MDMA cures cancer...

Quote:

The serotonin transporter (SLC6A4) is present in B-cell clones of diverse malignant origin: probing a potential antitumor target for psychotropics Elizabeth J. Meredith, Michelle J. Holder, Anita Chamba, Anita Challa, Adrian Drake Lee, Christopher M. Bunce, Mark T. Drayson, Geoffrey Pilkington, Randy D. Blakely, Martin J. S. Dyer, Nicholas M. Barnes, and John Gordon The FASEB Journal Express Article doi:10.1096/fj.04-3477fje Published online May 3, 2005 Abstract Following our previous description of the serotonin transporter (SERT) acting as a conduit to 5-hydroxytryptamine (5-HT)-mediated apoptosis, specifically in Burkitt's lymphoma, we now detail its expression among a broad spectrum of B cell malignancy, while exploring additional SERT substrates for potential therapeutic activity. SERT was readily detected in derived B cell lines with origins as diverse as B cell precursor acute lymphoblastic leukemia, mantle cell lymphoma, diffuse large B cell lymphoma, and multiple myeloma. Concentration and timecourse kinetics for the antiproliferative and proapoptotic activities of the amphetamine derivatives fenfluramine (an appetite suppressant) and 3,4-methylenedioxymethamphetamine (MDMA; "Ecstasy" revealed them as being similar to the endogenous indoleamine. A tricyclic antidepressant, clomipramine, instead mirrored the behavior of the selective serotonin reuptake inhibitor fluoxetine, both being effective in the low micromolar range. A majority of neoplastic clones were sensitive to one or more of the serotonergic compounds. Dysregulated bcl-2 expression, either by t(14;1(q32;q21) translocation or its introduction as a constitutively active transgene, provided protection from proapoptotic but not antiproliferative outcomes. These data indicate a potential for SERT as a novel anti-tumor target for amphetamine analogs, while evidence is presented that the seemingly more promising antidepressants are likely impacting malignant B cells independently of the transporter itself.

And the general public's introduction can be found here.

Sorry, I don't have anything smart or witty of my own to add, I just thought this could be an interesting topic to initiate!


Edit: !A la verrga! Why can't I get the formatting and code to work? It works half-way?! I give up. Maybe one of you mods can figure out what the deal is and fix it? I know you love me, vulture!

[Edited on 13-7-2005 by lahthffire]

[Edited on 13-7-2005 by lahthffire]

Abuse of MDMA may or may not lead to the death of brain cells containing the SERT (serotonin transporter), but I don't think this article is necessarily suggesting so.

It's not saying that cells harbouring the SERT can be killed with the mentioned amphetamine derivatives, but rather they discuss it's use as a conduit for transporting these species into the cell where they can trigger the 5-hydroxytryptamine (5-HT, serotonin) mediated apoptosis. (apoptosis - programmed cell death)

So apparently some cell types contain some mechanism for self destruction which is triggered by serotonin (5-HT). And the drugs they mentioned, which we already know share similar properties with serotonin in the brain, apparently also are capable of triggering the self-destruct mechanism.

What I get from this article is that the tumor cells of certain types of B-cell malignancies (in other words, certain types of lymphoma) do undergo this 5-HT mediated apoptosis, and that many amphetamine derivatives (as well as other serotonin related drugs) are also proving to be capable of doing the mediation. And that identification of malignancies that have the SERT could be a good way of identifying possible candidates for this type of treatment.

I find it HIGHLY unlikely that our brain cells would ever undergo 5-HT mediated apoptosis, considering that if they did, every second of normal brain operation would be triggering massive cell death!

Would it be too much to ask if you could please attach the article?

sparky (~_~)