Any time something related to a medical use for cannabis is found, it makes headlines. Mostly, the interest is generated by the relationship to an illegal drug. Sometimes, though, the media do a decent job of reporting the real issue.
Researchers at the
California Pacific Medical Center Research Institute have announced that one of the compounds found in cannabis, cannabidiol, inhibits a gene that is important for the growth and metastasis of breast cancer.
Note that this has nothing to do with medical marijuana, really. Cannabidiol is not psychoactive: it does not produce euphoria. Moreover, it is not possible to get enough into your body by smoking cannabis.
This has been reported by the
Washington Post,
UPI,
BBC,
ABC, and others. Most of the reporting is good, although there is one glaring error in the Washington Post article (I'll get to that).
The action is centered upon a pair of genes that are involved in the regulation of cell growth. Both genes code for proteins that are essential for normal growth. However, when growth is not regulated normally, it can get out of control. The result may be the development of a malignant tumor that can spread to various other body sites. If the expression of the genes is not properly regulated, then the proteins they encode are produced in unhealthy amounts. Thus, the regulation of gene expression is crucial for the proper regulation of cell growth.
The researchers involved in the studies included Sean McAllister, Ph.D., and Pierre Desprez, Ph.D.
They have been studying two genes: inhibitor of DNA binding-1 (Id-1), and inhibitor of DNA binding-2 (Id-2). In general, Id proteins tend to stop the differentiation of cells, and promote cell division. The do this by regulating transcription factors.
The CPMCRI researchers report that, in cultures of mouse breast cancer cells, the two proteins have opposite effects. Id-1 tends to promote proliferation of the cells, whereas Id-2 tends to restrain breast cancer cell proliferation.
What Desprez and McAllister found is that cannabidiol suppresses the Id-1 gene. This results in lower levels of the associated protein, which in turn results in less tumor growth and less metastasis.
Obviously, this is all very preliminary. The work so far has been done with cultured mouse cells. That is a lot different than cells in a live human. The news articles were careful to point that out.
The Washington Post article, however, contains an odd statement:
Quote:
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In humans, the Id-1 gene is found only in metastatic cancer cells, said Desprez, a staff scientist at the institute. Before birth, they are present and involved in the development of human embryos, but after birth, they go silent -- and should stay that way, he said.
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I don't think Desprez said that. Rather, the reporter (Carolyn Colwell) inferred that from something else. I don't think the gene simply disappears and then comes back. Rather, the protein that the gene encodes is what comes and goes. When the gene is silent, the protein goes away. When the gene is turned back on, the protein comes back. This point is peripheral to the main points in the article. I don't blame the reporter (too much), because it is a complex subject. It is easy to get confused. But I don't want to perpetuate the confusion by failing to point this out.
The results of the research have been published in the journal, Molecular Cancer Therapeutics.
Quote:
Abstract
Invasion and metastasis of aggressive breast cancer cells is the final and fatal step during cancer progression, and is the least understood genetically. Clinically, there are still limited therapeutic interventions for aggressive and metastatic breast cancers available. Clearly, effective and nontoxic therapies are urgently required. Id-1, an inhibitor of basic helix-loop-helix transcription factors, has recently been shown to be a key regulator of the metastatic potential of breast and additional cancers. Using a mouse model, we previously determined that metastatic breast cancer cells became significantly less invasive in vitro and less metastatic in vivo when Id-1 was down-regulated by stable transduction with antisense Id-1. It is not possible at this point, however, to use antisense technology to reduce Id-1 expression in patients with metastatic breast cancer. Here, we report that cannabidiol (CBD), a cannabinoid with a low-toxicity profile, could down-regulate Id-1 expression in aggressive human breast cancer cells. The CBD concentrations effective at inhibiting Id-1 expression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. CBD was able to inhibit Id-1 expression at the mRNA and protein level in a concentration-dependent fashion. These effects seemed to occur as the result of an inhibition of the Id-1 gene at the promoter level. Importantly, CBD did not inhibit invasiveness in cells that ectopically expressed Id-1. In conclusion, CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.
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Note especially that the authors state that CBD inhibits the proliferation of the cells, makes tham less invasive, and makes them less aggressive. They do not say anything about a cure.
On the CPMCRI website, they do not say that they expect CBD to be useful clinically. Rather, they say that it may serve as a template for other compounds that might turn out to be clinically useful.
Looking at the Medline database, these researchers have been at this for at least ten years already, just to get to this point. I won't even try to guess how long it may be before anything clinically useful may come of it. Even so, it is exciting to see a prospect for a safe drug that may have little or none of the unpleasantness that is so troublesome in so many anticancer drugs.
scienceblogs.com
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