CBL, CBLB, TET2, ASXL1, and IDH1/2 mutations and additional chromosomal aberrations constitute molecular events in chronic myelogenous leukemia. - Wikidata - wikimedia - TriplyDB

CBL, CBLB, TET2, ASXL1, and IDH1/2 mutations and additional chromosomal aberrations constitute molecular events in chronic myelogenous leukemia.

CBL, CBLB, TET2, ASXL1, and IDH1/2 mutations and additional chromosomal aberrations constitute molecular events in chronic myelogenous leukemia.

http://www.wikidata.org/entity/Q35030952

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IDH1/2 mutations target a key hallmark of cancer by deregulating cellular metabolism in glioma Myeloid malignancies: mutations, models and management Molecular-defined clonal evolution in patients with chronic myeloid leukemia independent of the BCR-ABL status.Mutant Cbl proteins as oncogenic drivers in myeloproliferative disorders Ten-Eleven-Translocation 2 (TET2) negatively regulates homeostasis and differentiation of hematopoietic stem cells in mice The distinct biological implications of Asxl1 mutation and its roles in leukemogenesis revealed by a knock-in mouse model STAT3 mutations indicate the presence of subclinical T-cell clones in a subset of aplastic anemia and myelodysplastic syndrome patients.The promise of whole-exome sequencing in medical genetics.PRPF8 defects cause missplicing in myeloid malignancies.Genome-wide characterization of pancreatic adenocarcinoma patients using next generation sequencing.Pathogenesis of myelodysplastic syndromes: an overview of molecular and non-molecular aspects of the disease.Functionally deregulated AML1/RUNX1 cooperates with BCR-ABL to induce a blastic phase-like phenotype of chronic myelogenous leukemia in mice.TET proteins and the control of cytosine demethylation in cancer.Disruption of the ASXL1 gene is frequent in primary, post-essential thrombocytosis and post-polycythemia vera myelofibrosis, but not essential thrombocytosis or polycythemia vera: analysis of molecular genetics and clinical phenotypes BMI1 reprogrammes histone acetylation and enhances c-fos pathway via directly binding to Zmym3 in malignant myeloid progression Mutations in the spliceosome machinery, a novel and ubiquitous pathway in leukemogenesis A novel mouse model identifies cooperating mutations and therapeutic targets critical for chronic myeloid leukemia progression.Genomic instability may originate from imatinib-refractory chronic myeloid leukemia stem cells.Use of CBL exon 8 and 9 mutations in diagnosis of myeloproliferative neoplasms and myelodysplastic/myeloproliferative disorders: an analysis of 636 cases.Somatic SETBP1 mutations in myeloid malignancies Patterns of missplicing due to somatic U2AF1 mutations in myeloid neoplasms.Epigenetic regulation in adult stem cells and cancers.Dissecting the gray zone between follicular lymphoma and marginal zone lymphoma using morphological and genetic features.The genetic basis of myelodysplasia and its clinical relevance ASXL1, TP53 and IKZF3 mutations are present in the chronic phase and blast crisis of chronic myeloid leukemia.Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice Molecular pathogenesis of myelodysplastic syndromes.Transformation of a chronic myeloproliferative neoplasm to acute myelogenous leukemia: does anything work?Genetic mechanisms of chronic myeloid leukemia blastic transformation.Chronic myeloid leukemia stem cell biology.Hematopoietic stem cells, progenitor cells and leukemic stem cells in adult myeloproliferative neoplasms.Isocitrate dehydrogenase mutations in leukemia.Genetic events other than BCR-ABL1.Genomic determinants of chronic myelomonocytic leukemia.ASXL1 mutation correction by CRISPR/Cas9 restores gene function in leukemia cells and increases survival in mouse xenografts.ASXL1 interacts with the cohesin complex to maintain chromatid separation and gene expression for normal hematopoiesis.Somatic SETBP1 mutations in myeloid neoplasms.Cytoplasmatic compartmentalization by Bcr-Abl promotes TET2 loss-of-function in chronic myeloid leukemia.The concomitant occurrence of JAK2V617F mutation and BCR/ABL transcript with phenotypic expression - an overlapping myeloproliferative disorder or two distinct diseases? - case report.Very long survival in complete cytogenetic remission in an adolescent with lymphoid blast crisis of chronic myeloid leukemia after treatment with intensive ALL-directed chemotherapy combined with continuous imatinib.

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CBL, CBLB, TET2, ASXL1, and IDH1/2 mutations and additional chromosomal aberrations constitute molecular events in chronic myelogenous leukemia.

http://www.wikidata.org/entity/Q35030952

description

2011 nî lūn-bûn

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2011 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2011 թվականի փետրվարին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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CBL, CBLB, TET2, ASXL1, and ID ...... chronic myelogenous leukemia.

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CBL, CBLB, TET2, ASXL1, and ID ...... chronic myelogenous leukemia.

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CBL, CBLB, TET2, ASXL1, and ID ...... chronic myelogenous leukemia.

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CBL, CBLB, TET2, ASXL1, and ID ...... chronic myelogenous leukemia.

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CBL, CBLB, TET2, ASXL1, and ID ...... chronic myelogenous leukemia.

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CBL, CBLB, TET2, ASXL1, and ID ...... n chronic myelogenous leukemia

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Anjali Advani

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Anna M Jankowska

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Bartlomiej Przychodzen

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Christine O'Keefe

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Courtney Prince

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Eric Hsi

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Hadrian Szpurka

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Harish Siddaiah

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Heather Cazzolli

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Hideki Makishima

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P2860

Conversion of 5-methylcytosine to 5-hydroxymethylcytosine in mammalian DNA by MLL partner TET1

Cancer-associated IDH1 mutations produce 2-hydroxyglutarate

Recurring mutations found by sequencing an acute myeloid leukemia genome

FISH and SNP-A karyotyping in myelodysplastic syndromes: improving cytogenetic detection of del(5q), monosomy 7, del(7q), trisomy 8 and del(20q)

An integrated genomic analysis of human glioblastoma multiforme

IDH1 and IDH2 mutations in gliomas

Novel mutations and their functional and clinical relevance in myeloproliferative neoplasms: JAK2, MPL, TET2, ASXL1, CBL, IDH and IKZF1

TET2 mutation is an independent favorable prognostic factor in myelodysplastic syndromes (MDSs).

ASXL1 represses retinoic acid receptor-mediated transcription through associating with HP1 and LSD1

Loss-of-function Additional sex combs like 1 mutations disrupt hematopoiesis but do not cause severe myelodysplasia or leukemia

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