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  • 1
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    Forcing cells to change lineages (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-12-04
    Description: The ability to produce stem cells by induced pluripotency (iPS reprogramming) has rekindled an interest in earlier studies showing that transcription factors can directly convert specialized cells from one lineage to another. Lineage reprogramming has become a powerful tool to study cell fate choice during differentiation, akin to inducing mutations for the discovery of gene functions. The lessons learnt provide a rubric for how cells may be manipulated for therapeutic purposes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Graf, Thomas -- Enver, Tariq -- MC_U137973817/Medical Research Council/United Kingdom -- England -- Nature. 2009 Dec 3;462(7273):587-94. doi: 10.1038/nature08533.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genomic Regulation and ICREA, 08003 Barcelona, Spain. thomas.graf@crg.es〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19956253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Lineage/*physiology ; Cellular Reprogramming/*genetics ; *Gene Expression Regulation, Developmental ; Gene Regulatory Networks/physiology ; Humans ; Pluripotent Stem Cells/cytology/*metabolism ; Transcription Factors/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Developmental biology: Instructions writ in blood (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-09-11
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enver, Tariq -- Jacobsen, Sten Eirik W -- G0501838/Medical Research Council/United Kingdom -- G0801073/Medical Research Council/United Kingdom -- MC_U137973817/Medical Research Council/United Kingdom -- England -- Nature. 2009 Sep 10;461(7261):183-4. doi: 10.1038/461183a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19741696" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Lineage/*drug effects ; Granulocyte Colony-Stimulating Factor/*pharmacology ; Hematopoiesis/*drug effects ; Hematopoietic Stem Cells/*cytology/*drug effects/metabolism ; Humans ; Macrophage Colony-Stimulating Factor/*pharmacology ; MafB Transcription Factor/metabolism ; Mice ; *Models, Biological ; Multipotent Stem Cells/cytology/drug effects/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Autonomous developmental control of human embryonic globin gene switching in transgenic mice (1990)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1990-11-23
    Description: The mechanisms by which expression of the beta-like globin genes are developmentally regulated are under intense investigation. The temporal control of human embryonic (epsilon) globin expression was analyzed. A 3.7-kilobase (kb) fragment that contained the entire human epsilon-globin gene was linked to a 2.5-kb cassette of the locus control region (LCR), and the developmental time of expression of this construct was studied in transgenic mice. The human epsilon-globin transgene was expressed in yolk sac-derived primitive erythroid cells, but not in fetal liver or bone marrow-derived definitive erythroid cells. The absence of epsilon gene expression in definitive erythroid cells suggests that the developmental regulation of the epsilon-globin gene depends only on the presence of the LCR and the epsilon-globin gene itself (that is, an autonomous negative control mechanism). The autonomy of epsilon-globin gene developmental control distinguishes it from the competitive mechanism of regulation of gamma and beta-globin genes, and therefore, suggests that at least two distinct mechanisms function in human hemoglobin switching.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Raich, N -- Enver, T -- Nakamoto, B -- Josephson, B -- Papayannopoulou, T -- Stamatoyannopoulos, G -- DK 3132/DK/NIDDK NIH HHS/ -- HL 20899/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1990 Nov 23;250(4984):1147-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Medical Genetics, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2251502" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow/embryology ; Bone Marrow Cells ; Erythroid Precursor Cells/metabolism ; Erythropoiesis ; Fetus/*metabolism ; *Gene Expression Regulation ; Globins/*genetics ; Hemoglobins/biosynthesis ; Humans ; Liver/cytology/embryology ; Mice ; Mice, Transgenic ; Regulatory Sequences, Nucleic Acid ; Yolk Sac/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Genetic variegation of clonal architecture and propagating cells in leukaemia (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-12-17
    Description: Little is known of the genetic architecture of cancer at the subclonal and single-cell level or in the cells responsible for cancer clone maintenance and propagation. Here we have examined this issue in childhood acute lymphoblastic leukaemia in which the ETV6-RUNX1 gene fusion is an early or initiating genetic lesion followed by a modest number of recurrent or 'driver' copy number alterations. By multiplexing fluorescence in situ hybridization probes for these mutations, up to eight genetic abnormalities can be detected in single cells, a genetic signature of subclones identified and a composite picture of subclonal architecture and putative ancestral trees assembled. Subclones in acute lymphoblastic leukaemia have variegated genetics and complex, nonlinear or branching evolutionary histories. Copy number alterations are independently and reiteratively acquired in subclones of individual patients, and in no preferential order. Clonal architecture is dynamic and is subject to change in the lead-up to a diagnosis and in relapse. Leukaemia propagating cells, assayed by serial transplantation in NOD/SCID IL2Rgamma(null) mice, are also genetically variegated, mirroring subclonal patterns, and vary in competitive regenerative capacity in vivo. These data have implications for cancer genomics and for the targeted therapy of cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anderson, Kristina -- Lutz, Christoph -- van Delft, Frederik W -- Bateman, Caroline M -- Guo, Yanping -- Colman, Susan M -- Kempski, Helena -- Moorman, Anthony V -- Titley, Ian -- Swansbury, John -- Kearney, Lyndal -- Enver, Tariq -- Greaves, Mel -- MC_U137973817/Medical Research Council/United Kingdom -- England -- Nature. 2011 Jan 20;469(7330):356-61. doi: 10.1038/nature09650. Epub 2010 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Haemato-Oncology, The Institute of Cancer Research, Sutton SM2 5NG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21160474" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Clone Cells/metabolism/*pathology ; Core Binding Factor Alpha 2 Subunit ; DNA Copy Number Variations/genetics ; DNA Mutational Analysis ; Disease Progression ; Genetic Variation/*genetics ; Genotype ; Humans ; Immunophenotyping ; In Situ Hybridization, Fluorescence ; Interleukin Receptor Common gamma Subunit/deficiency/genetics ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neoplasm Transplantation ; Oncogene Proteins, Fusion/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics/*pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Activation of developmentally mutated human globin genes by cell fusion (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-11-18
    Description: Human fetal globin genes are not expressed in hybrid cells produced by the fusion of normal human lymphocytes with mouse erythroleukemia cells. In contrast, when lymphocytes from persons with globin gene developmental mutations (hereditary persistence of fetal hemoglobin) are used for these fusions, fetal globin is expressed in the hybrid cells. Thus, mutations of developmental origin can be reconstituted in vitro by fusing mutant lymphoid cells with differentiated cell lines of the proper lineage. This system can readily be used for analyses, such as globin gene methylation, that normally require large numbers of pure nucleated erythroid cells, which are difficult to obtain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Papayannopoulou, T -- Enver, T -- Takegawa, S -- Anagnou, N P -- Stamatoyannopoulos, G -- DK30852/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1988 Nov 18;242(4881):1056-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology, University of Washington, Seattle 98195.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2461587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Fusion ; Chromosome Deletion ; Fetal Hemoglobin/*genetics ; Gene Expression Regulation ; Globins/*genetics ; Hemoglobinopathies/*genetics ; Humans ; Leukemia, Erythroblastic, Acute ; Mice ; Mutation ; Promoter Regions, Genetic ; RNA, Messenger/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    NOV (CCN3) functions as a regulator of human hematopoietic stem or progenitor cells (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-04-28
    Description: Clinically successful hematopoietic cell transplantation is dependent on hematopoietic stem and progenitor cells. Here we identify the matricellular protein Nephroblastoma Overexpressed (Nov, CCN3) as being essential for their functional integrity. Nov expression is restricted to the primitive (CD34) compartments of umbilical vein cord blood, and its knockdown in these cells by lentivirus-mediated RNA interference abrogates their function in vitro and in vivo. Conversely, forced expression of Nov and addition of recombinant Nov protein both enhance primitive stem and/or progenitor activity. Taken together, our results identify Nov (CCN3) as a regulator of human hematopoietic stem or progenitor cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gupta, Rajeev -- Hong, Dengli -- Iborra, Francisco -- Sarno, Samantha -- Enver, Tariq -- MC_U137961143/Medical Research Council/United Kingdom -- MC_U137973816/Medical Research Council/United Kingdom -- MC_U137973817/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2007 Apr 27;316(5824):590-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Headington, OX3 9DS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17463287" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; Cell Line ; Cells, Cultured ; Colony-Forming Units Assay ; Connective Tissue Growth Factor ; Genetic Vectors ; Hematopoiesis ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology/*physiology ; Humans ; Immediate-Early Proteins/genetics/*physiology ; Intercellular Signaling Peptides and Proteins/genetics/*physiology ; Lentivirus/genetics ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Nephroblastoma Overexpressed Protein ; RNA Interference ; Recombinant Proteins/metabolism ; Transfection ; Transplantation, Heterologous
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Initiating and cancer-propagating cells in TEL-AML1-associated childhood leukemia (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-01-19
    Description: Understanding cancer pathogenesis requires knowledge of not only the specific contributory genetic mutations but also the cellular framework in which they arise and function. Here we explore the clonal evolution of a form of childhood precursor-B cell acute lymphoblastic leukemia that is characterized by a chromosomal translocation generating a TEL-AML1 fusion gene. We identify a cell compartment in leukemic children that can propagate leukemia when transplanted in mice. By studying a monochorionic twin pair, one preleukemic and one with frank leukemia, we establish the lineal relationship between these "cancer-propagating" cells and the preleukemic cell in which the TEL-AML1 fusion first arises or has functional impact. Analysis of TEL-AML1-transduced cord blood cells suggests that TEL-AML1 functions as a first-hit mutation by endowing this preleukemic cell with altered self-renewal and survival properties.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hong, Dengli -- Gupta, Rajeev -- Ancliff, Philip -- Atzberger, Ann -- Brown, John -- Soneji, Shamit -- Green, Joanne -- Colman, Sue -- Piacibello, Wanda -- Buckle, Veronica -- Tsuzuki, Shinobu -- Greaves, Mel -- Enver, Tariq -- MC_U137961143/Medical Research Council/United Kingdom -- MC_U137973817/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2008 Jan 18;319(5861):336-9. doi: 10.1126/science.1150648.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Molecular Haematology Unit, Weatherall Institute for Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18202291" target="_blank"〉PubMed〈/a〉
    Keywords: Acute Disease ; Animals ; Antigens, CD19/analysis ; Antigens, CD34/analysis ; Antigens, CD38/analysis ; Apoptosis ; Bone Marrow Transplantation ; Child, Preschool ; Core Binding Factor Alpha 2 Subunit/analysis/*genetics/physiology ; *Diseases in Twins/genetics/metabolism/pathology ; Female ; Fetal Blood/transplantation ; Gene Rearrangement, B-Lymphocyte, Heavy Chain ; Humans ; Male ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Neoplasm Transplantation ; Neoplastic Stem Cells/pathology ; Oncogene Proteins, Fusion/analysis/*genetics/physiology ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/*genetics/metabolism/*pathology ; Precursor Cells, B-Lymphoid/chemistry/physiology ; Preleukemia/genetics/metabolism/*pathology ; Recombination, Genetic ; Transplantation, Heterologous ; Twins, Monozygotic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Electronic Resource
    Electronic Resource
    Analysis of Human γ-To-β Switching in Transgenic Mice (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 612 (1990), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1990.tb24298.x
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  • 9
    Electronic Resource
    Electronic Resource
    Simultaneous purification of DNA and RNA from small numbers of eukaryotic cells
    Amsterdam : Elsevier
    Analytical Biochemistry 180 (1989), S. 303-306 
    Details
    ISSN: 0003-2697
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0003-2697(89)90435-1
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  • 10
    Electronic Resource
    Electronic Resource
    Primary structure of the goat β-globin locus control region
    Amsterdam : Elsevier
    Genomics 9 (1991), S. 488-499 
    Details
    ISSN: 0888-7543
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0888-7543(91)90415-B
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