I’ve had a couple of requests for these:
This first one is from the National Cancer Institute in the USA. I’d recommend reading this first. If you look at the tab on the top of the page you’ll notice it’s for medical professionals, so there’s a bit of jargon but it’s still easy to understand what they’re saying. There’s also a long list of relevant research papers at the end of the article for anyone interested in further research:
Here’s the relevant bit about anti-tumour effects at the time of writing:
One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors. During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenomatumors and hepatocellular carcinoma (HCC) was observed in the mice. Decreased incidences ofbenign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, andpancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo . In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[5–8]
Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis invasion and metastasis.[9–12] One review summarizes the molecular mechanisms of action of cannabinoids as antitumor agents. Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce apoptosis in gliomacells in culture and induce regression of glioma tumors in mice and rats. Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.
The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC. Both agents reduced the viability of HCC cells in vitro and demonstrated antitumor effects in HCC subcutaneous xenografts in nude mice. The investigations documented that the anti-HCC effects are mediated by way of the CB2 receptor. Similar to findings in glioma cells, the cannabinoids were shown to trigger cell death through stimulation of an endoplasmic reticulum stress pathway that activates autophagy and promotes apoptosis. Other investigations have confirmed that CB1 and CB2 receptors may be potential targets in non-small cell lung carcinoma  and breast cancer.
An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors. CBD inhibited the survival of both estrogen receptor–positive and estrogen receptor–negative breast cancercell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic, mammary cells.
CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer. In the experimental system, azoxymethane increased premalignant and malignant lesionsin the mouse colon. Animals treated with azoxymethane and CBD concurrently were protected from developing premalignant and malignant lesions. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation.
Another investigation into the antitumor effects of CBD examined the role of intercellular adhesion molecule-1 (ICAM-1). ICAM-1 expression has been reported to be negatively correlated with cancer metastasis. In lung cancer cell lines, CBD upregulated ICAM-1, leading to decreased cancer cell invasiveness.
In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines. Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.[21,22]
In addition, both plant-derived and endogenous cannabinoids have been studied for anti-inflammatoryeffects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation. As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment ofcolorectal cancer has been developed.[24–27]
CBD may also enhance uptake of cytotoxic drugs into malignant cells. Activation of the transient receptor potential vanilloid type 2 (TRPV2) has been shown to inhibit proliferation of human glioblastoma multiforme cells and overcome resistance to the chemotherapy agent carmustine. In an in vitro model, CBD increased TRPV2 activation and increased uptake of cytotoxic drugs, leading to apoptosis of glioma cells without affecting normal human astrocytes. This suggests that coadministration of CBD with cytotoxic agents may increase drug uptake and potentiate cell death in human glioma cells.
Pretty interesting stuff. Interesting that the same site also provides patient information that says:
- Cannabis has been shown to kill cancer cells in the laboratory and to affect the immune system. However, there is no evidence that Cannabis’ effects on the immune system help the body fight cancer. (my emphasis)
- At this time, there is not enough evidence to recommend that patients inhale or ingest Cannabisas a treatment for cancer-related symptoms or side effects of cancer therapy.
- Cannabis is not approved by the FDA for use as a cancer treatment.
Here’s the link if you want to read more.
I don’t know about you, but I think their definition of evidence must be very different from the general understanding of that word. I’d say research that shows cancer cells dying in response to cannabis, even in vitro or in rats, was still evidence. I accept that you don’t rush from there to making it freely available but surely you’d be advocating human trials and further studies, particularly when there’s also this:
Which includes this quote:
“Another Spanish team, led by Dr Manuel Guzmon, wanted to see whether they could prevent a form of cancer (glioblastoma multiforme) from growing by cutting off its blood supply. Glioblastoma multiforme is one of the most difficult cancers to treat – it seldom responds to any medical intervention, especially conventional methods which poisoning and primatively destroy cells such as radiotherapy, chemotherapy and surgery.
The mice were given a cancer similar to the human brain cancer (glioblastoma multiforme). The mice were then given cannabinoids and the genes examined. The genes associated with blood vessel growth in tumors through the production of a chemical called vascular endothelial growth factor (VEGF) had their activity reduced.
Cannabinoids halt VEGF production by producing Ceramide. Ceramide controls cell death.
Dr Guzmon said: “As far as we know, this is the first report showing that ceramide depresses VEGF pathway by interfering with VEGF production.”
They then wanted to see if this would also happen with humans.
They selected two patients who had glioblastoma multiforme and had not responded to chemotherapy, radiotherapy or surgery. The scientists took samples from them before and after treating them with a cannabinoids solution – this was administered directly into the tumor.
Amazingly, both patients experienced reduced VEGF levels in the tumor as a result of treatment with cannabinoids.”
Hmm. I like to think we’re balanced at that point in history where a great breakthrough is about to happen. It seems likely that there will soon be either compelling evidence that cannabis cures cancer or compelling evidence that it doesn’t. Based on the research so far it’s certainly a substance worthy of human trials, particularly when we’re dealing with a disease with no shortage of patients that have exhausted all available medical options.
Even if the only benefit is to provide people with pain and nausea relief prior to death it’s a valuable drug. If you’ve ever seen a terminally ill person on morphine (as I did with my Dad) you’ll appreciate the need for something with less side effects.
As I’ve said, I’m not advocating that anyone break the law but I certainly support calls for more research and human trials in relation to cannabis. Wouldn’t it be ironic if something that’s been illegal for so long turns out to be the cure for cancer.