排序方式: 共有8条查询结果,搜索用时 156 毫秒
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Zhang J Ding L Holmfeldt L Wu G Heatley SL Payne-Turner D Easton J Chen X Wang J Rusch M Lu C Chen SC Wei L Collins-Underwood JR Ma J Roberts KG Pounds SB Ulyanov A Becksfort J Gupta P Huether R Kriwacki RW Parker M McGoldrick DJ Zhao D Alford D Espy S Bobba KC Song G Pei D Cheng C Roberts S Barbato MI Campana D Coustan-Smith E Shurtleff SA Raimondi SC Kleppe M Cools J Shimano KA Hermiston ML Doulatov S Eppert K Laurenti E Notta F Dick JE Basso G Hunger SP Loh ML Devidas M Wood B Winter S 《Nature》2012,481(7380):157-163
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Zhang J Benavente CA McEvoy J Flores-Otero J Ding L Chen X Ulyanov A Wu G Wilson M Wang J Brennan R Rusch M Manning AL Ma J Easton J Shurtleff S Mullighan C Pounds S Mukatira S Gupta P Neale G Zhao D Lu C Fulton RS Fulton LL Hong X Dooling DJ Ochoa K Naeve C Dyson NJ Mardis ER Bahrami A Ellison D Wilson RK Downing JR Dyer MA 《Nature》2012,481(7381):329-334
Retinoblastoma is an aggressive childhood cancer of the developing retina that is initiated by the biallelic loss of RB1. Tumours progress very quickly following RB1 inactivation but the underlying mechanism is not known. Here we show that the retinoblastoma genome is stable, but that multiple cancer pathways can be epigenetically deregulated. To identify the mutations that cooperate with RB1 loss, we performed whole-genome sequencing of retinoblastomas. The overall mutational rate was very low; RB1 was the only known cancer gene mutated. We then evaluated the role of RB1 in genome stability and considered non-genetic mechanisms of cancer pathway deregulation. For example, the proto-oncogene SYK is upregulated in retinoblastoma and is required for tumour cell survival. Targeting SYK with a small-molecule inhibitor induced retinoblastoma tumour cell death in vitro and in vivo. Thus, retinoblastomas may develop quickly as a result of the epigenetic deregulation of key cancer pathways as a direct or indirect result of RB1 loss. 相似文献
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Yooseph S Nealson KH Rusch DB McCrow JP Dupont CL Kim M Johnson J Montgomery R Ferriera S Beeson K Williamson SJ Tovchigrechko A Allen AE Zeigler LA Sutton G Eisenstadt E Rogers YH Friedman R Frazier M Venter JC 《Nature》2010,468(7320):60-66
The understanding of marine microbial ecology and metabolism has been hampered by the paucity of sequenced reference genomes. To this end, we report the sequencing of 137 diverse marine isolates collected from around the world. We analysed these sequences, along with previously published marine prokaryotic genomes, in the context of marine metagenomic data, to gain insights into the ecology of the surface ocean prokaryotic picoplankton (0.1-3.0?μm size range). The results suggest that the sequenced genomes define two microbial groups: one composed of only a few taxa that are nearly always abundant in picoplanktonic communities, and the other consisting of many microbial taxa that are rarely abundant. The genomic content of the second group suggests that these microbes are capable of slow growth and survival in energy-limited environments, and rapid growth in energy-rich environments. By contrast, the abundant and cosmopolitan picoplanktonic prokaryotes for which there is genomic representation have smaller genomes, are probably capable of only slow growth and seem to be relatively unable to sense or rapidly acclimate to energy-rich conditions. Their genomic features also lead us to propose that one method used to avoid predation by viruses and/or bacterivores is by means of slow growth and the maintenance of low biomass. 相似文献
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Novel mutations target distinct subgroups of medulloblastoma 总被引:1,自引:0,他引:1
Robinson G Parker M Kranenburg TA Lu C Chen X Ding L Phoenix TN Hedlund E Wei L Zhu X Chalhoub N Baker SJ Huether R Kriwacki R Curley N Thiruvenkatam R Wang J Wu G Rusch M Hong X Becksfort J Gupta P Ma J Easton J Vadodaria B Onar-Thomas A Lin T Li S Pounds S Paugh S Zhao D Kawauchi D Roussel MF Finkelstein D Ellison DW Lau CC Bouffet E Hassall T Gururangan S Cohn R Fulton RS Fulton LL Dooling DJ Ochoa K Gajjar A Mardis ER Wilson RK Downing JR Zhang J Gilbertson RJ 《Nature》2012,488(7409):43-48
Medulloblastoma is a malignant childhood brain tumour comprising four discrete subgroups. Here, to identify mutations that drive medulloblastoma, we sequenced the entire genomes of 37 tumours and matched normal blood. One-hundred and thirty-six genes harbouring somatic mutations in this discovery set were sequenced in an additional 56 medulloblastomas. Recurrent mutations were detected in 41 genes not yet implicated in medulloblastoma; several target distinct components of the epigenetic machinery in different disease subgroups, such as regulators of H3K27 and H3K4 trimethylation in subgroups 3 and 4 (for example, KDM6A and ZMYM3), and CTNNB1-associated chromatin re-modellers in WNT-subgroup tumours (for example, SMARCA4 and CREBBP). Modelling of mutations in mouse lower rhombic lip progenitors that generate WNT-subgroup tumours identified genes that maintain this cell lineage (DDX3X), as well as mutated genes that initiate (CDH1) or cooperate (PIK3CA) in tumorigenesis. These data provide important new insights into the pathogenesis of medulloblastoma subgroups and highlight targets for therapeutic development. 相似文献
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Zusammenfassung Verschiedene biochemische und elektronenoptische Techniken wurden dazu benützt, eine partikuläre Speicherform für Glukose inPhysarum polycephalum zu identifizieren. Die Ergebnisse zeigen, dass es sich um Glykogen handelt. 相似文献
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Weir BA Woo MS Getz G Perner S Ding L Beroukhim R Lin WM Province MA Kraja A Johnson LA Shah K Sato M Thomas RK Barletta JA Borecki IB Broderick S Chang AC Chiang DY Chirieac LR Cho J Fujii Y Gazdar AF Giordano T Greulich H Hanna M Johnson BE Kris MG Lash A Lin L Lindeman N Mardis ER McPherson JD Minna JD Morgan MB Nadel M Orringer MB Osborne JR Ozenberger B Ramos AH Robinson J Roth JA Rusch V Sasaki H Shepherd F Sougnez C Spitz MR Tsao MS Twomey D Verhaak RG Weinstock GM Wheeler DA Winckler W 《Nature》2007,450(7171):893-898
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