angiogenesis and tumor spreading since they have been reported to inhibit angiogenesis, cell
migration and metastasis in different types of cancer, pointing to a potential role of the endocannabinoid system as a target for a therapeutic approach of such malignant diseases. The potential use of cannabinoids to retard tumor growth and spreading is even more appealing considering that they show
a good safety profile, regarding toxicity, and are already used in cancer patients as palliatives to stimulate appetite and to prevent devastating effects such as nausea, vomiting and pain.

Therefore, even if further basic and preclinical research are required to clarify the molecular mechanisms of cannabinoids action in cancer and to test their effectiveness in patients, targeting the endocannabinoid system represents a very promising therapeutic approach for the treatment of different
types of cancer. Cannabinoids have the great advantage of being well tolerated, regarding toxicity, and of having such remarkable palliative effects in cancer patients that their use has already been approved for clinical practice (5).

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=9653194
Proc Natl Acad Sci U S A. 1998 July 7; 95(14): 8375–8380.  PMCID: PMC20983

The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation

Luciano De Petrocellis,*† Dominique Melck,*‡ Antonella Palmisano,§ Tiziana Bisogno,‡ Chiara Laezza,¶ Maurizio Bifulco,¶ and Vincenzo Di Marzo‡‖
†Istituto di Cibernetica and ‡Istituto per la Chimica di Molecole di Interesse Biologico (affiliated with the National Institute for the Chemistry of Biological Systems, Consiglio Nazionale delle Ricerche), Consiglio Nazionale delle Ricerche, Via Toiano 6, 80072 Arco Felice, Naples, Italy;

The anti-proliferative effect of anandamide was not due to toxicity or to apoptosis of cells but was accompanied by a reduction of cells in the S phase of the cell cycle.

In conclusion, we have shown that anandamide is a potent and selective inhibitor of the proliferation of HBC cells and that activation of a cannabinoid receptor, whose occurrence had never been described previously in these cells, is at least in part responsible for this effect.

http://en.wikipedia.org/wiki/Anandamide
Anandamide, also known as N-arachidonoylethanolamine or AEA, is an endogenous cannabinoid neurotransmitter found in animal and human organs, especially in the brain. It was isolated and its structure was first described by Czech analytical chemist Lumír Ondřej Hanuš and American molecular pharmacologist William Anthony Devane in the Laboratory of Raphael Mechoulam, at the Hebrew University in Jerusalem, Israel in 1992. The name is taken from the Sanskrit word ananda, which means "bliss, delight", and amide.[1][2] It is degraded by the fatty acid amide hydrolase (FAAH) enzyme which converts anandamide into ethanolamine and arachidonic acid. As such, inhibitors of FAAH lead to elevated anandamide levels and are being pursued for therapeutic use.

A study published in 1998 shows that anandamide inhibits human breast cancer cell proliferation.[14]

Paracetamol, or acetaminophen (in the U.S.A.) functions as a FAAH inhibitor. Subsequently, anandamide levels in the body and brain are elevated. This action may be partially or fully responsible for the analgesic effects of acetaminophen.

http://www.scielo.br/pdf/bjmbr/v39n4/6164.pdf
Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug
BCraanznilaiabnid Jiooul ransa al no fa Mntiepdsiyccahl oatnicd dBriuoglogical Research (2006) 39: 421-429

1Departamento de Farmacologia,2Departamento de Neurologia, Psiquiatria e Psicologia Médica,
Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brasil

Abstract
A high dose of Δ9-tetrahydrocannabinol, the main Cannabis sativa
(cannabis) component, induces anxiety and psychotic-like symptoms
in healthy volunteers. These effects of Δ9-tetrahydrocannabinol are
significantly reduced by cannabidiol (CBD), a cannabis constituent
which is devoid of the typical effects of the plant. This observation led
us to suspect that CBD could have anxiolytic and/or antipsychotic
actions. Studies in animal models and in healthy volunteers clearly
suggest an anxiolytic-like effect of CBD. The antipsychotic-like
properties of CBD have been investigated in animal models using
behavioral and neurochemical techniques which suggested that CBD
has a pharmacological profile similar to that of atypical antipsychotic
drugs. The results of two studies on healthy volunteers using perception
of binocular depth inversion and ketamine-induced psychotic
symptoms supported the proposal of the antipsychotic-like properties
of CBD. In addition, open case reports of schizophrenic patients
treated with CBD and a preliminary report of a controlled clinical trial
comparing CBD with an atypical antipsychotic drug have confirmed
that this cannabinoid can be a safe and well-tolerated alternative
treatment for schizophrenia.

http://jpet.aspetjournals.org/cgi/content/full/318/3/1375
Antitumor Activity of Plant Cannabinoids with Emphasis on the Effect of Cannabidiol on Human Breast Carcinoma
Alessia Ligresti, Aniello Schiano Moriello, Katarzyna Starowicz, Isabel Matias, Simona Pisanti, Luciano De Petrocellis, Chiara Laezza, Giuseppe Portella, Maurizio Bifulco, and Vincenzo Di Marzo
Endocannabinoid Research Group, Istituto di Chimica Biomolecolare (A.L., A.S.M., K.S., I.M., V.D.M.), and Istituto di Cibernetica (A.S.M., L.D.P.), Consiglio Nazionale delle Ricerche Pozzuoli, Italy; Dipartimento di Biologia e Patologia Cellulare e Molecolare "L. Califano", Università di Napoli "Federico II", Napoli, Italy (S.P., C.L., G.P., M.B.); and Dipartimento di Scienze Farmaceutiche, Università degli Studi di Salerno, Fisciano, Italy (S.P., M.B.)

The isolation of 9-tetrahydrocannabinol (THC), the main psychoactive component of Cannabis (Gaoni and Mechoulam, 1964),
cannabidiol is nonpsychotropic

Indeed, C. sativa contains at least 400 chemical components, of which 66 have been identified to belong to the class of the cannabinoids
To date, cannabinoids have been successfully used in the treatment of nausea and vomiting (for review, see Robson, 2005), two common side effects that accompany chemotherapy in cancer patients. Nevertheless, the use of cannabinoids in oncology might be somehow underestimated since increasing evidence exist that plant, synthetic, and endogenous cannabinoids (endocannabinoids) are able to exert a growth-inhibitory action on various cancer cell types.

9-Tetrahydrocannabinol (THC) exhibits antitumor effects on various cancer cell types, but its use in chemotherapy is limited by its psychotropic activity. We investigated the antitumor activities of other plant cannabinoids, i.e., cannabidiol, cannabigerol, cannabichromene, cannabidiol acid and THC acid, and assessed whether there is any advantage in using Cannabis extracts (enriched in either cannabidiol or THC) over pure cannabinoids. Results obtained in a panel of tumor cell lines clearly indicate that, of the five natural compounds tested, cannabidiol is the most potent inhibitor of cancer cell growth (IC50 between 6.0 and 10.6 µM), with significantly lower potency in noncancer cells. The cannabidiol-rich extract was equipotent to cannabidiol, whereas cannabigerol and cannabichromene followed in the rank of potency. Both cannabidiol and the cannabidiol-rich extract inhibited the growth of xenograft tumors obtained by s.c. injection into athymic mice of human MDA-MB-231 breast carcinoma or rat v-K-ras-transformed thyroid epithelial cells and reduced lung metastases deriving from intrapaw injection of MDA-MB-231 cells. Judging from several experiments on its possible cellular and molecular mechanisms of action, we propose that cannabidiol lacks a unique mode of action in the cell lines investigated. At least for MDA-MB-231 cells, however, our experiments indicate that cannabidiol effect is due to its capability of inducing apoptosis via: direct or indirect activation of cannabinoid CB2 and vanilloid transient receptor potential vanilloid type-1 receptors and cannabinoid/vanilloid receptor-independent elevation of intracellular Ca2+ and reactive oxygen species. Our data support the further testing of cannabidiol and cannabidiol-rich extracts for the potential treatment of cancer.

In conclusion, our data indicate that cannabidiol, and possibly Cannabis extracts enriched in this natural cannabinoid, represent a promising nonpsychoactive antineoplastic strategy. In particular, for a highly malignant human breast carcinoma cell line, we have shown here that cannabidiol and a cannabidiol-rich extract counteract cell growth both in vivo and in vitro as well as tumor metastasis in vivo. Cannabidiol exerts its effects on these cells through a combination of mechanisms that include either direct or indirect activation of CB2 and TRPV1 receptors and induction of oxidative stress, all contributing to induce apoptosis.

Mice treated with either pure cannabidiol or the cannabidiol-rich extract exhibited significantly smaller tumors in comparison with control mice. A strong and statistically significant antitumor effect was observed

http://en.wikipedia.org/wiki/Cannabinoid_receptor
Synthetic Δ9-THC is prescribed today under the generic name Dronabinol, to treat vomiting and for enhancement of appetite, mainly in AIDS patients.

http://en.wikipedia.org/wiki/American_Medical_Marijuana_Association
The American Medical Marijuana Association (AMMA) is an organization formed to promote and protect the legal access to medical marijuana.

http://americanmarijuana.org/
The American Medical Marijuana Association

http://americanmarijuana.org/Guzman-Cancer.pdf
CANNABINOIDS: POTENTIAL ANTICANCER AGENTS Manuel Guzmán
Cannabinoids — the active components of Cannabis sativa and their derivatives — exert palliative effects in cancer patients by preventing nausea, vomiting and pain and by stimulating appetite. In addition, these compounds have been shown to inhibit the growth of tumour cells in culture and animal models by modulating key cell-signalling pathways. Cannabinoids are usually
well tolerated, and do not produce the generalized toxic effects of conventional chemotherapies. So, could cannabinoids be used to develop new anticancer therapies?

http://videos.med.wisc.edu/videoInfo.php?videoid=1107
Cannabis and Cannabinoids in the 21st Century: Medical Marijuana
David Bearman, MD, a Santa Barbara, California physician and surgeon with Wisconsin roots, speaks on "Cannabis and Cannabinoids in 21st Century Medicine: Medical Marijuana in the Clinic".

Bearman is one of the leading physicians in the U.S. in the field of medical marijuana.

Major Uses of Cannabis:
pain
sleep insomnia
nausea
arthritis-
fibromyalgia , resless leg, compelx pain.

ADD/ADHD
Migraine headace-William OSler textbook
Seizures
Glaucoma
diabetic peripheral neuropathy
Crohn's Disease- decrease reliance on steroids, more solid stools, less abdominal pain.
Depression-
Cyclical Vomiting Syndrome

mental health issues
anxiety
depression
OCD
Tourettes
Bi-Polar Disorder
Panic Attacks
Migraine headaches....marijuana cookie prevented migraines
Patient with back surgery.  Went scuba diving. 
Became a quad for 9 months and then a para. Pain from T10 on down.
Cannabis relieved pain.
PTSD Iraq War Vets- Decrease in opiate use.

Safety MArinol APproved by FDA, upgraded to schedule three drug.
Sativex sold in cancada since 2005
Tincture of cannabis...approved for phase three clinical trial.
483 chemicals in cannabis.

Cannabinoid system is the Largest neuritransmitter system of the brain. moderates sensory input.  There is an excesive amount of dopamin transporter.  Endocannabinoid system causes dopamine to come back to the neuron and depolarizes and makes it more difficult.  Controls anger impulses.

CBD- Cannabidiol

http://finola.com/CBDreview2008.pdf
Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action  Antonio Waldo Zuardi1 Department of Neurology, Psychiatry and Medical Psychology, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP),

CBD- 1963 its exact chemical structure was elucidated by Mechoulam and Shvo. The interest in studies about cannabis was renewed in the early 1990’s, by the description and cloning of specific receptors for the cannabinoids in the nervous system and the subsequent isolation of anandamide, an endogenous cannabinoid.



Jeffrey Dach MD
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