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Cannabinoids induce cancer cell proliferation

Blowmonkey

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Cannabinoids induce cancer cell proliferation via tumor necrosis factor alpha-converting enzyme (TACE/ADAM17)-mediated transactivation of the epidermal growth factor receptor.

Hart S, Fischer OM, Ullrich A.

Department of Molecular Biology, Max-Planck-Institute of Biochemistry, Am Klopferspitz 18A, D-82152 Martinsried, Germany.


Cannabinoids, the active components of marijuana and their endogenous counterparts were reported as useful analgetic agents to accompany primary cancer treatment by preventing nausea, vomiting, and pain and by stimulating appetite. Moreover, they have been shown to inhibit cell growth and to induce apoptosis in tumor cells. Here, we demonstrate that anandamide, Delta(9)-tetrahydrocannabinol (THC), HU-210, and Win55,212-2 promote mitogenic kinase signaling in cancer cells. Treatment of the glioblastoma cell line U373-MG and the lung carcinoma cell line NCI-H292 with nanomolar concentrations of THC led to accelerated cell proliferation that was completely dependent on metalloprotease and epidermal growth factor receptor (EGFR) activity. EGFR signal transactivation was identified as the mechanistic link between cannabinoid receptors and the activation of the mitogen-activated protein kinases extracellular signal-regulated kinase 1/2 as well as prosurvival protein kinase B (Akt/PKB) signaling. Depending on the cellular context, signal cross-communication was mediated by shedding of proAmphiregulin (proAR) and/or proHeparin-binding epidermal growth factor-like growth factor (proHB-EGF) by tumor necrosis factor alpha converting enzyme (TACE/ADAM17). Taken together, our data show that concentrations of THC comparable with those detected in the serum of patients after THC administration accelerate proliferation of cancer cells instead of apoptosis and thereby contribute to cancer progression in patients.

PubMed

Uhm, this is cointradictory to everything that I've read uptill now.. Someone please elaborate on the subject.
 
Yes, I remeber when this article came out, it caused quite a stir in some of the very pro-cannabis news groups I frequent (talk.politics.drugs).

This is quite a tight article. Its published by reputable scientists, from a very reputable reaseach lab, in a reputable journal. Its introduction doesn't give away any blatant anti-cannabis biases.

The article has far too many blots for me to ever be bothered completely understanding it, and although I feel that some of the logic in it is a bit dodgy (THC has this effect, we block enzyme X and the effect stops, hence THC was activating enzyme X), the results seem sound, and show in line with other results that high doses of cannabinoids (4-10µM THC) induce cancer apoptosis.

The problem is, this thing is very in vivo. I was talking to a cancer researcher who thinks that there is nothing wrong with dealing with cancer cell lines and extrapolating; and I think that idea is rather prevalent in cancer research (the idea is laughed at in neuro circules.. 'oh, but that was in culture')

The need to implant those cell lines in an animal, and dose it with very low doses of THC.
 
*Bump*

Send off a copy to "Advanced Drug Discussion"..

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from h**p://www.chanvre-info.ch/info/en/article1946.html

"This findings could lead to the creation of antiviral drugs based on nonpsychoactive derivatives of THC.

The compound in marijuana that produces a high, delta-9 tetrahydrocannbinol or THC, may block the spread of several forms of cancer causing herpes viruses, University of South Florida College of Medicine scientists report. "

Source: Medical News Today, 23.9.2004

so it blocks the spread of cancer causing diseases, only to cause cancer itself?

thats rather conflicting news, isnt it?
 
Here's a link to the abstract of the article discussed above, and becasue it was published in a BMC journal, you can get free access to it. But the concentration is completely unreasobable... they're talking micromolar, those concentrations are probably neurotoxic... I don't know anything about virology, but there seems to be some odd comments on the cannabinoids receptor depedence of this effect... myabe DJDannyUhOh can comment...
 
I have no experience with any cannabinoid related viral RNA inhibition so I can't make an accurate guess as to why research in this specific area is conflicting. All I can say that we do not fully understand the complete function of each and every cannabinoid. The patients I currently work with I believe are being treated by their doctors with synthesized cannabinoids such as Dronabinol, Nabilone, Levonantradol, and BRL-4664 but they merely treat the side effects of chemo and not the cancer itself. However all of the patients report the medication does not work some of the time leading one to believe that there is some other force that affects the mechanisms of cannabinoid receptors. Besides, glioblastomas and other lesser known brain/nervous tissue cancers are the most difficult to understand. We barely understand the basic difference between a healthy lymphocyte and a cancer lymphocyte much beyond the fact its surface proteins slightly change in structure. Then, when you have a virus that throws lysogenic conversion into the equation, it becomes a huge mess.

Edit: Actually come to think of it, anything smoked should be assumed to contain carcinogens as a product of combustion and any research that "links" different outcomes at this point should be taken with a grain of salt.
 
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If I remember that article properly THC prohibits gamma herpes virus' from getting into cells and the gamma herpes virus is not herpes simplex III. Peace.
 
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