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Karen Yook's insight:
"Cancer is incredibly complex, with significant heterogeneity among patients, even with tumors of similar characteristics, and there is significant intra-tumoral heterogeneity that evolves over time and in response to therapy," said Dr. Lincoln Stein, Director of OICR's Informatics and Bio-Computing Program and Director of the ICGC's Data Coordination Centre housed in Toronto, Canada."
"The ICGC, comprised of research organizations around the world, is committed to making data rapidly and freely available."
“#OpenWorm is an iphone app which allow you to look inside the body of C. elegans the most well researched model animal. Every embryonic cell division has been mapped, It has a complete connectome and...”
“Through his calculated cross breeding studies of garden peas, Mendel discovered a pattern of dominant and recessive traits which lead to groundbreaking (100 Greatest Discoveries Shorts: Genetics : Video : Science Channel”
“Illumina, the biggest maker of genomic sequencing machines, say they've broken the "sound barrier" of sequencing.”
Karen Yook's insight:
It was only a matter of time (and the right technology!). Glad we are there now. At this point there really can be no argument for the FDA to continue banning 23andMe from reporting health-impacting genome marker results to its customers.
New research in simple animals suggests that combining mutants can lead to radical lifespan extension. Scientists at the Buck Institute combined mutations in two pathways well-known for lifespan extension and report a synergistic five-fold extension of longevity in the nematode C. elegans. The research, done at the Buck Institute and published online in Cell Reports on December 12, 2013, introduces the possibility of combination therapy for aging and the maladies associated with it.
The mutations inhibited key molecules involved in insulin signaling (IIS) and the nutrient signaling pathway Target of Rapamycin (TOR). Lead scientist and Buck faculty Pankaj Kapahi, PhD, said single mutations in TOR (in this case RSKS-1) usually result in a 30 percent lifespan extension, while mutations in IIS (Daf-2) often result in a doubling of lifespan in the worms -- added together they would be expected to extend longevity by 130 percent. "Instead, what we have here is a synergistic five-fold increase in lifespan," Kapahi said. "The two mutations set off a positive feedback loop in specific tissues that amplified lifespan. Basically these worms lived to the human equivalent of 400 to 500 years."
Kapahi said the research points to the possibility of using combination therapies for aging, similar to what is done for cancer and HIV. "In the early years, cancer researchers focused on mutations in single genes, but then it became apparent that different mutations in a class of genes were driving the disease process," he said. "The same thing is likely happening in aging." Kapahi said this research could help explain why scientists are having a difficult time identifying single genes responsible for the long lives experienced by human centenarians. "It's quite probable that interactions between genes are critical in those fortunate enough to live very long, healthy lives."
Former Buck postdoctoral fellow Di Chen, PhD, now an associate professor at the Model Animal Research Center, Nanjing University, China, lead author of the study, said that the positive feedback loop (DAF-16 via the AMPK complex) originated in the germline tissue of worms. The germline is a sequence of reproductive cells that may be passed onto successive generations. "The germline was the key tissue for the synergistic gain in longevity -- we think it may be where the interactions between the two mutations are integrated," Chen said. "The finding has implications for similar synergy between the two pathways in more complex organisms."
Kapahi said ideally the research would move into mice as a way of determining if the lifespan-extending synergy extends into mammals. "The idea would be to use mice genetically engineered to have suppressed insulin signaling, and then treat them with the drug rapamycin, which is well-known to suppress the TOR pathway."
Pankaj Kapahi, PhD et al. Germline Signaling Mediates the Synergistically Prolonged Longevity by Double Mutations in daf-2 and rsks-1 in C. elegans. Cell Reports, December 2013
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