The origin and nature of tightly clustered BTG1 deletions in precursor B-cell acute lymphoblastic leukemia support a model of multiclonal evolution. - Wikidata - wikimedia - TriplyDB

The origin and nature of tightly clustered BTG1 deletions in precursor B-cell acute lymphoblastic leukemia support a model of multiclonal evolution.

The origin and nature of tightly clustered BTG1 deletions in precursor B-cell acute lymphoblastic leukemia support a model of multiclonal evolution.

http://www.wikidata.org/entity/Q34167952

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The anti-proliferative activity of BTG/TOB proteins is mediated via the Caf1a (CNOT7) and Caf1b (CNOT8) deadenylase subunits of the Ccr4-not complex The Philadelphia chromosome in leukemogenesis Clonal evolution in hematological malignancies and therapeutic implications eIF3 targets cell-proliferation messenger RNAs for translational activation or repression Control of the Normal and Pathological Development of Neural Stem and Progenitor Cells by the PC3/Tis21/Btg2 and Btg1 Genes Tumor suppressors BTG1 and IKZF1 cooperate during mouse leukemia development and increase relapse risk in B-cell precursor acute lymphoblastic leukemia patients.Loss of TBL1XR1 disrupts glucocorticoid receptor recruitment to chromatin and results in glucocorticoid resistance in a B-lymphoblastic leukemia model.MYC through miR-17-92 suppresses specific target genes to maintain survival, autonomous proliferation, and a neoplastic state.Rare allelic forms of PRDM9 associated with childhood leukemogenesis.KRAS and CREBBP mutations: a relapse-linked malicious liaison in childhood high hyperdiploid acute lymphoblastic leukemia.Protracted dormancy of pre-leukemic stem cells.Genomics and drug profiling of fatal TCF3-HLF-positive acute lymphoblastic leukemia identifies recurrent mutation patterns and therapeutic options.Tumor suppressor BTG1 promotes PRMT1-mediated ATF4 function in response to cellular stress.Genes commonly deleted in childhood B-cell precursor acute lymphoblastic leukemia: association with cytogenetics and clinical features.Integration of genetic and clinical risk factors improves prognostication in relapsed childhood B-cell precursor acute lymphoblastic leukemia.BTG1 expression correlates with the pathogenesis and progression of ovarian carcinomas COBL is a novel hotspot for IKZF1 deletions in childhood acute lymphoblastic leukemia.B-lineage transcription factors and cooperating gene lesions required for leukemia development.RAG-mediated recombination is the predominant driver of oncogenic rearrangement in ETV6-RUNX1 acute lymphoblastic leukemia.Mechanism of ETV6-RUNX1 Leukemia.Genetic alterations in glucocorticoid signaling pathway components are associated with adverse prognosis in children with relapsed ETV6/RUNX1-positive acute lymphoblastic leukemia.Molecular profiling of gene copy number abnormalities in key regulatory genes in high-risk B-lineage acute lymphoblastic leukemia: frequency and their association with clinicopathological findings in Indian patients.Molecular characterization of acute lymphoblastic leukemia with high CRLF2 gene expression in childhood.Diversity of clinical implication of B-cell translocation gene 1 expression by histopathologic and anatomic subtypes of gastric cancer.Single-cell mutational profiling and clonal phylogeny in cancer.MYC-Master Regulator of the Cancer Epigenome and Transcriptome.The DNA Damage Response Regulates RAG1/2 Expression in Pre-B Cells through ATM-FOXO1 Signaling.Transcriptome sequencing reveals a profile that corresponds to genomic variants in Waldenström macroglobulinemia.Tumor suppressors BTG1 and BTG2 regulate early mouse B-cell development.Clone-specific secondary aberrations are not detected in neonatal blood spots of children with ETV6-RUNX1-positive leukemia.Deletions of IKZF1 and SPRED1 are associated with poor prognosis in a population-based series of pediatric B-cell precursor acute lymphoblastic leukemia diagnosed between 1992 and 2011.The subclonal complexity of STIL-TAL1+ T-cell acute lymphoblastic leukaemia.The cancer genome: from structure to function.

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The origin and nature of tightly clustered BTG1 deletions in precursor B-cell acute lymphoblastic leukemia support a model of multiclonal evolution.

http://www.wikidata.org/entity/Q34167952

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2012 nî lūn-bûn

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2012 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2012年の論文

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The origin and nature of tight ...... odel of multiclonal evolution.

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JOURNAL.PGEN.1002533

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The origin and nature of tight ...... odel of multiclonal evolution.

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Ad Geurts van Kessel

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Blanca Scheijen

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Edwin Sonneveld

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Esmé Waanders

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Frank N van Leeuwen

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Laurens T van der Meer

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Liesbeth van Emst

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Peter M Hoogerbrugge

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Roland P Kuiper

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Simon V van Reijmersdal

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P2860

The leukemia-associated protein Btg1 and the p53-regulated protein Btg2 interact with the homeoprotein Hoxb9 and enhance its transcriptional activation

The mammalian immediate-early TIS21 protein and the leukemia-associated BTG1 protein interact with a protein-arginine N-methyltransferase

Interaction of BTG1 and p53-regulated BTG2 gene products with mCaf1, the murine homolog of a component of the yeast CCR4 transcriptional regulatory complex

Frequent mutation of histone-modifying genes in non-Hodgkin lymphoma

RAG2 PHD finger couples histone H3 lysine 4 trimethylation with V(D)J recombination

IKZF1 deletions predict relapse in uniformly treated pediatric precursor B-ALL.

The mammalian anti-proliferative BTG/Tob protein family

Genome-wide analysis of genetic alterations in acute lymphoblastic leukaemia

Coactivation of nuclear receptors and myogenic factors induces the major BTG1 influence on muscle differentiation.

Mechanism and regulation of class switch recombination

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Adrianus Henricus Maria Geurts van Kessel

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2012-02-16T00:00:00Z

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