New Study Finds Marijuana Compound Inhibits Breast Cancer Growth

[Smokin Moose]

San Francisco, CA -- A new study announced today by the California Pacific Medical Center Research Institute (CPMCRI) found that a non-psychoactive, naturally occurring compound in the cannabis plant (marijuana) called cannabidiol (CBD) inhibits the activity of breast cancer cells "in vitro" and in animals.

While previous studies have found that tetrahydrocannabinol, another cannabis compound known as THC, has properties found to inhibit cancer growth, the CPMCRI study is the first time that CBD has been shown to have a similar effect. According to CPMCRI, the study was accepted for publication in October.

"This pre-clinical research clearly demonstrates the therapeutic potential of marijuana's active compounds," said CPMCRI cannabinoid researcher Jahan Marcu, who is also on the Medical & Scientific Advisory Board of Americans for Safe Access (ASA). "The availability of a non-toxic substance that has the potential to fight breast cancer and likely other forms of cancer is of tremendous importance."

Despite mounting evidence verifying the medical efficacy of smoked marijuana and it's isolated compounds, the federal government continues to obstruct scientific research in this field. In the last 20 years, the FDA has approved only three studies using plant-derived marijuana or its constituent compounds, forcing researchers such as CPMCRI to use synthetic versions. One reason for a lack of U.S. research using naturally derived marijuana is that scientists must obtain it from the National Institute for Drug Abuse (NIDA), which has a stated disinterest in the investigation of marijuana's therapeutic qualities.

"It's time for NIDA and the federal government to end the monopoly on research cannabis," said Caren Woodson, Director of Government Affairs for ASA. "This study should compel our government to do everything in its power to conduct the long-overdue research recommended by the 1999 Academy of Sciences Institute of Medicine report." The Drug Enforcement Administration (DEA), which works with NIDA to restrict the availability of research cannabis, is currently refusing to license University of Massachusetts Amherst Professor Lyle Craker, despite a ruling earlier this year from Administrative Law Judge Mary Ellen Bittner that stated such research was "in the public interest."

The CBD compound used by CPMCRI for the study was synthetic due to the complications of obtaining research cannabis. However, compounds extracted from the marijuana plant are far cheaper and would be easier to acquire for the purpose of research if a competitive source of research grade marijuana were available. Coincidentally, the DEA is recommending that the natural form of THC be rescheduled under the Controlled Substances Act (CSA) so that the plant derived compound may be naturally extracted in order to facilitate the research and development of generic, natural THC-based therapeutic drugs. "This study provides clear evidence which suggests that DEA ought to further consider rescheduling other cannabinoids with clear medical benefit in order to jump-start the research and development of cannabis-based drugs so patients have access to these drugs sooner as opposed to later," continued Woodson.

Further information:
CPMCRI Study and Researcher Dr. Sean McAllister — California Pacific Medical Center - Research Institute Programs

Source: Science Daily
Copyright: Science Daily
Contact: Mcallis@cpmcri.org
Website: California Pacific Medical Center

 

[Smokin Moose]

This is from:
Sean D. McAllister, Ph.D.

Introduction
Our research team is studying the potential of the endocannabinoid system to control cell fate with the goal of developing therapeutic interventions for aggressive cancers. This newly discovered biological system can be regulated by many different classes of cannabinoid compounds that work through specific cellular receptors. The cloned cannabinoid receptors have been termed cannabinoid 1 (CB1) and (CB2).

∆9-tetrahydrocannabinol (THC), a mixed CB1 and CB2 receptor agonist, is the primary active constituent of Cannabis sativa and is currently being used in a clinical trial for the treatment of aggressive recurrent glioblastoma multiforme (GBM). Cannabinoids are also being used in clinical trials for purposes unrelated to their direct anticancer activity. The compounds have been reported to be well tolerated during chronic oral and systemic administration. In addition to Δ9-THC, cannabidiol (CBD), cannabinol (CBN) and cannabigerol (CBG) are also present in reasonable quantities in Cannabis. CBN has low affinity for CB1 and CB2 receptors, whereas the non-psychotropic cannabinoids, CBD and CBG, have negligible affinity for the cloned receptors. We have determined that these additional cannabinoids are also effective and inhibiting aggressive cancers. Importantly, we have discovered in vitro that a synergistic increase in the antiproliferative and apoptotic activity of cannabinoids can be produced by combining specific ratios of CB1 and CB2 receptors agonists with non-psychotropic cannabinoids.

We are currently determining the molecular mechanism that may explain the synergistic increase in anticancer activity that is observed with the combination treatments. We are also studying whether this combination strategy will lead to greater antitumor activity in vivo.

In addition to the combination therapy project, we are working in collaboration with Dr. Pierre Desprez to develop novel inhibitors of Id-1 using cannabinoid compounds. Id-1 is a helix-loop-helix protein that acts as an inhibitor of basic helix-loop-helix transcription factors that control cell differentiation, development and carcinogenesis. Past research of Id-1 expression in normal and cancerous breast cells, as well as in mouse mammary glands and in human breast cancer biopsies, demonstrated that increased Id-1 expression was associated with a proliferative and invasive phenotype. Specifically, it was found that Id-1 was constitutively expressed at a high level in aggressive breast cancer cells and human biopsies, and that aggressiveness was reverted in vitro and in vivo when Id-1 expression was targeted using antisense technology. Importantly, we have recently discovered that CBD, a nontoxic cannabinoid that lacks psychoactivity, can inhibit Id-1 gene expression in metastatic breast cancer cells and consequently their aggressive phenotype. The down-regulation of expression was the result of the inhibition of the endogenous Id-1 promoter and corresponding mRNA and protein levels. CBD and compounds based off of its structure can therefore potentially be used as therapeutic agents. CBD also inhibits breast cancer metastasis in vivo.

Based off of our recent findings, we are currently involved in 1) developing novel CBD analogs for the treat of aggressive breast cancers 2) discovering the detailed mechanisms through which cannabinoid compounds regulate Id-1 expression.

 

[Boss]

Wow, this is very cool news. One, because it came from California, two, because of the results of the test.

This is really awesome.