Cancer and Cannabis Research

[Sequoiacrone]

The Author 2007. Published by Oxford University Press.
ARTICLES


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
Correspondence to: Burkhard Hinz, PhD, Institute of Toxicology and Pharmacology, University of Rostock, Schillingallee 70, Rostock D-18057, Germany (e-mail: burkhard.hinz@med.uni-rostock.de (burkhard.hinz@med.uni-rostock.de) ). Background: Cannabinoids, in addition to having palliative benefits in cancer therapy, have been associated with anticarcinogenic effects. Although the antiproliferative activities of cannabinoids have been intensively investigated, little is known about their effects on tumor invasion.

for more information:
http://jnci.oxfordjournals.org/cgi/content/abstract/djm268v1

(I cannot resist posting their conclusion, as I realize, being a cancer survivor for 25 years, that HOPE will give one strength to fight this battle.~Sequoia)

Conclusion: Increased expression of TIMP-1 mediates an anti-invasive effect of cannabinoids. Cannabinoids may therefore offer a therapeutic option in the treatment of highly invasive cancers.

[Sequoiacrone]

Friday, August 26, 2005
Biotech

High times: Cal Pacific tests marijuana's cancer-killing potential


San Francisco Business Times - by Daniel S. Levine (http://www.bizjournals.com/search/results.html?Ntt=%22Daniel%20S.%20Levine%22&Ntk=All&Ntx=mode matchallpartial)



If you thought marijuana kills brain cells, it may be you only have half of the story.
New research being conducted at the California Pacific Medical Center (http://www.bizjournals.com/sanfrancisco/related_content.html?topic=California%20Pacific%20 Medical%20Center) in San Francisco finds that THC, the substance that puts the "wowwie" in Maui Wowwie, killed brain tumor cells without harming healthy brain cells in a lab dish.
Much of the discussion around the medical benefits of marijuana has focused on such things as its ability to treat nausea and stimulate the appetite, reduce pressure within the eye related to glaucoma and treat muscle spasms and pain related to multiple sclerosis. There is, however, a growing interest among scientists in the possible anti-cancer properties of THC and other so-called cannabinoids found in marijuana.
Yes, it's not just college kids experimenting with marijuana anymore.
Though tests since the 1970s have indicated anti-cancer properties of THC, it has only been in recent years that there have been concerted efforts to test its anti-cancer potential. Much of this work has been conducted in Spain around brain cancer and in Italy around breast cancer. Some, though, is taking place in San Francisco.
Researchers at California Pacific Medical Center, in a study published this month in the Journal of Neuro-Oncology, found that THC decreases cell proliferation and increases cell death of glial cancer cells while having no significant impact on normal glial cells. Glial cells support and protect neurons within the brain.

for the rest of the story....

http://www.bizjournals.com/sanfrancisco/stories/2005/08/29/newscolumn6.html

[Sequoiacrone]

Breakthrough Discovered in Medical Marijuana Cancer Treatment

Tim King Salem-News.com
Researchers learned that cannabinoids have been associated with anti-carcinogenic effects, which are responsible in preventing or delaying the development of cancer.




(SALEM, Ore.) - A new study reveals that Medical Marijuana can be an effective treatment for cancer, that is the word announced by doctors in Germany who concluded that this clarification of the mechanism of cannabinoid action may help investigators to further explore their therapeutic benefit.
The medical article was originally published in the Journal of the National Cancer Institute Advance Access and online on December 25th 2007.
Cancer cells that were treated with combinations of cannabinoids, antagonists of cannabinoid receptors, and small interfering ribo nucleic acid or 'siRNA' to tissue inhibitor of matrix metalloproteinases-1 (TIMP-1) were assessed for invasiveness, protein expression, and activation of signal transduction pathways.
The biggest contribution of this breakthrough discovery, is that the expression of TIMP-1 was shown to be stimulated by cannabinoid receptor activation and to mediate the anti-invasive effect of cannabinoids.
In other words, they learned that treatment with cannabinoids, one of the active ingredients of the medicinal side of marijuana, has been shown to reduce the invasiveness of cancer cells. Prior to now the cellular mechanisms underlying this effect were unclear and the relevance of the findings to the behavior of tumor cells in vivo remains to be determined.
It is already known that marijuana can stimulate the appetite of patients, but researchers have learned that cannabinoids, in addition to having palliative benefits in cancer therapy, have been associated with anti-carcinogenic effects, which are responsible in preventing or delaying the development of cancer.
"Although the anti-proliferative activities of cannabinoids have been intensively investigated, little is known about their effects on tumor invasion," the article stated.
Method
In this now completed round of research, Matrigel-coated and uncoated Boyden chambers were used to quantify invasiveness and migration, respectively, of human cervical cancer 'HeLa' cells that had been treated with cannabinoids.
The stable anandamide analog R(+)-methanandamide 'MA' and the phytocannabinoid 9-tetrahydrocannabinol 'THC' in the presence or absence of antagonists of the CB1 or CB2 cannabinoid receptors or of transient receptor potential vanilloid 1 (TRPV1) or inhibitors of p38 or p42/44 mitogen–activated protein kinase (MAPK) pathways.
A method known as 'reverse transcriptase–polymerase chain reaction' and immunoblotting were used to assess the influence of cannabinoids on the expression of matrix metalloproteinases and endogenous tissue inhibitors. The role of TIMP-1 in the anti-invasive action of cannabinoids was analyzed by transfecting HeLa, human cervical carcinoma, or human lung carcinoma cells cells with siRNA targeting TIMP-1.
They say all statistical tests were two-sided.
Results
Without modifying migration, MA and THC caused a time and concentration-dependent suppression of HeLa cell invasion through Matrigel that was accompanied by increased expression of TIMP-1.
At the lowest concentrations tested, MA and THC led to a decrease in cell invasion.
"The stimulation of TIMP-1 expression and suppression of cell invasion were reversed by pretreatment of cells with antagonists to CB1 or CB2 receptors, with inhibitors of MAPKs, or, in the case of MA, with an antagonist to TRPV1. Knockdown of cannabinoid-induced TIMP-1 expression by siRNA led to a reversal of the cannabinoid-elicited decrease in tumor cell invasiveness in HeLa, A549, and C33A cells."
The researchers concluded that increased expression of TIMP-1 mediates an anti-invasive effect of cannabinoids. That means that in our future, cannabinoids may offer a therapeutic option in the treatment of highly invasive cancers.

For the rest of the related story...

http://www.salem-news.com/articles/january112008/cancer_treatment_11008.php

[Sequoiacrone]

Science News



(http://www.sciencedaily.com/releases/2007/04/070417193338.htm#)


Marijuana Cuts Lung Cancer Tumor Growth In Half, Study Shows



ScienceDaily (Apr. 17, 2007) — The active ingredient in marijuana cuts tumor growth in common lung cancer in half and significantly reduces the ability of the cancer to spread, say researchers at Harvard University who tested the chemical in both lab and mouse studies.

They say this is the first set of experiments to show that the compound, Delta-tetrahydrocannabinol (THC), inhibits EGF-induced growth and migration in epidermal growth factor receptor (EGFR) expressing non-small cell lung cancer cell lines. Lung cancers that over-express EGFR are usually highly aggressive and resistant to chemotherapy.
THC that targets cannabinoid receptors CB1 and CB2 is similar in function to endocannabinoids, which are cannabinoids that are naturally produced in the body and activate these receptors. The researchers suggest that THC or other designer agents that activate these receptors might be used in a targeted fashion to treat lung cancer.
"The beauty of this study is that we are showing that a substance of abuse, if used prudently, may offer a new road to therapy against lung cancer," said Anju Preet, Ph.D., a researcher in the Division of Experimental Medicine.
Acting through cannabinoid receptors CB1 and CB2, endocannabinoids (as well as THC) are thought to play a role in variety of biological functions, including pain and anxiety control, and inflammation. Although a medical derivative of THC, known as Marinol, has been approved for use as an appetite stimulant for cancer patients, and a small number of U.S. states allow use of medical marijuana to treat the same side effect, few studies have shown that THC might have anti-tumor activity, Preet says. The only clinical trial testing THC as a treatment against cancer growth was a recently completed British pilot study in human glioblastoma.
In the present study, the researchers first demonstrated that two different lung cancer cell lines as well as patient lung tumor samples express CB1 and CB2, and that non-toxic doses of THC inhibited growth and spread in the cell lines. "When the cells are pretreated with THC, they have less EGFR stimulated invasion as measured by various in-vitro assays," Preet said.
Then, for three weeks, researchers injected standard doses of THC into mice that had been implanted with human lung cancer cells, and found that tumors were reduced in size and weight by about 50 percent in treated animals compared to a control group. There was also about a 60 percent reduction in cancer lesions on the lungs in these mice as well as a significant reduction in protein markers associated with cancer progression, Preet says.

For the rest of this article...
http://www.sciencedaily.com/releases/2007/04/070417193338.htm

[Sequoiacrone]

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.)
http://jpet.aspetjournals.org/math/Delta.gif9-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 ...


for the entire article see here:
http://jpet.aspetjournals.org/cgi/content/abstract/318/3/1375

[Sequoiacrone]

Copyright © 2000 by The Endocrine Society
ARTICLES

Suppression of Nerve Growth Factor Trk Receptors and Prolactin Receptors by Endocannabinoids Leads to Inhibition of Human Breast and Prostate Cancer Cell Proliferation1 (http://endo.endojournals.org/cgi/content/full/141/1/118#FN1)

Dominique Melck, Luciano De Petrocellis, Pierangelo Orlando, Tiziana Bisogno, Chiara Laezza, Maurizio Bifulco and Vincenzo Di Marzo

Istituto per la Chimica di Molecole di Interesse Biologico (D.M., T.B., V.D.M.), Istituto di Cibernetica (L.D.P.), and Istituto di Biochimica delle Proteine ed Enzimologia (P.O.), Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA); and Centro di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche, and Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli Federico II (C.L., M.B.), 80131 Naples, Italy
Address all correspondence and requests for reprints to: Dr. Vincenzo Di Marzo, Istituto per la Chimica di Molecole di Interesse Biologico, Consiglio Nazionale delle Ricerche, 80072 Arco Felice (NA), Italy. E-mail: vdm@trinc.icmib.na.cnr.it. (vdm@trinc.icmib.na.cnr.it)

See the full article:
http://endo.endojournals.org/cgi/content/abstract/141/1/118

[Sequoiacrone]

Science: Cannabidiol inhibits tumour growth in leukaemia and breast cancer in animal studies


Italian researchers investigated the anti-tumour effects of five natural cannabinoids of the cannabis plant (cannabidiol, cannabigerol, cannabichromene, cannabidiol-acid and THC-acid) in breast cancer. Cannabidiol (CBD) was the most potent cannabinoid in inhibiting the growth of human breast cancer cells that had been injected under the skin of mice. CBD also reduced lung metastases deriving from human breast cancer cells that had been injected into the paws of the animals.
Researchers found that the anti-tumour effects of CBD were caused by induction of apoptosis (programmed cell death). They concluded that their data "support the further testing of cannabidiol and cannabidiol-rich extracts for the potential treatment of cancer."
These observations are supported by investigations of US scientists who found out that exposure of leukaemia cells to CBD led to a reduction in cell viability and induction of apoptosis. In living animals CBD caused a reduction in number of leukaemia cells. The scientists noted that CBD "may be a novel and highly selective treatment for leukemia."
(Sources: Ligresti A, Schiano Moriello A, Starowicz K, Matias I, Pisanti S, De Petrocellis L, Laezza C, Portella G, Bifulco M, Di Marzo V. Anti-tumor activity of plant cannabinoids with emphasis on the effect of cannabidiol on human breast carcinoma. J Pharmacol Exp Ther. 2006 May 25; [electronic publication ahead of print]; McKallip RJ, Jia W, Schlomer J, Warren JW, Nagarkatti PS, Nagarkatti M. Cannabidiol-induced apoptosis in human leukemia cells: A novel role of cannabidiol in the regulation of p22phox and Nox4 expression. Mol Pharmacol. 2006 Jun 5; [electronic publication ahead of print])

http://www.cannabis-med.org/english/bulletin/ww_en_db_cannabis_artikel.php?id=220#2

Source: IACM Bulletin
freely distributed

[Sequoiacrone]

The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells: a possible role for cyclooxygenase 2

H A Patsos1, D J Hicks1</STRONG>, R R H Dobson1</STRONG>, A Greenhough1</STRONG>, N Woodman1</STRONG>, J D Lane2</STRONG>, A C Williams1</STRONG>, C Paraskeva1 </STRONG>

1 Cancer Research UK Colorectal Tumour Biology Group, Department of Pathology and Microbiology, School of Medical Sciences, University of Bristol, Bristol, UK
2 Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol, UK

Correspondence to:
Correspondence to:
Professor C Paraskeva
Cancer Research UK Colorectal Tumour Biology Group, Department of Pathology and Microbiology, School of Medical Sciences, University Walk, University of Bristol, Bristol BS8 1TD, UK; C.Paraskeva@bristol.ac.uk (C.Paraskeva@bristol.ac.uk)


ABSTRACT
Background and aims: Cyclooxygenase 2 (COX-2) is upregulated in most colorectal cancers and is responsible for metabolism of the endogenous cannabinoid, anandamide, into prostaglandin-ethanolamides (PG-EAs). The aims of this study were to determine whether anandamide and PG-EAs induce cell death in colorectal carcinoma (CRC) cells, and whether high levels of COX-2 in CRC cells could be utilised for their specific targeting for cell death by anandamide. Methods: We determined the effect of anandamide on human CRC cell growth by measuring cell growth and cell death, whether this was ....

read more here:
http://gut.bmj.com/cgi/content/abstract/54/12/1741

[Sequoiacrone]

Title[Dronabinol for supportive therapy in patients with malignant melanoma and liver metastases.] [Article in German]Author(s)Zutt M, Hanssle H, Emmert S, Neumann C, Kretschmer L.
Journal, Volume, IssueHautarzt 2006;57(5):423-7.

Major outcome(s)A significant increase in appetite and decrease in nausea in most patients.

IndicationNausea/vomiting;Appetite loss/weight loss;Cancer;Cancer chemotherapy
Abstract:
MedicationDelta-9-THCBACKGROUND: Loss of appetite and nausea can reduce the quality of life of patients with malignant melanoma and liver metastases. Often established antiemetic drugs fail to bring relief. Tetrahydrocannabinol (THC, Marinol (TM)), which is the active agent of Indian hemp, has been used successfully in this situation for other malignant tumors.
PATIENTS AND METHODS:
We treated 7 patients with hematogenous metastatic melanoma and liver metastases suffering from extensive loss of appetite and nausea supportively with dronabinol (Marinol((R))). All of these patients had previously received standard antiemetic therapy without adequate relief. Dronabinol is a synthetic Delta-tetrahydrocannabinol. The drug was administered in capsule form.
We evaluated the palliative effects of dronabinol with a special patient evaluation form, which was filled out at the beginning of the therapy and again after 4 weeks.
RESULTS:
The majority of patients described a significant increase in appetite and decrease in nausea. These effects remained for some weeks, but then decreased as metastases progressed and the general condition worsened. All of the patients experienced slight to moderate dizziness, but it was not sufficiently troubling to cause interruption or termination of therapy.
CONCLUSION:
Loss of appetite and nausea due to liver metastases of malignant melanoma can be treated in individual cases supportively with Dronabinol.
Route(s)OralDose(s)
variableDuration (days)
Participants7 patients with hematogenous metastatic melanoma
DesignOpen studyType of publicationMedical journalAddress of author(s)Hautklinik und Poliklinik der Georg-August-Universitat Gottingen, Germany
Full text available

Source: http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=180

[Sequoiacrone]

Cannabis Marijuana Reduces Skin Cancer


Cannabalm (anti-cancer) Ocean of Lotion (http://www.onlinepot.org/medical/cannabalm.htm) (http://www.onlinepot.org/medical/cannabalm.htm)

Inhibition of skin tumor growth and angiogenesis
in vivo by activation of cannabinoid receptors


M. Llanos Casanova1, Cristina Blázquez2, Jesús Martínez-Palacio1, Concepción Villanueva3, M. Jesús Fernández-Aceñero3, John W. Huffman4, José L. Jorcano1 and Manuel Guzmán2

1 Project on Cellular and Molecular Biology and Gene Therapy, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas, Madrid, Spain 2 Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, Madrid, Spain 3 Department of Pathology, Hospital General de Móstoles, Madrid, Spain 4 Department of Chemistry, Clemson University, Clemson, South Carolina, USA
Address correspondence to: Manuel Guzmán, Department of Biochemistry and Molecular Biology I, School of Biology, Complutense University, 28040 Madrid, Spain. Phone: 34-913944668; Fax: 34-913944672; E-mail: mgp@bbm1.ucm.es (mgp@bbm1.ucm.es).
Received for publication June 7, 2002, and accepted in revised form November 19, 2002.

Abstract
Nonmelanoma skin cancer is one of the most common malignancies in humans. Different therapeutic strategies for the treatment of these tumors are currently being investigated. Given the growth-inhibiting effects of cannabinoids on gliomas and the wide tissue distribution of the two subtypes of cannabinoid receptors (CB1 and CB2), we studied the potential utility of these compounds in anti–skin tumor therapy. Here we show that the CB1 and the CB2 receptor are expressed in normal skin and skin tumors of mice and humans. In cell culture experiments pharmacological activation of cannabinoid receptors induced the apoptotic death of tumorigenic epidermal cells, whereas the viability of nontransformed epidermal cells remained unaffected. Local administration of the mixed CB1/CB2 agonist WIN-55,212-2 or the selective CB2 agonist JWH-133 induced a considerable growth inhibition of malignant tumors generated by inoculation of epidermal tumor cells into nude mice. Cannabinoid-treated tumors showed an increased number of apoptotic cells. This was accompanied by impairment of tumor vascularization, as determined by altered blood vessel morphology and decreased expression of proangiogenic factors (VEGF, placental growth factor, and angiopoietin 2). Abrogation of EGF-R function was also observed in cannabinoid-treated tumors. These results support a new therapeutic approach for the treatment of skin tumors.

READ MORE:
http://www.onlinepot.org/medical/skincancerreport.htm

That link to the Cannabalm Lotion RECIPE is by an old and much respected OGF who is still working on cannabis medicines.

[Sequoiacrone]

Research Findings on Medicinal Properties of Marijuana
by Kevin B. Zeese (http://www.marijuanalibrary.org/Zeese_Research_0197.html#kbz), Esq.

January, 1997 President
Common Sense for Drug Policy (http://www.drugsense.org/csdp/)
3220 N Street, NW, #141
Washington, DC 20007
703-354-5694 (tel)
703-354-5695 (fax)
kevzeese@laser.net (kevzeese@laser.net) (e-mail)


(an excerpt from the article)



There have been several studies which have been published which focus on the medical value of smoked marijuana and cancer therapy. These include:

Vinciguerra et al., Inhalation Marijuana as an Antiemetic for Cancer Chemotherapy," The New York State Journal of Medicine, pgs., 525-527, October 1988 involved 56 patients who had no improvement with standard antiemetics. When treated with marijuana 78 percent demonstrated a positive response. No serious negative side effects were seen.
Chang et al., Delta-9-Tetrahydrocannabinol as an Antiemetic in Cancer Patients Receiving High Dose Methotrexate," Annals of Internal Medicine, Volume 91, Number 6, pg. 819-824, December 1979 is a randomized, double-blind, placebo controlled trial of THC and smoked marijuana which found a 72 percent reduction in nausea and vomiting. The research found that smoked THC (marijuana) was more reliable than oral THC.
Foltin, R.W., Brady, J.V. and Fischman, M.W. 1986. Behavioral analysis of marijuana effects on food intake in humans. Pharmacology, Biochemistry and Behavior. 25: 577-582 and Foltin, R.W. et al., 1988 Effects of Smoked Marijuana on Food Intake and Body Weight of Humans Living in a Residential Laboratory," Appetite 11:1-14; Greenberg, et al. 1976 Effects of Marijuana use on Body Weight and Caloric Intake in Humans," Psychopharmacology 49: 79-84. All demonstrate that marijuana increases appetite and food intake.
Doblin et al., Marijuana as Antiemetic Medicine: A Survey of Oncologists' Experiences and Attitudes," Journal of Clinical Oncology, Vol. 9, No. 7, July 1991. A random survey of clinical oncologists found that 44 percent of respondents report recommending the (illegal) use of marijuana for the control of emesis and 48 percent would prescribe marijuana to some patients if it were legal.
Sallan, S.E., Zinberg, N.E. and Frei, D., Antiemetic Effect of Delta-9-tetrahydrocannabinol in Patients Receiving Cancer Chemotherapy," New England Journal of Medicine, 293(16): 795-797 (1975). The researchers conducting this study of THC noticed that some patients were dropping out of the research and choosing to use marijuana from the street instead. They followed up on these patients. In their conclusion they reported on the marijuana patients and stated that natural marijuana was more successful than synthetic THC for some patients.
(historical reference from the above article)


The list of medical uses of cannabis from historical references includes: 11 (http://www.marijuanalibrary.org/Zeese_Research_0197.html#note11)
Anorexia, Asthma, Nausea,
Pain, Peptic Ulcer, Alcoholism
Glaucoma, Epilepsy, Depression
Migraine, Anxiety, Inflammation
Hypertension, Insomnia, Cancer
Interestingly, relief of many of the symptoms marijuana was used for in these illnesses are many of the same symptoms that have been proven in modern research. This should not be surprising unless we want to assume that all of the experience of thousands of years did not have some factual basis.

To read more from this 1997 article:
http://www.marijuanalibrary.org/Zeese_Research_0197.html#pt3a

[Sequoiacrone]

Anti-Tumor Effects
Anti Tumor Effects by GW Pharmaceuticals
Emerging research indicates that cannabinoids may help protect against the development of certain types of tumors. Most recently, a Spanish research team reported in Nature that injections of synthetic THC eradicated malignant brain tumors - so-called gliomas - in one-third of treated rats, and prolonged life in another third by as much as six weeks. (1 (http://www.ukcia.org/research/AntiTumorEffects.htm#1)) Team leader Manuel Guzman called the results "remarkable" and speculated that they "may provide a new therapeutic approach for the treatment of malignant gliomas. (2 (http://www.ukcia.org/research/AntiTumorEffects.htm#2)) An accompanying commentary remarked that this was the first convincing study to demonstrate that cannabis-based treatment may combat cancer. (3 (http://www.ukcia.org/research/AntiTumorEffects.htm#3)) Other journals have also recently reported on cannabinoids' antitumoral potential. (4 (http://www.ukcia.org/research/AntiTumorEffects.htm#4),5 (http://www.ukcia.org/research/AntiTumorEffects.htm#5),6 (http://www.ukcia.org/research/AntiTumorEffects.htm#6),7 (http://www.ukcia.org/research/AntiTumorEffects.htm#7))
Earlier studies also indicate that cannabinoids may successfully stave certain types of tumors. One study examined the effects of delta-9-tetrahydrocannabinol (THC), delta-8-THC, and cannabinol (CBN) on cancer cells in mice lungs. Researchers reported that cannabinoids reduced the size of the tumors by 25 to 82 percent, depending on dose and duration of treatment, with a corresponding increase in survival time. (8 (http://www.ukcia.org/research/AntiTumorEffects.htm#8)) A two-year federal study by the U.S. National Toxicology Program found that mice and rats given high doses of THC over long periods of time appeared to have greater protection against malignancies than untreated controls. Researchers concluded that in both mice and rats, "the incidence of benign and malignant neoplasms was decreased in a dose dependent manner." (9 (http://www.ukcia.org/research/AntiTumorEffects.htm#9),10 (http://www.ukcia.org/research/AntiTumorEffects.htm#10)) Dr. Lester Grinspoon writes in Marihuana: The Forbidden Medicine (with James Bakalar) that other animal studies also suggest that some cannabinoids have tumor-reducing properties. (11 (http://www.ukcia.org/research/AntiTumorEffects.htm#11))
An Italian research team reported in 1998 that the endocannabinoid anandamide, which binds to the same brain receptors as cannabis, "potently and selectively inhibits the proliferation of human breast cancer cells in vitro" by interfering with their DNA production cycle. (12 (http://www.ukcia.org/research/AntiTumorEffects.htm#12),13 (http://www.ukcia.org/research/AntiTumorEffects.htm#13)) Non-mammary tumor cells were not affected by anandamide. Clearly, further research is necessary and appropriate.

REFERENCES


I. Galve-Roperph et al. "Antitumoral action of cannabinoids: involvement of sustained ceramide accumulation of ERK activation." Nature Medicine 6 (2000): 313-319.
ACM Bulletin. "THC destroys brain cancer in animal research," March 5, 2000.
http://www.acmed.org/english/2000/eb000305.html
D. Piomelli. "Pot of gold for glioma therapy." Nature Medicine 6 (2000): 255-256.
J. Benard. "Cannabinoids, among others, send malignant tumors to nirvana." Bull Cancer 87 (2000): 299-300.
J. Molnar et al. "Membrane associated with antitumor effects of crocine-ginsenoside and cannabinoid derivatives." Anticancer Res 20 (2000): 861-867.
L. Ruiz et al. "Delta-9-tetrahydrocannabinol induces apoptosis in human prostate PC-3 cells via a receptor-independent mechanism." FEBS Letter 458 (1999): 400-404.
S. Baek et al. "Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells." Arch Pharm Res 21 (1998): 353-356.
L. Harris et al., "Anti-tumoral Properties of Cannabinoids," The Pharmacology of Marihuana, ed. M. Braude et al., 2 vols., New York: Raven Press (1976) 2: 773-776 as cited by L. Grinspoon et al., Marihuana: The Forbidden Medicine (second edition), New Haven, CT: Yale University Press (1997), 173.
J. James, "Unpublished Federal Study Found THC-Treated Rats Lived Longer, Had Less Cancer," AIDS Treatment News 263 (1997).
http://www.immunet.org/immunet/atn.nsf/page/a-263-04
"Toxicology and Carcinogenesis Studies of 1 trans-delta-9-tetrahydrocannabinol in F344N/N Rats and BC63F1 Mice," National Institutes of Health National Toxicology Program, NIH Publication No. 97-3362 (November 1996).
L. Grinspoon et al., Marihuana: "The Forbidden Medicine" (second edition), 173.
L. De Petrocellis et al., The endogenous cannabinoid anandamide inhibits human breast cancer cell proliferation, Proceedings of the National Academy of Sciences 95 (1998): 8375-8380.
http://www.pnas.org/cgi/content/abstract/95/14/8375
"Pot Chemicals Might Inhibit Breast Tumors, Stroke Damage," Dallas Morning News, July 13, 1998.
http://www.mapinc.org/drugnews