This is a useful agent for treating nausea, appetite loss, pain and insomnia that can occur as side effects of chemotherapy or cancer itself. Beyond that, some components of cannabis may have significant anti-cancer effects.
A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
CANCER- COLORECTAL & Cannabis studies completed
Eating a diet high in fiber may help prevent colorectal cancer and other common digestive system cancers, including stomach, mouth, and pharynx. Fiber is found in fruits, vegetables, and whole grains. In general, the more natural and unprocessed the food, the higher it is in fiber.
Cannabinoids and cancer: potential for colorectal cancer therapy. (may need free registration)
Biochem Soc Trans. 2005; 33(Pt 4):712-4 (ISSN: 0300-5127)
Patsos HA; Hicks DJ; Greenhough A; Williams AC; Paraskeva C
Despite extensive research into the biology of CRC (colorectal cancer), and recent advances in surgical techniques and chemotherapy, CRC continues to be a major cause of death throughout the world.
Therefore it is important to develop novel chemopreventive/chemotherapeutic agents for CRC. Cannabinoids are a class of compounds that are currently used in the treatment of chemotherapy-induced nausea and vomiting, and in the stimulation of appetite.
However, there is accumulating evidence that they could also be useful for the inhibition of tumour cell growth by modulating key survival signalling pathways. The chemotherapeutic potential for plant-derived and endogenous cannabinoids in CRC therapy is reviewed.
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Marijuana takes on colon cancer
The chemicals in marijuana could put the brakes on colon cancer, according to new research. That doesn't mean smoking a joint will help, though, as the chemicals only form part of the process.
Without this receptor, a protein called survivin, which stops cells from dying, increases unchecked and causes tumour growth.
To better understand the role that the receptor, called CB1, plays in cancer progression, the researchers manipulated its expression in mice that had been genetically engineered to spontaneously develop colon tumours.
"When we knocked out the receptor, the number of tumors went up dramatically," says DuBois. Alternatively, when mice with normal CB1 receptors were treated with a cannabinoid compound, their tumours shrank.
The findings suggest a two-step treatment plan for colon cancer, as well as for other cancers that might be linked to this receptor.
First, turn the CB1 receptor back on, and then activate it with drugs currently in development that mimic marijuana. But how to turn it on?
The researchers found that in human colon cancer cells, the gene that makes the receptor is blocked by a process called methylation, in which a small chemical group is added to the DNA.
Treating the cells with decitibine - a demethylating drug already approved for use in humans - removed the chemical group and the gene began making the receptor. Drugs that mimic marijuana might then activate the receptor, although DuBois did not test this.
Cannabis compound clue to colon cancer
06 August 2008 Magazine issue 2668.
SMOKING hash or marijuana may not be the healthiest way to do it, but taking substances similar to those found in cannabis might one day help to treat colon cancer.
Raymond DuBois and colleagues at the University of Texas, Houston, discovered that a key receptor for cannabinoids - compounds similar to the active ingredient of cannabis - is turned off in most types of human colon cancer cells.
Similarly, mice genetically engineered to develop colon tumours developed more of them if the receptor, called CB1, was knocked out (Cancer Research, DOI: 10.1158/0008-5472.CAN-08-0896). What's more, tumours shrank when the genetically engineered mice were injected with a cannabinoid.
One suggestion is that lack of CB1 encourages tumour growth because the receptor normally interacts with cannabinoids made by the body to prompt cells to die. This opens up a possible two-step treatment for colon cancer. First, switch CB1 back on using...
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Cannabis-Linked Cell Receptor Might Help Prevent Colon Cancer
Findings may serve as new path for better treatment of disease, study suggests
FRIDAY, Aug. 1 (HealthDay News) -- A cannabinoid receptor lying on the surface of cells may help suppress colorectal cancer, say U.S. researchers. When the receptor is turned off, tumor growth is switched on.
Cannabinoids are compounds related to the tetrahydrocannabinol (THC) found in the cannabis plant.
It's already known that the receptor, CB1, plays a role in relieving pain and nausea, elevating mood and stimulating appetite by serving as a docking station for the cannabinoid group of signaling molecules. This study suggests that CB1 may offer a new path for cancer prevention or treatment.
"We've found that CB1 expression is lost in most colorectal cancers, and when that happens, a cancer-promoting protein is free to inhibit cell death," senior author Dr. Raymond Dubois, provost and executive vice president of the University of Texas M.D. Anderson Cancer Center, said in a university news release.
In their study of human colorectal tumor specimens, the researchers also found that the drug decitabine can restore CB1 expression.
In addition, mice that are prone to developing intestinal tumors and also have functioning CB1 receptors developed fewer and smaller tumors when treated with a drug that mimics a cannabinoid receptor ligand, the researchers found. Ligands are molecules that function by binding to specific receptors.
"Potential application of cannabinoids as anti-tumor drugs is an exciting prospect, because cannabinoid agonists (synthetic molecules that mimic the action of natural molecules) are being evaluated now to treat the side effects of chemotherapy and radiation therapy," DuBois said. "Turning CB1 back on and than treating with a cannabinoid agonist could provide a new approach to colorectal cancer treatment or prevention."
The study was published in the Aug. 1 issue of the journal Cancer Research.
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Last updated 8/1/2008
Cannabinoids in intestinal inflammation and cancer
Pharmacol Res. 2009 Aug;60(2):117-25. Epub 2009 Mar 18.
Emerging evidence suggests that cannabinoids may exert beneficial effects in intestinal inflammation and cancer.
Adaptive changes of the endocannabinoid system have been observed in intestinal biopsies from patients with inflammatory bowel disease and colon cancer.
Studies on epithelial cells have shown that cannabinoids exert antiproliferative, antimetastatic and apoptotic effects as well as reducing cytokine release and promoting wound healing.
In vivo, cannabinoids - via direct or indirect activation of CB(1) and/or CB(2) receptors - exert protective effects in well-established models of intestinal inflammation and colon cancer.
Pharmacological elevation of endocannabinoid levels may be a promising strategy to counteract intestinal inflammation and colon cancer.
The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells: a possible role for cyclooxygenase 2
- H A Patsos
- D J Hicks
- R R H Dobson
- A Greenhough
- N Woodman
- J D Lane
- A C Williams
- C Paraskeva
- 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; [email protected]
- Accepted 5 July 2005
- Revised 24 June 2005
- Published Online First 11 August 2005
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 dependent on COX-2 protein expression or enzyme activity, and the potential involvement of PG-EAs in induction of cell death.
Results: Anandamide inhibited the growth of CRC cell lines HT29 and HCA7/C29 (moderate and high COX-2 expressors, respectively) but had little effect on the very low COX-2 expressing CRC cell line, SW480. Induction of cell death in HT29 and HCA7/C29 cell lines was partially rescued by the COX-2 selective inhibitor NS398. Cell death induced by anandamide was neither apoptosis nor necrosis.
Furthermore, inhibition of fatty acid amide hydrolase potentiated the non-apoptotic cell death, indicating that anandamide induced cell death was mediated via metabolism of anandamide by COX-2, rather than its degradation into arachidonic acid and ethanolamine. Interestingly, both PGE2-EA and PGD2-EA induced classical apoptosis.
Conclusions: These findings suggest anandamide may be a useful chemopreventive/therapeutic agent for colorectal cancer as it targets cells that are high expressors of COX-2, and may also be used in the eradication of tumour cells that have become resistant to apoptosis.