Cannabinoids and cancer

[Rich66]

1: Cancer Lett. 2009 May 11. [Epub ahead of print] Links

Cannabinoids in the treatment of cancer.

Alexander A, Smith PF, Rosengren RJ.
Department of Pharmacology and Toxicology, University of Otago, Dunedin 9001, New Zealand.
Cannabinoids, the active components of the hemp plant Cannabis sativa, along with their endogenous counterparts and synthetic derivatives, have elicited anti-cancer effects in many different in vitro and in vivo models of cancer. While the various cannabinoids have been examined in a variety of cancer models, recent studies have focused on the role of cannabinoid receptor agonists (both CB(1) and CB(2)) in the treatment of estrogen receptor-negative breast cancer. This review will summarize the anti-cancer properties of the cannabinoids, discuss their potential mechanisms of action, as well as explore controversies surrounding the results.
PMID: 19442435 [PubMed - as supplied by publisher]

[Rich66]

A more funnerer article:
http://pr.cannazine.co.uk/2009062310...rs-a-year.html

[Rich66]

J Pharmacol Exp Ther. 2009 Nov 4. [Epub ahead of print]
Antitumorigenic effects of cannabinoids beyond apoptosis.

Freimuth N, Ramer R, Hinz B.
University of Rostock.
According to the World Health Organization the cases of death caused by cancer will have been doubled until the year 2030. By 2010 cancer is expected to be the cause of death number one. It is therefore necessary to explore novel approaches for the treatment of cancer. During past years the antitumorigenic effects of cannabinoids have emerged as an exciting field in cancer research. Apart from their proapoptotic and antiproliferative action, recent research has shown that cannabinoids may likewise affect tumor cell angiogenesis, migration, invasion, adhesion and metastasation. This review will summarize the data concerning the influence of cannabinoids on these locomotive processes beyond modulation of cancer cell apoptosis and proliferation. The findings discussed here provide a new perspective on the antitumorigenic potential of cannabinoids.

PMID: 19889794 [PubMed - as supplied by publisher]

Mol Cancer Ther. 2009 Nov 3. [Epub ahead of print]
Synthetic cannabinoid receptor agonists inhibit tumor growth and metastasis of breast cancer.

Qamri Z, Preet A, Nasser MW, Bass CE, Leone G, Barsky SH, Ganju RK.
1Department of Pathology, The Ohio State University College of Medicine, 2Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, College of Medicine and Public Health, Department of Molecular Genetics, College of Biological Sciences, The Ohio State University, Columbus, Ohio; 3Division of Experimental Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts; 4Lombardi Comprehensive Cancer Center, Washington, District of Columbia; and 5Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Medical Center Boulevard Winston-Salem, North Carolina.
Cannabinoids have been reported to possess antitumorogenic activity. Not much is known, however, about the effects and mechanism of action of synthetic nonpsychotic cannabinoids on breast cancer growth and metastasis. We have shown that the cannabinoid receptors CB1 and CB2 are overexpressed in primary human breast tumors compared with normal breast tissue. We have also observed that the breast cancer cell lines MDA-MB231, MDA-MB231-luc, and MDA-MB468 express CB1 and CB2 receptors. Furthermore, we have shown that the CB2 synthetic agonist JWH-133 and the CB1 and CB2 agonist WIN-55,212-2 inhibit cell proliferation and migration under in vitro conditions. These results were confirmed in vivo in various mouse model systems. Mice treated with JWH-133 or WIN-55,212-2 showed a 40% to 50% reduction in tumor growth and a 65% to 80% reduction in lung metastasis. These effects were reversed by CB1 and CB2 antagonists AM 251 and SR144528, respectively, suggesting involvement of CB1 and CB2 receptors. In addition, the CB2 agonist JWH-133 was shown to delay and reduce mammary gland tumors in the polyoma middle T oncoprotein (PyMT) transgenic mouse model system. Upon further elucidation, we observed that JWH-133 and WIN-55,212-2 mediate the breast tumor-suppressive effects via a coordinated regulation of cyclooxygenase-2/prostaglandin E2 signaling pathways and induction of apoptosis. These results indicate that CB1 and CB2 receptors could be used to develop novel therapeutic strategies against breast cancer growth and metastasis. [Mol Cancer Ther 2009;8(11):3117-29].

[Ellie F]

Thanks Rich
I have a Canadian friend who believes a relative of hers was cured of advanced cancer by taking cannabis oil brewed in her own kitchen from the heads of the hemp plant. I was sceptical at first but who knows!!
Ellie

[Rich66]

On the other hand....

Toxicology. 2009 May 2;259(1-2):25-32. Epub 2009 Feb 4.
Modulation of Delta9-tetrahydrocannabinol-induced MCF-7 breast cancer cell growth by cyclooxygenase and aromatase.

Takeda S, Yamamoto I, Watanabe K.
Organization for Frontier Research in Preventive Pharmaceutical Sciences, Hokuriku University, Ho-3 Kanagawa-machi, Kanazawa 920-1181, Japan.
Delta(9)-Tetrahydrocannabinol (Delta(9)-THC), a major constituent of marijuana, has been shown to stimulate the growth of MCF-7 breast cancer cells through cannabinoid receptor-independent signaling [Takeda, S., Yamaori, S., Motoya, E., Matsunaga, T., Kimura, T., Yamamoto, I., Watanabe, K., 2008. Delta(9)-Tetrahydrocannabinol enhances MCF-7 cell proliferation via cannabinoid receptor-independent signaling. Toxicology 245, 141-146]. Although the growth of MCF-7 cells is known to be stimulated by 17beta-estradiol (E(2)), the interaction of Delta(9)-THC and E(2) in MCF-7 cell growth is not fully clarified so far. In the present study, by using E(2)-sensitive MCF-7 cells that have expressed cyclooxygenase-2 (COX-2) and cytochrome P450 19 (aromatase), we studied whether or not COX-2 and aromatase are involved in Delta(9)-THC-mediated MCF-7 cell proliferation. It was shown that Delta(9)-THC-induced MCF-7 cell growth was inhibited by COX-2 inhibitors and was stimulated by arachidonic acid (a COX substrate). However, the growth of MCF-7 cells induced by Delta(9)-THC was not stimulated by PGE(2), and the expression of aromatase was not affected by COX-2 inhibitors, arachidonic acid, and PGE(2), suggesting that there is a disconnection between COX-2 (PGE(2)) and aromatase in Delta(9)-THC-mediated MCF-7 cell proliferation. On the other hand, Delta(9)-THC-induced MCF-7 cell growth was elevated by two kinds of aromatase inhibitors. Taken together with the evidence that Delta(9)-THC-induced MCF-7 cell proliferation was interfered with testosterone (an aromatase substrate) and exogenously provided E(2), it is suggested that (1) the growth stimulatory effects of Delta(9)-THC are mediated by the product(s) of COX-2 except for PGE(2), (2) the action of Delta(9)-THC is modulated by E(2), and (3) COX-2 and aromatase are individually engaged in the proliferation of MCF-7 cells induced by Delta(9)-THC.

PMID: 19428940 [PubMed - indexed for MEDLINE]