Marijuana takes on colon cancer
August 1, 2008 | New Scientist
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.
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.
Journal reference: Cancer Research (vol 68, p 6468)
Cannabis compound clue to colon cancer
August 6, 2008 | New Scientist
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 decitibine, a drug already approved for use in humans which DuBois and his team showed stops blockage of the receptor in human colon cancer cells. Then give the patient cannabinoids to activate CB1.
The research also casts a shadow on the weight-loss drug rimonabant. The drug suppresses appetite by blocking CB1, which is involved in hunger as well as tumour growth. DuBois suggests that anyone on the drug be screened for colon cancer.