Scientists believe marijuana compound could fight cancer

“Scientists in California believe they may have discovered a compound in marijuana that can reduce the aggressiveness of some forms of cancer.

The San Francisco Gate reports on the data that has been years in the making. While marijuana has been shown to help reduce nausea and pain in cancer patients, scientists believe that a compound in marijuana has the ability to “turn off” the activity of a gene responsible for metastasis in breast and other types of cancers.

The research team is working out of San Francisco’s California Pacific Medical Center Research Institute and have been working for years on the study. The compound they’re focused on, called cannabidiol, does not produce the psychotropic high associated with marijuana.

Last year, the team published a small study showing the positive effects of cannabidiol on mice. New data is about to be released that expands upon the previous results that the researchers hope will help propel the study even further.

“The preclinical trial data is very strong, and there’s no toxicity. There’s really a lot of research to move ahead with and to get people excited,” said Sean McAllister, who is working alongside scientist Pierre Desprez in the study.

Desprez and McAllister believe that their merging of separate areas of study was serendipitous.

Desprez had been studying the protein ID-1, which he found to play an important role in how cancer could spread. McAllister, on the other hand, was focused on studying anabolic steroids in drug abuse. He soon became focused on with the role non-psychotropic cannabidiol, or CBD, interacts with cancer.

McAllister, after hearing an internal seminar from Desprez on his studies of ID-1, came up with the question “How effective would cannabidiol be on targeting metastatic cancer cells?”

The two then teamed up, with Desprez armed with ID-1 cancer-causing protein, and McAllister with CBD, his cancer-fighting compound.

For their experimentation, the doctors exposed ID-1 to CBD in a petri dish. In a shocking result, the ID-1, the cancer-causing protein, reverted to a normal state and stopped acting “crazy.”

“We thought we did the experiment the wrong way,” McAllister said of the overwhelming results.

However, their results proved to be consisted.

“I told Sean, ‘Maybe your drug is working through my gene,’ ” Desprez said.

What the researchers have discovered thus far in their research is that CBD turns off the overexpression of ID-1, which prevents it from traveling to foreign tissues. Thus, the metastasization – cancer’s fatal ability – is blocked.

In the wake of their positive results, the doctors were forced to emphasize that the CBD will only work in the presence of high levels of ID-1 and these do not include all cancerous tumors but, rather, aggressive, metastatic cells. High levels have been found in leukemia, colorectal, pancreatic, lung, ovarian, brain and other cancers.”
Read more: http://www.irishcentral.com/news/Scientists-believe-marijuana-compound-could-fight-cancer-170689736.html#ixzz29rQbc2oS

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NBC News Reports that Cannabidiol (CBD) “Turns Off” the Cancer Gene Involved in Metastasis Findings by Scientists at California Pacific Medical Center gives Scientific Support for Cannabis Science

“Cannabis Science (CBIS), a pioneering U.S. Biotech Company developing pharmaceutical products for global public health challenges, reports on a recent press release by the San Francisco NBC news, with new studies by Scientists at California Pacific Medical Center, which have shown that cannabidiol, (CBD -1.18%, news), has the ability to “turn off” a gene that causes breast and other types of cancers to metastasize, according to the San Francisco Chronicle newspaper.

NBC News reports, “The drug “has been shown to reduce pain and nausea” in cancer patients. AIDS patients also use cannabis to eat, sleep and otherwise be more functional. Turns out that cannabidiol has none of the psychotropic effects of marijuana as a whole. The researchers hope to move to clinical trials on humans soon to test the cannabidiol inhibition of metastasis, reported in the San Francisco Chronicle. “What they found is that the cannabinoid turns off the overexpression of ID-1, which makes the cells lose their ability to travel to distant tissues. In other words, it keeps the cells more local and blocks their ability to metastasize. (spread to a new location) The researchers stressed cannabidiol works only on cancer cells that have these high levels of ID-1 and these do not include all cancerous tumors but, rather, aggressive, metastatic cells. But they’ve found such high levels in leukemia, colorectal, pancreatic, lung, ovarian, brain and other cancers.””

http://money.msn.com/business-news/article.aspx?feed=BW&date=20120920&id=15582334

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Cannabinoids in intestinal inflammation and cancer.

Abstract

“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.”

http://www.ncbi.nlm.nih.gov/pubmed/19442536

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Turned-Off Cannabinoid Receptor Turns On Colorectal Tumor Growth

“CB1 is well-established for relieving pain and nausea, elevating mood and stimulating appetite by serving as a docking station for the cannabinoid group of signaling molecules. It now may serve as 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,” said senior author Raymond DuBois, M.D., Ph.D., provost and executive vice president of The University of Texas M. D. Anderson Cancer Center.

DuBois and collaborators from Vanderbilt-Ingram Cancer Center also show that CB1 expression can be restored with an existing drug, decitabine. They found that mice prone to developing intestinal tumors that also have functioning CB1 receptors develop fewer and smaller tumors when treated with a drug that mimics a cannabinoid receptor ligand. Ligands are molecules that function by binding to specific receptors. Agonists are synthetic molecules that mimic the action of a natural molecule.

“Potential application of cannabinoids as anti-tumor drugs is an exciting prospect, because cannabinoid agonists are being evaluated now to treat the side-effects of chemotherapy and radiation therapy,” DuBois said. “Turning CB1 back on and then treating with a cannabinoid agonist could provide a new approach to colorectal cancer treatment or prevention.”

Cannabinoids are a group of ligands that serve a variety of cell-signaling roles. Some are produced by the body internally (endocannabinoids). External cannabinoids include manmade versions and those present in plants, most famously the active ingredient in marijuana (THC).”

http://www.sciencedaily.com/releases/2008/08/080801074056.htm

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Could Pot Cure Colon Cancer?

“According to researchers at the University of Texas in Houston chemicals in marijuana could be a potential cure in the treatment of colon cancer. Don’t think lighting up a joint will help though, it’s all a chemical process.

 
The key receptors for cannabinoids are turned off in the human body when it’s attacked by most kinds of colon cancer. Those receptors are also found in marijuana.

 

Using test mice scientists turned off the receptor and found that tumors quickly developed.

 

“When we knocked out the receptor, the number of tumors went up dramatically,” says researcher Raymond DuBois. Alternatively, when mice with normal CB1 receptors were treated with a cannabinoid compound, their tumours shrank.

 

The researchers are advising a two step method to treat colon cancer.

 

Step One is to turn the CB1 receptor back on and then activate it with drugs that mimic marijuana. The drug decitibine is already approved and does help in making the receptor. Already the second step has not been worked out Dubuis believes that using drugs that mimic marijuana will shrunk tumors.”

 

 

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Cannabis-Linked Cell Receptor Might Help Prevent Colon Cancer – ABCNews

“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.

“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.””

http://abcnews.go.com/Health/Healthday/story?id=5496283&page=1

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Study: Marijuana Could Stop Growth of Colon Cancer Cells

“The administration of the non-psychotropic cannabis plant constituent cannabidiol (CBD) is protective in an experimental model of colon cancer, according to preclinical trial data published online in the Journal of Molecular Medicine.

Investigators at the University of Naples assessed the effect of CBD on colon carcinogenesis in mice. Researchers reported that CBD administration was associated with cancerous tumor reduction and reduced cell proliferation.

Authors wrote: “Although cannabidiol has been shown to kill glioma cells, to inhibit cancer cell invasion and to reduce the growth of breast carcinoma and lung metastases in rodents, its effect on colon carcinogenesis has not been evaluated to date. This is an important omission, since colon cancer affects millions of individuals in Western countries. In the present study, we have shown that cannabidiol exerts (1) protective effects in an experimental model of colon cancer and (2) antiproliferative actions in colorectal carcinoma cells.”

Authors also acknowledged that CBD possesses “an extremely safe profile in humans.” They concluded, “[O]ur findings suggest that cannabidiol might be worthy of clinical consideration in colon cancer prevention.””

http://www.opposingviews.com/i/society/drug-law/latest-science-non-psychotropic-cannabinoid-inhibits-colon-cancer-cell

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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.

Raymond DuBois and colleagues at the University of Texas in Houston discovered that a key receptor for cannabinoids, which are found in marijuana, is turned off in most types of human colon cancer.

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.

Dual attack

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.”

 

http://www.newscientist.com/article/dn14451-marijuana-takes-on-colon-cancer.html

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Cannabinoids and the digestive tract.

“In the digestive tract there is evidence for the presence of high levels of endocannabinoids (anandamide and 2-arachidonoylglycerol) and enzymes involved in the synthesis and metabolism of endocannabinoids. Immunohistochemical studies have shown the presence of CB1 receptors on myenteric and submucosal nerve plexuses along the alimentary tract. Pharmacological studies have shown that activation of CB1 receptors produces relaxation of the lower oesophageal sphincter, inhibition of gastric motility and acid secretion, as well as intestinal motility and secretion. In general, CB1-induced inhibition of intestinal motility and secretion is due to reduced acetylcholine release from enteric nerves. Conversely, endocannabinoids stimulate intestinal primary sensory neurons via the vanilloid VR1 receptor, resulting in enteritis and enhanced motility. The endogenous cannabinoid system has been found to be involved in the physiological control of colonic motility and in some pathophysiological states, including paralytic ileus, intestinal inflammation and cholera toxin-induced diarrhoea. Cannabinoids also possess antiemetic effects mediated by activation of central and peripheral CB1 receptors.

Pharmacological modulation of the endogenous cannabinoid system could provide a new therapeutic target for the treatment of a number of gastrointestinal diseases, including nausea and vomiting, gastric ulcers, secretory diarrhoea, paralytic ileus, inflammatory bowel disease, colon cancer and gastro-oesophageal reflux conditions.”

http://www.ncbi.nlm.nih.gov/pubmed/16596788

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

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 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.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774787/

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