What's new for 'JKB_daily1' in PubMed

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Wednesday, 2012 May 09
Search: (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

Items 1 - 10 of 10

1.	Lancet. 2012 Apr 21;379(9825):1484; author reply 1484-5. Paediatric hospital-acquired bacteraemia in developing countries. Wolkewitz M, Di Termini S, Cooper B, Meerpohl J, Schumacher M. Comment on Lancet. 2011 Dec 10;378(9808):2021-7.
	PMID: 22521064 [PubMed - indexed for MEDLINE]
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2.	Lancet. 2012 Apr 21;379(9825):1483-4; author reply 1484-5. Paediatric hospital-acquired bacteraemia in developing countries. Das RR. Comment on Lancet. 2011 Dec 10;378(9808):2021-7.
	PMID: 22521062 [PubMed - indexed for MEDLINE]
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3.	Lancet. 2012 Apr 21;379(9825):1462. New hope for sepsis. [No authors listed]
	PMID: 22521056 [PubMed - indexed for MEDLINE]
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4.	Science. 2012 Apr 20;336(6079):353-5. Recent plant diversity changes on Europe's mountain summits. Pauli H, Gottfried M, Dullinger S, Abdaladze O, Akhalkatsi M, Benito Alonso JL, Coldea G, Dick J, Erschbamer B, Fernández Calzado R, Ghosn D, Holten JI, Kanka R, Kazakis G, Kollár J, Larsson P, Moiseev P, Moiseev D, Molau U, Molero Mesa J, Nagy L, Pelino G, Puşcaş M, Rossi G, Stanisci A, Syverhuset AO, Theurillat JP, Tomaselli M, Unterluggauer P, Villar L, Vittoz P, Grabherr G. Source Institute of Mountain Research, Austrian Academy of Sciences, c/o University of Vienna, 1030 Wien, Austria. Abstract In mountainous regions, climate warming is expected to shift species' ranges to higher altitudes. Evidence for such shifts is still mostly from revisitations of historical sites. We present recent (2001 to 2008) changes in vascular plant species richness observed in a standardized monitoring network across Europe's major mountain ranges. Species have moved upslope on average. However, these shifts had opposite effects on the summit floras' species richness in boreal-temperate mountain regions (+3.9 species on average) and Mediterranean mountain regions (-1.4 species), probably because recent climatic trends have decreased the availability of water in the European south. Because Mediterranean mountains are particularly rich in endemic species, a continuation of these trends might shrink the European mountain flora, despite an average increase in summit species richness across the region.
	PMID: 22517860 [PubMed - indexed for MEDLINE]
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5.	Nature. 2012 Mar 29;483(7391):637-9. Epigenetics: Marked for success. Ledford H.
	PMID: 22468273 [PubMed - indexed for MEDLINE]
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6.	Nature. 2012 Mar 28;483(7391):603-7. doi: 10.1038/nature11003. The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity. Barretina J, Caponigro G, Stransky N, Venkatesan K, Margolin AA, Kim S, Wilson CJ, Lehár J, Kryukov GV, Sonkin D, Reddy A, Liu M, Murray L, Berger MF, Monahan JE, Morais P, Meltzer J, Korejwa A, Jané-Valbuena J, Mapa FA, Thibault J, Bric-Furlong E, Raman P, Shipway A, Engels IH, Cheng J, Yu GK, Yu J, Aspesi P Jr, de Silva M, Jagtap K, Jones MD, Wang L, Hatton C, Palescandolo E, Gupta S, Mahan S, Sougnez C, Onofrio RC, Liefeld T, MacConaill L, Winckler W, Reich M, Li N, Mesirov JP, Gabriel SB, Getz G, Ardlie K, Chan V, Myer VE, Weber BL, Porter J, Warmuth M, Finan P, Harris JL, Meyerson M, Golub TR, Morrissey MP, Sellers WR, Schlegel R, Garraway LA. Source The Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA. Comment in Nature. 2012 Mar 29;483(7391):544-5. Abstract The systematic translation of cancer genomic data into knowledge of tumour biology and therapeutic possibilities remains challenging. Such efforts should be greatly aided by robust preclinical model systems that reflect the genomic diversity of human cancers and for which detailed genetic and pharmacological annotation is available. Here we describe the Cancer Cell Line Encyclopedia (CCLE): a compilation of gene expression, chromosomal copy number and massively parallel sequencing data from 947 human cancer cell lines. When coupled with pharmacological profiles for 24 anticancer drugs across 479 of the cell lines, this collection allowed identification of genetic, lineage, and gene-expression-based predictors of drug sensitivity. In addition to known predictors, we found that plasma cell lineage correlated with sensitivity to IGF1 receptor inhibitors; AHR expression was associated with MEK inhibitor efficacy in NRAS-mutant lines; and SLFN11 expression predicted sensitivity to topoisomerase inhibitors. Together, our results indicate that large, annotated cell-line collections may help to enable preclinical stratification schemata for anticancer agents. The generation of genetic predictions of drug response in the preclinical setting and their incorporation into cancer clinical trial design could speed the emergence of 'personalized' therapeutic regimens. PMCID: PMC3320027 [Available on 2012/9/29]
	PMID: 22460905 [PubMed - indexed for MEDLINE]
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7.	Nature. 2012 Mar 28;483(7391):570-5. doi: 10.1038/nature11005. Systematic identification of genomic markers of drug sensitivity in cancer cells. Garnett MJ, Edelman EJ, Heidorn SJ, Greenman CD, Dastur A, Lau KW, Greninger P, Thompson IR, Luo X, Soares J, Liu Q, Iorio F, Surdez D, Chen L, Milano RJ, Bignell GR, Tam AT, Davies H, Stevenson JA, Barthorpe S, Lutz SR, Kogera F, Lawrence K, McLaren-Douglas A, Mitropoulos X, Mironenko T, Thi H, Richardson L, Zhou W, Jewitt F, Zhang T, O'Brien P, Boisvert JL, Price S, Hur W, Yang W, Deng X, Butler A, Choi HG, Chang JW, Baselga J, Stamenkovic I, Engelman JA, Sharma SV, Delattre O, Saez-Rodriguez J, Gray NS, Settleman J, Futreal PA, Haber DA, Stratton MR, Ramaswamy S, McDermott U, Benes CH. Source Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK. Comment in Nature. 2012 Mar 29;483(7391):544-5. Abstract Clinical responses to anticancer therapies are often restricted to a subset of patients. In some cases, mutated cancer genes are potent biomarkers for responses to targeted agents. Here, to uncover new biomarkers of sensitivity and resistance to cancer therapeutics, we screened a panel of several hundred cancer cell lines--which represent much of the tissue-type and genetic diversity of human cancers--with 130 drugs under clinical and preclinical investigation. In aggregate, we found that mutated cancer genes were associated with cellular response to most currently available cancer drugs. Classic oncogene addiction paradigms were modified by additional tissue-specific or expression biomarkers, and some frequently mutated genes were associated with sensitivity to a broad range of therapeutic agents. Unexpected relationships were revealed, including the marked sensitivity of Ewing's sarcoma cells harbouring the EWS (also known as EWSR1)-FLI1 gene translocation to poly(ADP-ribose) polymerase (PARP) inhibitors. By linking drug activity to the functional complexity of cancer genomes, systematic pharmacogenomic profiling in cancer cell lines provides a powerful biomarker discovery platform to guide rational cancer therapeutic strategies.
	PMID: 22460902 [PubMed - indexed for MEDLINE]
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8.	Nature. 2012 Mar 28;483(7391):546-8. doi: 10.1038/483546a. Cancer: Clinical trials unite mice and humans. Johnson L. Comment on Nature. 2012 Mar 29;483(7391):613-7.
	PMID: 22460895 [PubMed - indexed for MEDLINE]
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9.	Nature. 2012 Mar 28;483(7391):520-2. doi: 10.1038/483520a. Flu surveillance lacking. Butler D.
	PMID: 22460875 [PubMed - indexed for MEDLINE]
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10.	Nature. 2012 Mar 18;483(7391):613-7. doi: 10.1038/nature10937. A murine lung cancer co-clinical trial identifies genetic modifiers of therapeutic response. Chen Z, Cheng K, Walton Z, Wang Y, Ebi H, Shimamura T, Liu Y, Tupper T, Ouyang J, Li J, Gao P, Woo MS, Xu C, Yanagita M, Altabef A, Wang S, Lee C, Nakada Y, Peña CG, Sun Y, Franchetti Y, Yao C, Saur A, Cameron MD, Nishino M, Hayes DN, Wilkerson MD, Roberts PJ, Lee CB, Bardeesy N, Butaney M, Chirieac LR, Costa DB, Jackman D, Sharpless NE, Castrillon DH, Demetri GD, Jänne PA, Pandolfi PP, Cantley LC, Kung AL, Engelman JA, Wong KK. Source Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, USA. Comment in Nature. 2012 Mar 29;483(7391):546-8. Abstract Targeted therapies have demonstrated efficacy against specific subsets of molecularly defined cancers. Although most patients with lung cancer are stratified according to a single oncogenic driver, cancers harbouring identical activating genetic mutations show large variations in their responses to the same targeted therapy. The biology underlying this heterogeneity is not well understood, and the impact of co-existing genetic mutations, especially the loss of tumour suppressors, has not been fully explored. Here we use genetically engineered mouse models to conduct a 'co-clinical' trial that mirrors an ongoing human clinical trial in patients with KRAS-mutant lung cancers. This trial aims to determine if the MEK inhibitor selumetinib (AZD6244) increases the efficacy of docetaxel, a standard of care chemotherapy. Our studies demonstrate that concomitant loss of either p53 (also known as Tp53) or Lkb1 (also known as Stk11), two clinically relevant tumour suppressors, markedly impaired the response of Kras-mutant cancers to docetaxel monotherapy. We observed that the addition of selumetinib provided substantial benefit for mice with lung cancer caused by Kras and Kras and p53 mutations, but mice with Kras and Lkb1 mutations had primary resistance to this combination therapy. Pharmacodynamic studies, including positron-emission tomography (PET) and computed tomography (CT), identified biological markers in mice and patients that provide a rationale for the differential efficacy of these therapies in the different genotypes. These co-clinical results identify predictive genetic biomarkers that should be validated by interrogating samples from patients enrolled on the concurrent clinical trial. These studies also highlight the rationale for synchronous co-clinical trials, not only to anticipate the results of ongoing human clinical trials, but also to generate clinically relevant hypotheses that can inform the analysis and design of human studies.
	PMID: 22425996 [PubMed - indexed for MEDLINE]
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