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

Sent on Wednesday, 2014 August 13
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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1.	N Engl J Med. 2014 Jul 31;371(5):411-23. doi: 10.1056/NEJMoa1314981. Spread of artemisinin resistance in Plasmodium falciparum malaria. Ashley EA1, Dhorda M, Fairhurst RM, Amaratunga C, Lim P, Suon S, Sreng S, Anderson JM, Mao S, Sam B, Sopha C, Chuor CM, Nguon C, Sovannaroth S, Pukrittayakamee S, Jittamala P, Chotivanich K, Chutasmit K, Suchatsoonthorn C, Runcharoen R, Hien TT, Thuy-Nhien NT, Thanh NV, Phu NH, Htut Y, Han KT, Aye KH, Mokuolu OA, Olaosebikan RR, Folaranmi OO, Mayxay M, Khanthavong M, Hongvanthong B, Newton PN, Onyamboko MA, Fanello CI, Tshefu AK, Mishra N, Valecha N, Phyo AP, Nosten F, Yi P, Tripura R, Borrmann S, Bashraheil M, Peshu J, Faiz MA, Ghose A, Hossain MA, Samad R, Rahman MR, Hasan MM, Islam A, Miotto O, Amato R, MacInnis B, Stalker J, Kwiatkowski DP, Bozdech Z, Jeeyapant A, Cheah PY, Sakulthaew T, Chalk J, Intharabut B, Silamut K, Lee SJ, Vihokhern B, Kunasol C, Imwong M, Tarning J, Taylor WJ, Yeung S, Woodrow CJ, Flegg JA, Das D, Smith J, Venkatesan M, Plowe CV, Stepniewska K, Guerin PJ, Dondorp AM, Day NP, White NJ; Tracking Resistance to Artemisinin Collaboration (TRAC). Author information: 1The authors' affiliations are listed in the Appendix. Comment in Treatment of malaria--a continuing challenge. [N Engl J Med. 2014] Treatment of malaria--a continuing challenge.Greenwood B. N Engl J Med. 2014 Jul 31; 371(5):474-5. Abstract BACKGROUND: Artemisinin resistance in Plasmodium falciparum has emerged in Southeast Asia and now poses a threat to the control and elimination of malaria. Mapping the geographic extent of resistance is essential for planning containment and elimination strategies. METHODS: Between May 2011 and April 2013, we enrolled 1241 adults and children with acute, uncomplicated falciparum malaria in an open-label trial at 15 sites in 10 countries (7 in Asia and 3 in Africa). Patients received artesunate, administered orally at a daily dose of either 2 mg per kilogram of body weight per day or 4 mg per kilogram, for 3 days, followed by a standard 3-day course of artemisinin-based combination therapy. Parasite counts in peripheral-blood samples were measured every 6 hours, and the parasite clearance half-lives were determined. RESULTS: The median parasite clearance half-lives ranged from 1.9 hours in the Democratic Republic of Congo to 7.0 hours at the Thailand-Cambodia border. Slowly clearing infections (parasite clearance half-life >5 hours), strongly associated with single point mutations in the "propeller" region of the P. falciparum kelch protein gene on chromosome 13 (kelch13), were detected throughout mainland Southeast Asia from southern Vietnam to central Myanmar. The incidence of pretreatment and post-treatment gametocytemia was higher among patients with slow parasite clearance, suggesting greater potential for transmission. In western Cambodia, where artemisinin-based combination therapies are failing, the 6-day course of antimalarial therapy was associated with a cure rate of 97.7% (95% confidence interval, 90.9 to 99.4) at 42 days. CONCLUSIONS: Artemisinin resistance to P. falciparum, which is now prevalent across mainland Southeast Asia, is associated with mutations in kelch13. Prolonged courses of artemisinin-based combination therapies are currently efficacious in areas where standard 3-day treatments are failing. (Funded by the U.K. Department of International Development and others; ClinicalTrials.gov number, NCT01350856.). Free Article
	PMID: 25075834 [PubMed - in process]
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2.	N Engl J Med. 2014 Jul 31;371(5):403-10. doi: 10.1056/NEJMoa1315860. Spiroindolone KAE609 for falciparum and vivax malaria. White NJ1, Pukrittayakamee S, Phyo AP, Rueangweerayut R, Nosten F, Jittamala P, Jeeyapant A, Jain JP, Lefèvre G, Li R, Magnusson B, Diagana TT, Leong FJ. Author information: 1From the Mahidol-Oxford Tropical Medicine Research Unit (N.J.W., F.N., A.J.) and the Department of Clinical Tropical Medicine (S.P., P.J.), Faculty of Tropical Medicine, Mahidol University, Bangkok, and the Shoklo Malaria Research Unit, Faculty of Tropical Medicine, Mahidol-Oxford Tropical Medicine Research Unit, Mahidol University (A.P.P., F.N.), and Mae Sot General Hospital (R.R.), Mae Sot - all in Thailand; the Centre for Tropical Medicine, Nuffield Department of Medicine, University of Oxford, Oxford, United Kingdom (N.J.W., F.N.); Novartis Healthcare, Hyderabad, India (J.P.J.); Novartis, Basel, Switzerland (G.L., B.M.); Novartis Institute of Biomedical Research, Beijing (R.L.); and Novartis Institute for Tropical Diseases, Singapore (T.T.D., F.J.L.). Comment in Treatment of malaria--a continuing challenge. [N Engl J Med. 2014] Treatment of malaria--a continuing challenge.Greenwood B. N Engl J Med. 2014 Jul 31; 371(5):474-5. Abstract BACKGROUND: KAE609 (cipargamin; formerly NITD609, Novartis Institute for Tropical Diseases) is a new synthetic antimalarial spiroindolone analogue with potent, dose-dependent antimalarial activity against asexual and sexual stages of Plasmodium falciparum. METHODS: We conducted a phase 2, open-label study at three centers in Thailand to assess the antimalarial efficacy, safety, and adverse-event profile of KAE609, at a dose of 30 mg per day for 3 days, in two sequential cohorts of adults with uncomplicated P. vivax malaria (10 patients) or P. falciparum malaria (11). The primary end point was the parasite clearance time. RESULTS: The median parasite clearance time was 12 hours in each cohort (interquartile range, 8 to 16 hours in patients with P. vivax malaria and 10 to 16 hours in those with P. falciparum malaria). The median half-lives for parasite clearance were 0.95 hours (range, 0.68 to 2.01; interquartile range, 0.85 to 1.14) in the patients with P. vivax malaria and 0.90 hours (range, 0.68 to 1.64; interquartile range, 0.78 to 1.07) in those with P. falciparum malaria. By comparison, only 19 of 5076 patients with P. falciparum malaria (<1%) who were treated with oral artesunate in Southeast Asia had a parasite clearance half-life of less than 1 hour. Adverse events were reported in 14 patients (67%), with nausea being the most common. The adverse events were generally mild and did not lead to any discontinuations of the drug. The mean terminal half-life for the elimination of KAE609 was 20.8 hours (range, 11.3 to 37.6), supporting a once-daily oral dosing regimen. CONCLUSIONS: KAE609, at dose of 30 mg daily for 3 days, cleared parasitemia rapidly in adults with uncomplicated P. vivax or P. falciparum malaria. (Funded by Novartis and others; ClinicalTrials.gov number, NCT01524341.). Free Article
	PMID: 25075833 [PubMed - in process]
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3.	Nat Genet. 2014 Jun;46(6):530-1. doi: 10.1038/ng.2993. Exploring new models of easiRNA biogenesis. Sarazin A, Voinnet O. Author information: Department of Biology at the Swiss Federal Institute of Technology Zürich, Zürich, Switzerland. Comment on miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis. [Nature. 2014] miRNAs trigger widespread epigenetically activated siRNAs from transposons in Arabidopsis.Creasey KM, Zhai J, Borges F, Van Ex F, Regulski M, Meyers BC, Martienssen RA. Nature. 2014 Apr 17; 508(7496):411-5. Epub 2014 Mar 16. Abstract Although silent transposons in plants can be reactivated by stress or during development, their potential deleterious effects are prevented by transposon-derived epigenetically activated small interfering RNAs (easiRNAs). A new study shows how serendipitous interactions between reactivated transposons and endogenous microRNAs might initiate easiRNA biogenesis, establishing an unexpected link between these two classes of silencing small RNAs.
	PMID: 24866189 [PubMed - in process]
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4.	Nat Genet. 2014 Jun;46(6):567-72. doi: 10.1038/ng.2987. Epub 2014 May 18. Genome sequence of the cultivated cotton Gossypium arboreum. Li F1, Fan G2, Wang K1, Sun F2, Yuan Y 1, Song G1, Li Q3, Ma Z4, Lu C5, Zou C5, Chen W6, Liang X6, Shang H5, Liu W6, Shi C6, Xiao G7, Gou C6, Ye W5, Xu X6, Zhang X5, Wei H5, Li Z5, Zhang G8, Wang J6, Liu K5, Kohel RJ9, Percy RG9, Yu JZ9, Zhu YX7, Wang J10, Yu S5. Author information: 11] State Key Laboratory of Cotton Biology, Institute of Cotton Research of the Chinese Academy of Agricultural Sciences, Anyang, China. [2]. 21] BGI-Shenzhen, Shenzhen, China. [2]. 31] State Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China. [2]. 41] Key Laboratory for Crop Germplasm Resources of Hebei, Agricultural University of Hebei, Baoding, China. [2]. 5State Key Laboratory of Cotton Biology, Institute of Cotton Research of the Chinese Academy of Agricultural Sciences, Anyang, China. 6BGI-Shenzhen, Shenzhen, China. 7State Key Laboratory of Protein and Plant Gene Research, College of Life Sciences, Peking University, Beijing, China. 8Key Laboratory for Crop Germplasm Resources of Hebei, Agricultural University of Hebei, Baoding, China. 9Crop Germplasm Research Unit, Southern Plains Agricultural Research Center, US Department of Agriculture-Agricultural Research Service (USDA-ARS), College Station, Texas, USA. 101] BGI-Shenzhen, Shenzhen, China. [2] Department of Biology, University of Copenhagen, Copenhagen, Denmark. [3] King Abdulaziz University, Jeddah, Saudi Arabia. [4] Macau University of Science and Technology, Macau, China. [5] Department of Medicine, University of Hong Kong, Hong Kong. [6] State Key Laboratory of Pharmaceutical Biotechnology, University of Hong Kong, Hong Kong. Abstract The complex allotetraploid nature of the cotton genome (AADD; 2n = 52) makes genetic, genomic and functional analyses extremely challenging. Here we sequenced and assembled the Gossypium arboreum (AA; 2n = 26) genome, a putative contributor of the A subgenome. A total of 193.6 Gb of clean sequence covering the genome by 112.6-fold was obtained by paired-end sequencing. We further anchored and oriented 90.4% of the assembly on 13 pseudochromosomes and found that 68.5% of the genome is occupied by repetitive DNA sequences. We predicted 41,330 protein-coding genes in G. arboreum. Two whole-genome duplications were shared by G. arboreum and Gossypium raimondii before speciation. Insertions of long terminal repeats in the past 5 million years are responsible for the twofold difference in the sizes of these genomes. Comparative transcriptome studies showed the key role of the nucleotide binding site (NBS)-encoding gene family in resistance to Verticillium dahliae and the involvement of ethylene in the development of cotton fiber cells.
	PMID: 24836287 [PubMed - in process]
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5.	Nat Genet. 2014 Jun;46(6):588-94. doi: 10.1038/ng.2981. Epub 2014 May 4. Pan-cancer genetic analysis identifies PARK2 as a master regulator of G1/S cyclins. Gong Y1, Zack TI2, Morris LG3, Lin K4, Hukkelhoven E5, Raheja R5, Tan IL4, Turcan S1, Veeriah S1, Meng S1, Viale A6, Schumacher SE7, Palmedo P8, Beroukhim R9, Chan TA10. Author information: 1Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. 21] Broad Institute, Cambridge, Massachusetts, USA. [2] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. [3] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. [4] Center for Cancer Genome Characterization, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. [5] Biophysics Program, Harvard University, Boston, Massachusetts, USA. 3Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. 4Weill Cornell College of Medicine, New York, New York, USA. 5Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. 6Genomics Core, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. 7Broad Institute, Cambridge, Massachusetts, USA. 81] Broad Institute, Cambridge, Massachusetts, USA. [2] Center for Biomedical Informatics, Harvard University, Boston, Massachusetts, USA. 91] Broad Institute, Cambridge, Massachusetts, USA. [2] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. [3] Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. [4] Center for Cancer Genome Characterization, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. 101] Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. [2] Department of Radiation Oncology, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. [3] Brain Tumor Center, Memorial Sloan-Kettering Cancer Center, New York, New York, USA. Comment in PARK2 orchestrates cyclins to avoid cancer. [Nat Genet. 2014] PARK2 orchestrates cyclins to avoid cancer.Bartek J, Hodny Z. Nat Genet. 2014 Jun; 46(6):527-8. Abstract Coordinate control of different classes of cyclins is fundamentally important for cell cycle regulation and tumor suppression, yet the underlying mechanisms are incompletely understood. Here we show that the PARK2 tumor suppressor mediates this coordination. The PARK2 E3 ubiquitin ligase coordinately controls the stability of both cyclin D and cyclin E. Analysis of approximately 5,000 tumor genomes shows that PARK2 is a very frequently deleted gene in human cancer and uncovers a striking pattern of mutual exclusivity between PARK2 deletion and amplification of CCND1, CCNE1 or CDK4-implicating these genes in a common pathway. Inactivation of PARK2 results in the accumulation of cyclin D and acceleration of cell cycle progression. Furthermore, PARK2 is a component of a new class of cullin-RING-containing ubiquitin ligases targeting both cyclin D and cyclin E for degradation. Thus, PARK2 regulates cyclin-CDK complexes, as does the CDK inhibitor p16, but acts as a master regulator of the stability of G1/S cyclins.
	PMID: 24793136 [PubMed - in process]
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6.	Nat Genet. 2014 Jun;46(6):558-66. doi: 10.1038/ng.2965. Epub 2014 Apr 28. Deep transcriptome profiling of mammalian stem cells supports a regulatory role for retrotransposons in pluripotency maintenance. Fort A1, Hashimoto K1, Yamada D2, Salimullah M3, Keya CA3, Saxena A1, Bonetti A3, Voineagu I1, Bertin N1, Kratz A3, Noro Y3, Wong CH4, de Hoon M3, Andersson R5, Sandelin A5, Suzuki H3, Wei CL4, Koseki H2; FANTOM Consortium, Hasegawa Y3, Forrest AR3, Carninci P3. Author information: 11] Division of Genomic Technologies, RIKEN Center for Life Science Technologies, Yokohama, Japan. [2]. 2Laboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan. 3Division of Genomic Technologies, RIKEN Center for Life Science Technologies, Yokohama, Japan. 4Sequencing Technology Group, Joint Genome Institute, Lawrence Berkeley National Laboratory, Walnut Creek, California, USA. 5Bioinformatics Centre, Department of Biology and Biotech Research and Innovation Centre, University of Copenhagen, Copenhagen, Denmark. Abstract The importance of microRNAs and long noncoding RNAs in the regulation of pluripotency has been documented; however, the noncoding components of stem cell gene networks remain largely unknown. Here we investigate the role of noncoding RNAs in the pluripotent state, with particular emphasis on nuclear and retrotransposon-derived transcripts. We have performed deep profiling of the nuclear and cytoplasmic transcriptomes of human and mouse stem cells, identifying a class of previously undetected stem cell-specific transcripts. We show that long terminal repeat (LTR)-derived transcripts contribute extensively to the complexity of the stem cell nuclear transcriptome. Some LTR-derived transcripts are associated with enhancer regions and are likely to be involved in the maintenance of pluripotency.
	PMID: 24777452 [PubMed - in process]
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7.	Nat Genet. 2014 Jun;46(6):607-12. doi: 10.1038/ng.2953. Epub 2014 Apr 20. Integrated genomic characterization of adrenocortical carcinoma. Assié G1, Letouzé E2, Fassnacht M3, Jouinot A4, Luscap W4, Barreau O5, Omeiri H4, Rodriguez S4, Perlemoine K4, René-Corail F4, Elarouci N6, Sbiera S7, Kroiss M8, Allolio B9, Waldmann J10, Quinkler M11, Mannelli M12, Mantero F13, Papathomas T14, De Krijger R14, Tabarin A15, Kerlan V16, Baudin E17, Tissier F18, Dousset B19, Groussin L5, Amar L20, Clauser E21, Bertagna X22, Ragazzon B4, Beuschlein F23, Libé R22, de Reyniès A2, Bertherat J24. Author information: 11] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. [5]. 21] Programme Cartes d'Identité des Tumeurs (CIT), Ligue Nationale Contre Le Cancer, Paris, France. [2]. 31] Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, University of Munich, Munich, Germany. [2] Endocrine and Diabetes Unit, Department of Internal Medicine I, University Hospital of Würzburg, Würzburg, Germany. [3] Comprehensive Cancer Center Mainfranken, University of Würzburg, Würzburg, Germany. 41] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. 51] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. 6Programme Cartes d'Identité des Tumeurs (CIT), Ligue Nationale Contre Le Cancer, Paris, France. 71] Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, University of Munich, Munich, Germany. [2] Endocrine and Diabetes Unit, Department of Internal Medicine I, University Hospital of Würzburg, Würzburg, Germany. 8Comprehensive Cancer Center Mainfranken, University of Würzburg, Würzburg, Germany. 9Endocrine and Diabetes Unit, Department of Internal Medicine I, University Hospital of Würzburg, Würzburg, Germany. 10Visceral, Thoracic and Vascular Surgery, University Hospital Giessen and Marburg, Marburg, Germany. 11Department of Clinical Endocrinology, Charité Campus Mitte, Charité University Medicine, Berlin, Germany. 12Department of Experimental and Clinical Biomedical Sciences, University of Florence, Florence, Italy. 13Endocrinology Unit, Department of Medicine, University of Padova, Padova, Italy. 14Department of Pathology, Josephine Nefkens Institute, Erasmus MC University Medical Center, Rotterdam, The Netherlands. 151] Department of Endocrinology, Diabetes and Metabolic Diseases, University Hospital of Bordeaux, Bordeaux, France. [2] Rare Adrenal Cancer Network COMETE, Paris, France. 161] Rare Adrenal Cancer Network COMETE, Paris, France. [2] Department of Endocrinology, Diabetes and Metabolic Diseases, University Hospital of Brest, Brest, France. 171] Rare Adrenal Cancer Network COMETE, Paris, France. [2] Department of Nuclear Medicine and Endocrine Oncology, Institut Gustave Roussy, Université Paris-Sud, Villejuif, France. 181] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Department of Pathology, Assistance Publique-Hôpitaux de Paris, Hôpital Pitié-Salpétrière, Pierre et Marie Curie Université, Paris, France. 191] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. [5] Department of Digestive and Endocrine Surgery, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. 20Hypertension Unit, Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Paris, France. 21Oncogenetic Laboratory, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. 221] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. [5] Rare Adrenal Cancer Network COMETE, Paris, France. 23Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, University of Munich, Munich, Germany. 241] INSERM U1016, Institut Cochin, Paris, France. [2] CNRS UMR 8104, Paris, France. [3] Université Paris Descartes, Sorbonne Paris Cité, Paris, France. [4] Center for Rare Adrenal Diseases, Department of Endocrinology, Assistance Publique-Hôpitaux de Paris, Hôpital Cochin, Paris, France. [5] Rare Adrenal Cancer Network COMETE, Paris, France. [6]. Abstract Adrenocortical carcinomas (ACCs) are aggressive cancers originating in the cortex of the adrenal gland. Despite overall poor prognosis, ACC outcome is heterogeneous. We performed exome sequencing and SNP array analysis of 45 ACCs and identified recurrent alterations in known driver genes (CTNNB1, TP53, CDKN2A, RB1 and MEN1) and in genes not previously reported in ACC (ZNRF3, DAXX, TERT and MED12), which we validated in an independent cohort of 77 ACCs. ZNRF3, encoding a cell surface E3 ubiquitin ligase, was the most frequently altered gene (21%) and is a potential new tumor suppressor gene related to the β-catenin pathway. Our integrated genomic analyses further identified two distinct molecular subgroups with opposite outcome. The C1A group of ACCs with poor outcome displayed numerous mutations and DNA methylation alterations, whereas the C1B group of ACCs with good prognosis displayed specific deregulation of two microRNA clusters. Thus, aggressive and indolent ACCs correspond to two distinct molecular entities driven by different oncogenic alterations.
	PMID: 24747642 [PubMed - in process]
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8.	Dev Comp Immunol. 2014 Feb;42(2):278-85. doi: 10.1016/j.dci.2013.09.011. Epub 2013 Sep 29. Production and characterisation of a monoclonal antibody that recognises the chicken CSF1 receptor and confirms that expression is restricted to macrophage-lineage cells. Garcia-Morales C1, Rothwell L, Moffat L, Garceau V, Balic A, Sang HM, Kaiser P, Hume DA. Author information: 1The Roslin Institute & Royal (Dick) School of Veterinary Studies, University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK. Abstract Macrophages contribute to innate and acquired immunity as well as many aspects of homeostasis and development. Studies of macrophage biology and function in birds have been hampered by a lack of definitive cell surface markers. As in mammals, avian macrophages proliferate and differentiate in response to CSF1 and IL34, acting through the shared receptor, CSF1R. CSF1R mRNA expression in the chicken is restricted to macrophages and their progenitors. To expedite studies of avian macrophage biology, we produced an avian CSF1R-Fc chimeric protein and generated a monoclonal antibody (designated ROS-AV170) against the chicken CSF1R using the chimeric protein as immunogen. Specific binding of ROS-AV170 to CSF1R was confirmed by FACS, ELISA and immunohistochemistry on tissue sections. CSF1 down-regulated cell surface expression of the CSF1R detected with ROS-AV170, but the antibody did not block CSF1 signalling. Expression of CSF1R was detected on the surface of bone marrow progenitors only after culture in the absence of CSF1, and was induced during macrophage differentiation. Constitutive surface expression of CSF1R distinguished monocytes from other myeloid cells, including heterophils and thrombocytes. This antibody will therefore be of considerable utility for the study of chicken macrophage biology. Copyright © 2013. Published by Elsevier Ltd.
	PMID: 24084378 [PubMed - in process]
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