Starving ER+ breast cancer cells by blocking their amino acid transporter (necessary)

[Rich66]

The compound they used is alpha-methyl-DL-tryptophan, already used in humans for short periods when they are getting a PET scan in certain areas of the brain.

Already being used..gotta love that.


Here is the full research paper:
http://www.jbc.org/content/early/201...11.229518.long

In conclusion, the present studies provide the proof-of-principle that SLC6A14 is a potential drug target for the treatment of ER-positive breast cancer. α-MT in itself represents a viable drug for this purpose. It could also serve as a lead compound for the design and development of more potent blockers of SLC6A14 for future use.

Article mentioning AMT and serotonin level monitoring via PET:

http://www.nature.com/jcbfm/journal/.../9590848a.html

Alpha-methyl-L-tryptophan (AMT) is an analog of tryptophan, the precursor of the neurotransmitter serotonin (5-HT, 5-hydroxytryptamine). For the past decade, Diksic and colleagues performed numerous studies of radiolabeled AMT in rats and dogs with the goal of validating AMT as a tracer for the measurement of the rate of sertonin synthesis in vivo in humans with positron emission tomography (PET).

In summary, we believe that the rat studies demonstrate unequivocably the presence of irreversible uptake of AMT. However, these studies also demonstrate that the serotonin synthesis component is a fraction of the irreversible uptake of the tracer (Fig. 5). Thus, although lacking properties for measuring the absolute synthesis rate, AMT uptake is useful as an index or capacity for serotonin synthesis.

This all begs the question of whether available anxiety/depression drugs or supplements that alter serotonin levels might be useful in this ER+ cancer equation.