Germline finding of a genetic variant that could be linked to SPOP mutations. https://www.nature.com/articles/s41467-017-00046-0
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“The NCI will continue to supply the NCI-60 cell lines to researchers, but will eventually refocus its drug screening on newer models. It is developing hundreds of ‘patient-derived xenografts’ (PDXs), which are created by implanting small chunks of human tumours into mice. There, the tumours grow in an environment that, although not human, better mimics their native environment”
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$GOOG’s Road Map to Global Domination
http://www.NYTimes.com/2013/12/15/magazine/googles-plan-for-global-domination-dont-ask-why-ask-where.html Old article but discussion on #opendata v closed maps still relevant
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“O’Reilly is more skeptical. “An open-hardware play broke the IBM monopoly, an open-software play broke the Microsoft monopoly, and eventually an open-data play will prevail,” O’Reilly admits, but he points out that those earlier cases were not instances of direct competition between rival companies. “It wasn’t a plug-compatible mainframe clone that dethroned IBM; it wasn’t a free operating system like Linux that dethroned Windows.” Rather, he says, “it was this toy, the personal computer, it was the global operating system that we call the Internet.”
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“Current treatments for diseases related to ageing “just exchange one disease for another”, says physician Nir Barzilai of the Albert Einstein College of Medicine in New York. That is because people treated for one age-related disease often go on to die from another relatively soon thereafter. “What we want to show is that if we delay ageing, that’s the best way to delay disease.”
Barzilai and other researchers plan to test that notion in a clinical trial called Targeting Aging with Metformin, or TAME. They will give the drug metformin to thousands of people who already have one or two of three conditions — cancer, heart disease or cognitive impairment — or are at risk of them. People with type 2 diabetes cannot be enrolled because metformin is already used to treat that disease.
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http://www.nature.com/news/anti-ageing-pill-pushed-as-bona-fide-drug-1.17769
Make Pharma Great Again w. AI, by @mostafabenh
https://Medium.com/@mostafab/make-pharma-great-again-with-artificial-intelligence-some-challenges-50e91ea9988d Optimism-inducing Moore’s law in tech vs. #Eroom’s law for drugs
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Drug discovery is getting increasingly tough and expensive. Despite technological progress, the cost of developing a new drug doubles every nine years. That’s Eroom’s law of Pharma, which mirrors Moore’s law for computer performance.
….
Drugs are getting more expensive
In the tech industry, the situation is different. Optimism prevails. Tech is fueled by Moore’s law, the fact that computer performance is doubling every 18 months.
Moore’s law
This exponential progress keeps prices low. For example, Google gives away the use of its new TPU chip for free, for some scientific projects. Tech companies are more generous due to their feeling of abundance. How can Tech help Pharma, especially at a time of expansion for Artificial Intelligence?
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‘Make Pharma Great Again with Artificial Intelligence: some Challenges’
Clues from the resilient
http://www.ScienceMag.org/content/344/6187/970.full Potential 2nd site mutations that neutralize #Mendelian-disease mutations
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“For 127 catastrophic Mendelian diseases (those caused by a single gene such as cystic fibrosis and ataxia-telangiectasia), there are presently 164 genes harboring 685 known recurrent variants that are highly penetrant and causal for deleterious traits, most typically manifesting in individuals before the age of 18 (). …For common diseases, the observed small effect sizes of individual gene variants limit diagnostic potential, and given that most variants identified have an unclear function, how to target the corresponding gene for therapeutic intervention is typically unclear. For rarer Mendelian disorders, although genetics directly implicate a specific gene in a disease, a majority of such cases relate to loss-of-function mutations. Designing small molecules to fix the corresponding broken protein has proven difficult….
The prominent role of second-site mutations and environmental factors that enable resistance to (or buffer against) disease traits has been well established in a multitude of model organisms from yeast to mice (–). Screening for second-site mutations in “resilient” individuals that prevent disease-causing alleles from manifesting their effects could identify targets to which drugs would be designed to disrupt their function, as opposed to targeting the disease-causing gene directly. Genetic studies examining seemingly healthy people have revealed, for example, rare mutations in chemokine (C-C motif) receptor type 5 (the co-receptor for human immunodeficiency virus) that block HIV infection (), and secondary mutations in fetal globin genes that modify the severity of sickle cell disease by buffering primary mutations in β-globin genes ()
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Studies published in 2013 indicate that high levels of TMAO in the blood are associated with an increased risk of major adverse cardiovascular events.[9] The concentration of TMAO in the blood increases after consuming foods containing carnitine[10] or
lecithin[9] if the bacteria that convert those substances to TMAO are present in the gut.[11] High concentrations of carnitine are found in red meat, some energy drinks, and some dietary supplements;
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https://en.m.wikipedia.org/wiki/Trimethylamine_N-oxide
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A peculiar cross reaction with a specific food exists with Lipitor and other “statin” drugs used to lower cholesterol. Grapefruit juice blocks special enzymes in the wall of the small intestine that actually destroy many medications, including Lipitor, and prevents their absorption into the body.
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http://www.rxlist.com/script/main/mobileart-rx.asp?articlekey=87598