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  1. 1
    A. R. Forrest ; H. Kawaji ; M. Rehli ; J. K. Baillie ; M. J. de Hoon ; V. Haberle ; T. Lassmann ; I. V. Kulakovskiy ; M. Lizio ; M. Itoh ; R. Andersson ; C. J. Mungall ; T. F. Meehan ; S. Schmeier ; N. Bertin ; M. Jorgensen ; E. Dimont ; E. Arner ; C. Schmidl ; U. Schaefer ; Y. A. Medvedeva ; C. Plessy ; M. Vitezic ; J. Severin ; C. Semple ; Y. Ishizu ; R. S. Young ; M. Francescatto ; I. Alam ; D. Albanese ; G. M. Altschuler ; T. Arakawa ; J. A. Archer ; P. Arner ; M. Babina ; S. Rennie ; P. J. Balwierz ; A. G. Beckhouse ; S. Pradhan-Bhatt ; J. A. Blake ; A. Blumenthal ; B. Bodega ; A. Bonetti ; J. Briggs ; F. Brombacher ; A. M. Burroughs ; A. Califano ; C. V. Cannistraci ; D. Carbajo ; Y. Chen ; M. Chierici ; Y. Ciani ; H. C. Clevers ; E. Dalla ; C. A. Davis ; M. Detmar ; A. D. Diehl ; T. Dohi ; F. Drablos ; A. S. Edge ; M. Edinger ; K. Ekwall ; M. Endoh ; H. Enomoto ; M. Fagiolini ; L. Fairbairn ; H. Fang ; M. C. Farach-Carson ; G. J. Faulkner ; A. V. Favorov ; M. E. Fisher ; M. C. Frith ; R. Fujita ; S. Fukuda ; C. Furlanello ; M. Furino ; J. Furusawa ; T. B. Geijtenbeek ; A. P. Gibson ; T. Gingeras ; D. Goldowitz ; J. Gough ; S. Guhl ; R. Guler ; S. Gustincich ; T. J. Ha ; M. Hamaguchi ; M. Hara ; M. Harbers ; J. Harshbarger ; A. Hasegawa ; Y. Hasegawa ; T. Hashimoto ; M. Herlyn ; K. J. Hitchens ; S. J. Ho Sui ; O. M. Hofmann ; I. Hoof ; F. Hori ; L. Huminiecki ; K. Iida ; T. Ikawa ; B. R. Jankovic ; H. Jia ; A. Joshi ; G. Jurman ; B. Kaczkowski ; C. Kai ; K. Kaida ; A. Kaiho ; K. Kajiyama ; M. Kanamori-Katayama ; A. S. Kasianov ; T. Kasukawa ; S. Katayama ; S. Kato ; S. Kawaguchi ; H. Kawamoto ; Y. I. Kawamura ; T. Kawashima ; J. S. Kempfle ; T. J. Kenna ; J. Kere ; L. M. Khachigian ; T. Kitamura ; S. P. Klinken ; A. J. Knox ; M. Kojima ; S. Kojima ; N. Kondo ; H. Koseki ; S. Koyasu ; S. Krampitz ; A. Kubosaki ; A. T. Kwon ; J. F. Laros ; W. Lee ; A. Lennartsson ; K. Li ; B. Lilje ; L. Lipovich ; A. Mackay-Sim ; R. Manabe ; J. C. Mar ; B. Marchand ; A. Mathelier ; N. Mejhert ; A. Meynert ; Y. Mizuno ; D. A. de Lima Morais ; H. Morikawa ; M. Morimoto ; K. Moro ; E. Motakis ; H. Motohashi ; C. L. Mummery ; M. Murata ; S. Nagao-Sato ; Y. Nakachi ; F. Nakahara ; T. Nakamura ; Y. Nakamura ; K. Nakazato ; E. van Nimwegen ; N. Ninomiya ; H. Nishiyori ; S. Noma ; T. Noazaki ; S. Ogishima ; N. Ohkura ; H. Ohimiya ; H. Ohno ; M. Ohshima ; M. Okada-Hatakeyama ; Y. Okazaki ; V. Orlando ; D. A. Ovchinnikov ; A. Pain ; R. Passier ; M. Patrikakis ; H. Persson ; S. Piazza ; J. G. Prendergast ; O. J. Rackham ; J. A. Ramilowski ; M. Rashid ; T. Ravasi ; P. Rizzu ; M. Roncador ; S. Roy ; M. B. Rye ; E. Saijyo ; A. Sajantila ; A. Saka ; S. Sakaguchi ; M. Sakai ; H. Sato ; S. Savvi ; A. Saxena ; C. Schneider ; E. A. Schultes ; G. G. Schulze-Tanzil ; A. Schwegmann ; T. Sengstag ; G. Sheng ; H. Shimoji ; Y. Shimoni ; J. W. Shin ; C. Simon ; D. Sugiyama ; T. Sugiyama ; M. Suzuki ; N. Suzuki ; R. K. Swoboda ; P. A. t Hoen ; M. Tagami ; N. Takahashi ; J. Takai ; H. Tanaka ; H. Tatsukawa ; Z. Tatum ; M. Thompson ; H. Toyodo ; T. Toyoda ; E. Valen ; M. van de Wetering ; L. M. van den Berg ; R. Verado ; D. Vijayan ; I. E. Vorontsov ; W. W. Wasserman ; S. Watanabe ; C. A. Wells ; L. N. Winteringham ; E. Wolvetang ; E. J. Wood ; Y. Yamaguchi ; M. Yamamoto ; M. Yoneda ; Y. Yonekura ; S. Yoshida ; S. E. Zabierowski ; P. G. Zhang ; X. Zhao ; S. Zucchelli ; K. M. Summers ; H. Suzuki ; C. O. Daub ; J. Kawai ; P. Heutink ; W. Hide ; T. C. Freeman ; B. Lenhard ; V. B. Bajic ; M. S. Taylor ; V. J. Makeev ; A. Sandelin ; D. A. Hume ; P. Carninci ; Y. Hayashizaki
    Nature Publishing Group (NPG)
    Published 2014
    Staff View
    Publication Date:
    2014-03-29
    Publisher:
    Nature Publishing Group (NPG)
    Print ISSN:
    0028-0836
    Electronic ISSN:
    1476-4687
    Topics:
    Biology
    Chemistry and Pharmacology
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Animals ; *Atlases as Topic ; Cell Line ; Cells, Cultured ; Cluster Analysis ; Conserved Sequence/genetics ; Gene Expression Regulation/genetics ; Gene Regulatory Networks/genetics ; Genes, Essential/genetics ; Genome/genetics ; Humans ; Mice ; *Molecular Sequence Annotation ; Open Reading Frames/genetics ; Organ Specificity ; Promoter Regions, Genetic/*genetics ; RNA, Messenger/analysis/genetics ; Transcription Factors/metabolism ; Transcription Initiation Site ; Transcription, Genetic/genetics ; Transcriptome/*genetics
    Published by:
    http://www.nature.com/

    Latest Papers from Table of Contents or Articles in Press
  2. 2
    Staff View
    ISSN:
    0257-8972
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics
    Physics
    Type of Medium:
    Electronic Resource
    URL:
    http://linkinghub.elsevier.com/retrieve/pii/0257-8972(93)90131-7

    Articles: DFG German National Licenses
  3. 3
    Staff View
    ISSN:
    1433-0415
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Die aktuellen Empfehlungen zum Vorgehen bei Anthrazyklin-Extravasaten sind weitgehend empirischer Natur und basieren ausschließlich auf Tierversuchen und klinischen Fallberichten. Die konservative Behandlung hat die Vermeidung paravasatbedingter lokaler Gewebsschäden sowie die Erhaltung der funktionalen und morphologischen Hautintegrität zum Ziel und ermöglicht in der Regel eine plangerechte Fortsetzung der Chemotherapie. Im Gegensatz zur konservativen Therapie stellt das chirurgische Debridement mit konsekutiver Hauttransplantation ein Verfahren dar, das mit operationsassoziierter Morbidität, Transplantatproblemen und Wundheilungsstörungen einhergehen kann und deshalb nur als ultima ratio Anwendung finden sollte. Die vorliegende Übersicht fasst die aktuellen Fragestellungen zur Extravasation von Anthrazyklinen zusammen, wobei Doxorubicin, Epirubicin, Daunorubicin und Idarubicin als Beispiele “lokal toxischer” antineoplastischer Verbindungen gelten können, die nach Extravasation zur Gewebsnekrose führen können. Als Grundlage wurden publizierte Tierversuche, klinische Erfahrungsberichte und verfügbare Einzelfalldokumentationen sowie Literaturübersichten seit 1976 berücksichtigt.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/s007610050043

    Articles: DFG German National Licenses
  4. 4
    Staff View
    ISSN:
    1434-0879
    Keywords:
    ICAM-1 ; Molecular regulation ; Renal cell carcinoma ; Cytokines ; Protein kinase C activator
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract Intercellular adhesion molecule-1 (ICAM-1) mediates two important functional. aspects of tumor biology, namely enhancement of tumor metastasis and mediation of host defense mechanisms such as lymphocyte-mediated tumor cytotoxicity. Since ICAM-1 is expressed by most renal cell carcinomas (RCC), the regulation of ICAM-1 expression is important in understanding the biological behavior of RCC. We report an investigation on ICAM-1 expression and molecular regulation by cytokines and protein kinase C activator on RCC cell lines. Of the various cytokines, tumor necrosis factor αa (TNFα), interferon-γ (IFNγ), and phorbol myristate acetate (PMA) strongly upregulated ICAM-1 protein expression on RCC. The kinetics of ICAM-1 message induction was studied by Northern analysis of total RNA extracted from RCC and normal kidney proximal tubular (NKPT) cells. Time course studies showed that ICAM-1 mRNA was upregulated by INFγ, TNFα, and PMA, plateaued after 2 h, and remained increased for up to 24 h. Although ICAM-1 mRNA in NKPT cells was upregulated by these cytokines, their messages returned to basal levels after 24 h. ICAM-1 mRNA stability assays showed that both unstimulated and stimulated RCC cells had very stable ICAM-1 mRNA up to 24 h. In order to investigate whether increased gene transcription contributes to ICAM-1 upregulation, RCC cells were treated with TNFα, IFNγ, or PMA with or without simultaneous addition of actinomycin D. ICAM-1 message induction-blocking studies suggested that primary upregulation of ICAM-1 mRNA may be caused by transcriptional upregulation. These results suggest that long-lasting ICAM-1 message upregulation in response to cytokines or PMA may be due to transcriptional upregulation in the early phase and stabilization of ICAM-1 message in the later phase (after 4 h). These observations suggest that RCC may lack the normal downregulatory mechanisms which control ICAM-1 expression and may explain the high frequency of ICAM-1 expression observed on primary human RCC.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF00942091

    Articles: DFG German National Licenses
  5. 5
    Staff View
    ISSN:
    1434-0879
    Keywords:
    Kidney neoplasms ; Tumor cells ; Cultures ; Cell adhesion molecules
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract In order to investigate the importance of cell adhesion molecules (CAMs) in renal cell carcinoma (RCC), a cell line, designated as CCF-RC7, was established from a human RCC of the clear cell type. CCF-RC7 was passaged over 50 times in vitro for 31/2 years. The cell line has an epithelial morphology and a doubling time of 30 h, forming colonies in soft agar with an average efficiency of 10.4% and producing clear cell tumors in athymic nude mice. CCF-RC7 cells have an aneuploid-hypotetraploid karyotype with a modal chromosome number of 82 and rearrangements in chromosomes 9, 12 and 14. Immunohistochemical and flow immunocytometric analyses revealed high expression of ICAM-1 (CD54), and Hermes antigen (CD44), which was significantly upregulated by cytokine and PMA treatment. VLA-4 was expressed on approximately 20% of tumor cells and could not be altered by cytokine or PMA stimulation. High expression of sialyl Lewis X was also demonstrated by immunohistological examination. This newly characterized cell line will serve as a useful model for the study of CAMs during hematogenous metastasis and host defense mechanisms in human RCC.
    Type of Medium:
    Electronic Resource
    URL:
    http://dx.doi.org/10.1007/BF00389570

    Articles: DFG German National Licenses