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Cannabinoids could be useful for treating cancer - cannabis is not

Cannabinoids could be useful for treating cancer but cannabis is not.

Researchers in Spain have published results in this week’s British Journal of Cancer showing that certain cannabinoids – molecules so-called because they were originally found in cannabis – could hold promise for treating prostate cancer.

So does this mean that smoking cannabis could treat the disease?

Certainly not.  In this paper the researchers were using purified man-made cannabinoids. And they were investigating how to harness the cancer-fighting powers of these chemicals without the mind-bending ones.

Cannabinoids and cancer

Certain cannabinoids, such as THC, the main active ingredient in cannabis, have well-documented mind-altering properties. But other cannabinoids have been known for some years to have biological effects elsewhere in the body. Of most interest to cancer researchers is the evidence showing that they can slow the growth and spread of cancer cells, or even kill them.

For example, Cancer Research UK is funding the work of Professor Chris Paraskeva in Bristol, who is investigating the anti-cancer properties of cannabinoids, as part of his research into the prevention and treatment of bowel cancer.

It needs to be stressed that these studies have all been done with purified cannabinoid chemicals – not cannabis itself, which contains cannabinoids along with a cocktail of other chemicals. There is no reliable evidence to suggest that smoking cannabis can treat cancer.

How do they work?

Cannabinoids affect cells’ behaviour by sticking to receptor molecules on their surface, and triggering a cascade of events within them. There are two main types of cannabinoid receptor, known as CB1 and CB2, although researchers think there may be others out there.

CB1 is mainly found on nerve cells in the brain – so its likely to be the important one when it comes to the mind-altering effects of cannabis.  CB2 is mainly found elsewhere in the body, and is the prime suspect for controlling the other effects of cannabinoids on the body.

In nerve cells, cannabinoids sticking to CB1 receptors  can lead to changes in the signalling pathways (causing the mind-altering and pain-relieving effects of cannabis). We also now know that cannabinoids can trigger other events within the cell, including halting growth or even kick-starting cell death.

The new research

In their recent paper, Professor Ines Diaz-Laviada and her team at the University of Alcala in Madrid studied the effects of two cannabinoids – the catchily named Methanandamide (MET) and JWH-015.  These are synthetic chemicals that don’t occur naturally in cannabis, although they are similar to compounds found in the plant.

The researchers tested the chemicals on different human prostate cancer cell lines grown in the lab, and found that they could slow down their growth and trigger cell death.  An interesting finding, but which of the two cannabinoid receptors is at work?

By using drugs that block either one receptor or the other,  or a genetic technique called RNA interference to ‘knock out’ CB1 or CB2 in turn, the scientists found that the anti-cancer effects of MET and JWH-015 were brought about by CB2.

This is an important finding, because it tells us that it should be possible to develop drugs that target CB2, which will have an anti-cancer effect, but which – crucially – won’t have the mind-altering effects of many cannabinoids.

As a last step, the researchers tested the effects of JWH-015 on mice that had been transplanted with human prostate cancer cells. The chemical helped to slow the growth of tumours, compared with a saltwater control. And blocking the CB2 receptors with a highly-specific drug called SR2 wiped out the effect of JWH-015, proving that it works through the CB2 pathway.

What does it mean for cancer treatment?

Although this work is still at an early stage, it provides a tantalising suggestion that drugs that activate the CB2 receptor could be useful for treating prostate cancer.  There’s still more research to be done before we know if MET or JWH-015 are suitable for testing in clinical trials involving patients – and no guarantee that these trials would be successful.

As part of this research, the scientists also investigated the cellular pathways that cannabinoids activate (or block) when they bind to CB2 receptors on prostate cancer cells. By understanding these cellular responses in greater detail, we might discover new targets for cancer treatment.

So can smoking cannabis treat cancer?

No.  This is a classic fallacy – assuming that because cannabinoids can kill cancer cells in the lab, then cannabis (containing cannabinoids) must be able to treat cancer. Ed has previously written extensively about this, with regard to red wine and cancer.

This research has been done using man-made chemicals that mimic the compounds found in cannabis, rather than unpurified marijuana.  Smoking cannabis, particularly when mixed with tobacco, is likely to increase rather that decrease cancer risk, although the evidence for this is mixed.   And, of course, cannabis is classified as an illegal drug in the UK.



Olea-Herrero, N. et al. (2009). Inhibition of human tumour prostate PC-3 cell growth by cannabinoids R(+)-Methanandamide and JWH-015: Involvement of CB2 British Journal of Cancer DOI: 10.1038/sj.bjc.6605248


Dennis Smith December 5, 2011

Regarding the value of cannabis when eaten, I have an anecdote to offer. My mother had pancreatic cancer. She decided to accept radiation and chemo. She also agreed to take alternative measures as well. She was able to obtain a license for cannabis. She ate a small amount of finely ground cannabis (1/8 -1/2 teaspoon) twice a day mixed with butter on toast or in a scrambled egg. Her psychoactive experience never exceeded mild euphoria. The chemotherapist was kind enough to provide us with her tumour marker printouts at each of our visits. For the first year her cancer did not grow or spread, and her tumour markers stayed low except for the two times when she stopped taking the cannabis to see what would happen. This supports the research suggesting that cannabinoids prevent angiogenisis. Her chemo treatments included 5-flourouracil, gemcitabine, and a breast cancer med. Eventually, her liver failed and she rapidly went downhill and died more than two years after diagnosis.

Peter Reynolds August 31, 2011

Yes Dave, both the method of ingestion and the use of synthetic compounds are red herrings but used as excuses for inaction.

The anger expressed by Oliver is legitimate. Big Pharma rules. Government submits. Big Charity succumbs.

Meanwhile, people suffer, often unnecessarily.

Sativa Indica August 31, 2011

Anecdotal Evidence leads to the restriction of drugs and their withdrawl from the market; as when Thalidomide was found to cause birth defects, and when the Fen-Phen combination was found to cause heart valve problems. Anecdotal evidence often leads to new uses for a medication; for example the morning sickness drug, Thalidomide, is now used for treatment of Cancer and Leprosy, and the anticonvulsant drug, tegretol, is now used to treat seizures, chronic pain and bipolar disorder. Anecdotal evidence may prompt a physician to alter a dosage, change medications, or discontinue a medication, based solely on the individual responses of any given patient.

Anecdotal evidence is obviously not as conclusive as clinical trials, however automatically disregarding all evidence because its anecdotal is problematic.

Im not a medical professional, so perhaps im wrong, but dont the vast majority of drugs prescribed today have ‘mind altering effects’? its with this in mind that i ask, why is the search for cannabinoids that dont alter your mind that important when the alternatives offered clearly do?

Dave Hand August 31, 2011

The author of the article seems ever-so eager to point out that smoking cannabis cannot cure cancer.

Bearing in mind cannabis can be eaten, vapourised and applied topically, would she feel so confident saying the same thing about these other methods of application?

Peter Reynolds August 31, 2011

Oliver, you make some good points. Please don’t kill the debate by suffocating it!

I hope to hear more from Ms Arney

Oliver Stieber May 10, 2011

Is their serious risk of injury of disability from practicing the experiment of disengagement by unsubstantial authority and not seeking to inform the experimentee of the nature not just the substance?

Are you suitably attempting to establishing the action of the observer on the experiment?

Oliver Stieber May 10, 2011

are you saying it’s impossible to determine to and margin of error the measurable effects of a gross substance which has been in use by man for a great period of time and had significant research into negative effects.

Are you saying that it is then impossible to refine that gross substance?

Are you saying that results based on a single chemical compound has zero margin of error?

Are you saying that it’s impossible to promote provision of means by which someone can be provided with established measures by which to interdependently qualify data?

Are you saying that it’s impossible to qualify if someone is capable of then independently using such measures?

Are you saying that it’s impossible to then extract further information using meta data analysis?

Are you saying that is is not cost effective? (Data please).

Are you saying that this is not valid under established research protocols such as :

“No experiment should be conducted where there is an a priori reason to believe that death or disabling injury will occur; except, perhaps, in those experiments where the experimental physicians also serve as subjects…”

See Larenzo.

Oliver Stieber May 10, 2011

(1) “you don’t seem to grasp the obvious real problems of testing cannabis.”
Mark says:
December 20, 2009 at 4:51 am
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If read the tread you will find that it was quoting someone else.

Is your remit to actively promote REASERCH or actively promote authority?

Are there possible avenues for more independent research that are actively being discouraged due to protocol over substance.

This is being moderated in a way I consider to be unacceptable and I refuse to disengage from highlighting this hypocriticy since I release that people need to be made aware that you must always consider the action of the observer in the observation.

(b) Your last statement is totally incomprehensible.

Is the basis for the authority weighted toward existing authoritative protocol over research, especially given that some of the protocols in that existing authority are totally contradictory but have still been accepted by said same authority as acceptable methods with real effects for ‘lesser’ conditions.

Is your motive therefore more weighted to being an authority over research and to attempt to assert that authority with no sound basis over opinion and failing that disengaging?