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Berlin Brandenburg

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  • 1
    Language: English
    In: Cancer Cell, 08 January 2018, Vol.33(1), pp.3-5
    Description: In this issue of , Kleppe et al. describe a combination strategy designed to inhibit BET bromodomain and JAK/STAT signaling as a method for effectively inhibiting NF-κB and cytokine production in myeloproliferative neoplasms (MPNs). The results provide a strong rationale for clinical evaluation of dual BET/JAK inhibition in MPNs. In this issue of , Kleppe et al. describe a combination strategy designed to inhibit BET bromodomain and JAK/STAT signaling as a method for effectively inhibiting NF-κB and cytokine production in myeloproliferative neoplasms (MPNs). The results provide a strong rationale for clinical evaluation of dual BET/JAK inhibition in MPNs.
    Keywords: Medicine
    ISSN: 1535-6108
    E-ISSN: 1878-3686
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  • 2
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 15 January 2013, Vol.110(3), pp.1041-1046
    Description: The molecular etiology of human progenitor reprogramming into self-renewing leukemia stem cells (LSC) has remained elusive. Although DNA sequencing has uncovered spliceosome gene mutations that promote alternative splicing and portend leukemic transformation, isoform diversity also may be generated by RNA editing mediated by adenosine deaminase acting on RNA (ADAR) enzymes that regulate stem cell maintenance. In this study, wholetranscriptome sequencing of normal, chronic phase, and serially transplantable blast crisis chronic myeloid leukemia (CML) progenitors revealed increased IFN-γ pathway gene expression in concert with BCR-ABL amplification, enhanced expression of the IFN-responsive ADAR1 p150 isoform, and a propensity for increased adenosine-to-inosine RNA editing during CML progression. Lentiviral overexpression experiments demonstrate that ADAR1 p150 promotes expression of the myeloid transcription factor PU. 1 and induces malignant reprogramming of myeloid progenitors. Moreover, enforced ADAR1 p150 expression was associated with production of a misspliced form of GSK3β implicated in LSC self-renewal. Finally, functional serial transplantation and shRNA studies demonstrate that ADAR1 knockdown impaired in vivo self-renewal capacity of blast crisis CML progenitors. Together these data provide a compelling rationale for developing ADAR1-based LSC detection and eradication strategies.
    Keywords: Biological sciences -- Biology -- Genetics ; Biological sciences -- Biology -- Cytology ; Health sciences -- Medical conditions -- Diseases ; Biological sciences -- Biology -- Cytology ; Biological sciences -- Biology -- Physiology ; Physical sciences -- Chemistry -- Chemical compounds ; Biological sciences -- Biology -- Genetics ; Biological sciences -- Biology -- Genetics ; Health sciences -- Medical conditions -- Diseases ; Biological sciences -- Biology -- Cytology
    ISSN: 00278424
    E-ISSN: 10916490
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  • 3
    In: Nature, 2009, Vol.460(7253), p.359
    Description: DNA-damage-induced SOS mutations arise when Escherichia coli DNA polymerase (pol) V, activated by a RecA nucleoprotein filament (RecA *), catalyses translesion DNA synthesis. Here we address two longstanding enigmatic aspects of SOS mutagenesis, the molecular composition of mutagenically active polV and the role of RecA *. We show that RecA * transfers a single RecA-ATP stoichiometrically from its DNA 3'-end to free polV (UmuD' [sub.2]C) to form an active mutasome (polV Mut) with the composition UmuD' [sub.2]C-RecA-ATP. PolV Mut catalyses TLS in the absence of RecA * and deactivates rapidly upon dissociation from DNA. Deactivation occurs more slowly in the absence of DNA synthesis, while retaining RecA-ATP in the complex. Reactivation of polV Mut is triggered by replacement of RecA-ATP from RecA *. Thus, the principal role of RecA * in SOS mutagenesis is to transfer RecA-ATP to polV, and thus generate active mutasomal complex for translesion synthesis.
    Keywords: Dna Polymerases -- Physiological Aspects ; Dna Polymerases -- Research ; Dna Synthesis -- Research ; Escherichia Coli -- Physiological Aspects ; Escherichia Coli -- Genetic Aspects ; Escherichia Coli -- Research;
    ISSN: 0028-0836
    E-ISSN: 14764687
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  • 4
    Language: English
    In: Cancer Research, 10/01/2014, Vol.74(19 Supplement), pp.1912-1912
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 5
    Language: English
    In: Cancer Research, 07/01/2017, Vol.77(13 Supplement), pp.299-299
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 6
    Language: English
    In: Cancer Research, 10/01/2014, Vol.74(19 Supplement), pp.5103-5103
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 7
    Language: English
    In: Cancer Research, 10/01/2014, Vol.74(19 Supplement), pp.375-375
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 8
    Language: English
    In: PLoS ONE, 2012, Vol.7(6), p.e39725
    Description: Leukemia initiating cells (LIC) contribute to therapeutic resistance through acquisition of mutations in signaling pathways, such as NOTCH1, that promote self-renewal and survival within supportive niches. Activating mutations in NOTCH1 occur commonly in T cell acute lymphoblastic leukemia (T-ALL) and have been implicated in therapeutic resistance. However, the cell type and context specific consequences of NOTCH1 activation, its role in human LIC regeneration, and sensitivity to NOTCH1 inhibition in hematopoietic microenvironments had not been elucidated. ; We established humanized bioluminescent T-ALL LIC mouse models transplanted with pediatric T-ALL samples that were sequenced for NOTCH1 and other common T-ALL mutations. In this study, CD34 cells from T-ALL samples had higher leukemic engraftment and serial transplantation capacity than CD34 cells in hematopoietic niches, suggesting that self-renewing LIC were enriched within the CD34 fraction. Humanized NOTCH1 monoclonal antibody treatment reduced LIC survival and self-renewal in T-ALL LIC-engrafted mice and resulted in depletion of CD34CD2CD7 cells that harbor serial transplantation capacity. ; These results reveal a functional hierarchy within the LIC population based on NOTCH1 activation, which renders LIC susceptible to targeted NOTCH1 inhibition and highlights the utility of NOTCH1 antibody targeting as a key component of malignant stem cell eradication strategies.
    Keywords: Research Article ; Biology ; Medicine ; Cell Biology ; Hematology ; Oncology ; Developmental Biology
    E-ISSN: 1932-6203
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  • 9
    Language: English
    In: Cancer Research, 04/15/2011, Vol.71(8 Supplement), pp.974-974
    ISSN: 0008-5472
    E-ISSN: 1538-7445
    Source: CrossRef
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  • 10
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