Hello, everyone, and welcome to another working week. We hope the weekend was refreshing and invigorating as you prepare to resume the usual routine of meetings and deadlines. This may be mid-summer, but there is, as always, much to do. So please join us as we fortify ourselves with a mandatory cup of stimulation and get ready to attack our own to-list. Meanwhile, here are some tidbits. Hope your day goes well and let us know if you hear about anything interesting...
FDA OKs Novartis' Afinitor For Breast Cancer (Reuters)
Onyx Gets FDA Approval For Myeloma Drug (Xconomy)
California County To Vote On Drug Disposal (San Francisco Chronicle)
All HIV Patients Should Be Treated With ARVs: Panel (Reuters)
Merck Bets Its New Sleeping Pill Is No Yawner (Bloomberg News)
Pfizer Gets Positive EU Review Of Lung Cancer Drug (Bloomberg News)
Higher Severance For Merck KGgA Workers: Panel (World Radio Switzerland)
J&J Appeals $1.2 Billion Risperdal Ruling (Bloomberg News)
Pfizer Loses Prempro Ruling And Must Pay $10.4 Million (Bloomberg News)
EDITOR'S NOTE: Please check this post for updates during the day
3 Comments
However, according to some private researchers, they have found that there are actually two separate forms of mTOR, TORC1 and TORC2, and they sit at a critical point in cellular determination. Stimulated by the insulin growth pathway, cells must decide whether they will grow in size or divide. The mTOR proteins participate in this process by regulating protein synthesis and glucose uptake among other functions.
In turn, the mTOR pathway is regulated by numerous other factors like AMP kinase and AKT. The current crop of mTOR inhibitors all target TORC1. More interesting are the compounds that influence upstream signaling, including phosphoinositol kinase (PI3K) and AKT.
What we are coming to learn is that these are not targets but collections of targets. Indeed, the PI3K inhibitors themselves have influence on one, two or all of the distinct classes of phosphoinositol kinases.
Most of the studies to date have used compounds that affect all the classes equally (pan-inhibitors). Pharmaceutical companies are now developing highly selective inhibitors of this fundamental pathway. In addition, duel inhibitors that target both PI3K and mTOR are in clinical trials. What we are coming to realize is the complexity of these pathways.
What may prove more vexing still is their redundancy. One well-established by-product of successful inhibition of mTOR (principally TORC1) is the upstream activity of AKT via a feedback loop. This has the undesirable affect of redoubling mTOR stimulation through the very pharmacological manipulation that was designed to inhibit it. An unintended consequence of a well laid plan.
To unravel the complexities and redundancies of these processes, some private researchers have utilized the human tumor primary culture platform. It enables them to examine the end result of signal inhibition and dissect disease specific profiles. Using this approach they can define the specific operative pathways in each disease entity.
The technology is at our doorstwp. Scientists at Univ Utah and UCSF have discovered the DEC2 gene that allows mice to sleep less. If we could identify the same gene in humans and then develop drugs to turn on the activity of the gene this would be a tremendous advance. For anybody interested in getting ahead this would be a natural choice. And aren't we all interested in that? Multibillison dollar product, no brainer. Moreover it would allow the Adderall junkies to spare their drug for the real ADD kids.
http://www.sciencecodex.com/gene_variation_that_lets_people_get_by_on_fewer_zees_transferred_to_create_insomniac_mice