What's new for 'JKB_daily1' in PubMed
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Sender's message: Sepsis or genomics or altitude: JKB_daily1
Sent on Thursday, 2013 March 07Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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PubMed Results |
1. | Nat Med. 2013 Jan;19(1):9. doi: 10.1038/nm0113-9.Straight talk with...Stephen O'Brien. Interviewed by Elie Dolgin.O'Brien S.AbstractStephen O'Brien joined the US National Cancer Institute as a post doc in 1971 and climbed the ranks to become head of the institute's Laboratory of Genomic Diversity, a position he held for 25 years. But, after four decades at the government agency, O'Brien was ready for something new. In December 2011, he stepped down and took up a three-year, $5 million 'megagrant' in Russia through a program started a year earlier by the Russian Ministry of Education and Science to attract big-name researchers to work at least part-time in that country. O'Brien used his money to help launch the Theodosius Dobzhansky Center for Genome Bioinformatics at Saint Petersburg State University. Although O'Brien is a cancer researcher, he has diverse scientific interests. He led the team that discovered the CCR5-Δ32 mutation that confers resistance to HIV, and he has helped document the remarkable genetic uniformity of African cheetahs. Recently, he and two California scientists started the Genome 10K project, which aims to sequence the genetic blueprints of 10,000 vertebrate species. On a trip back to the US, O'Brien spoke with Elie Dolgin about how comparative genomics and his new Russian center will help advance the search for new therapeutics. |
PMID: 23295996 [PubMed - indexed for MEDLINE] | |
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2. | Nat Med. 2013 Jan;19(1):57-64. doi: 10.1038/nm.2999. Epub 2012 Dec 2.Chemotherapy-triggered cathepsin B release in myeloid-derived suppressor cells activates the Nlrp3 inflammasome and promotes tumor growth.Bruchard M, Mignot G, Derangère V, Chalmin F, Chevriaux A, Végran F, Boireau W, Simon B, Ryffel B, Connat JL, Kanellopoulos J, Martin F, Rébé C, Apetoh L, Ghiringhelli F.Institut National de Santé et de Recherche Médicale (INSERM) U866, Dijon, France. Comment in
AbstractChemotherapeutic agents are widely used for cancer treatment. In addition to their direct cytotoxic effects, these agents harness the host's immune system, which contributes to their antitumor activity. Here we show that two clinically used chemotherapeutic agents, gemcitabine (Gem) and 5-fluorouracil (5FU), activate the NOD-like receptor family, pyrin domain containing-3 protein (Nlrp3)-dependent caspase-1 activation complex (termed the inflammasome) in myeloid-derived suppressor cells (MDSCs), leading to production of interleukin-1β (IL-1β), which curtails anticancer immunity. Chemotherapy-triggered IL-1β secretion relied on lysosomal permeabilization and the release of cathepsin B, which bound to Nlrp3 and drove caspase-1 activation. MDSC-derived IL-1β induced secretion of IL-17 by CD4(+) T cells, which blunted the anticancer efficacy of the chemotherapy. Accordingly, Gem and 5FU exerted higher antitumor effects when tumors were established in Nlrp3(-/-) or Casp1(-/-) mice or wild-type mice treated with interleukin-1 receptor antagonist (IL-1Ra). Altogether, these results identify how activation of the Nlrp3 inflammasome in MDSCs by 5FU and Gem limits the antitumor efficacy of these chemotherapeutic agents. |
PMID: 23202296 [PubMed - indexed for MEDLINE] | |
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