Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA? - Wikidata - awgldk - TriplyDB

Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?

Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?

http://www.wikidata.org/entity/Q37060144

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Defective control of pre-messenger RNA splicing in human disease Potential relationship between inadequate response to DNA damage and development of myelodysplastic syndrome.Development of cancer-initiating cells and immortalized cells with genomic instability.Thrombopoietin promotes NHEJ DNA repair in hematopoietic stem cells through specific activation of Erk and NF-κB pathways and their target, IEX-1 SRSF2 Is Essential for Hematopoiesis, and Its Myelodysplastic Syndrome-Related Mutations Dysregulate Alternative Pre-mRNA Splicing.Fucoidan inhibits proliferation of the SKM-1 acute myeloid leukaemia cell line via the activation of apoptotic pathways and production of reactive oxygen species.Haploinsufficiency of del(5q) genes, Egr1 and Apc, cooperate with Tp53 loss to induce acute myeloid leukemia in mice.Adult Stem Cells and Diseases of Aging.DNA damage accumulation and repair defects in acute myeloid leukemia: implications for pathogenesis, disease progression, and chemotherapy resistance.On the potential role of DNMT1 in acute myeloid leukemia and myelodysplastic syndromes: not another mutated epigenetic driver.Telomere dysfunction drives aberrant hematopoietic differentiation and myelodysplastic syndrome.Progressive genomic instability in the Nup98-HoxD13 model of MDS correlates with loss of the PIG-A gene product Telomeres and Telomerase in Hematopoietic Dysfunction: Prognostic Implications and Pharmacological Interventions.Differential expression of homologous recombination DNA repair genes in the early and advanced stages of myelodysplastic syndrome.MTHFR, TS and XRCC1 genetic variants may affect survival in patients with myelodysplastic syndromes treated with supportive care or azacitidine.The Augmented R-Loop Is a Unifying Mechanism for Myelodysplastic Syndromes Induced by High-Risk Splicing Factor Mutations.

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Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?

http://www.wikidata.org/entity/Q37060144

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article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 30 April 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?

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Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?

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type

label

Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?

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Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?

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Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?

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Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?

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J.EXPHEM.2013.04.008

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Experimental Hematology

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Myelodysplastic syndrome: an inability to appropriately respond to damaged DNA?

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Alexander J R Bishop

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Christi A Walter

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Linda M Scott

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Paul Hasty

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Ting Zhou

http://www.w3.org/2001/XMLSchema#string

Vivienne I Rebel

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P2860

Altered hematopoiesis in mice lacking DNA polymerase mu is due to inefficient double-strand break repair

The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes

Hematopoietic fingerprints: an expression database of stem cells and their progeny

SALL4, a novel oncogene, is constitutively expressed in human acute myeloid leukemia (AML) and induces AML in transgenic mice

Epidemiology of myelodysplastic syndromes

Two regression models and a scoring system for predicting survival and planning treatment in myelodysplastic syndromes: a multivariate analysis of prognostic factors in 370 patients

Inactivation of Fac in mice produces inducible chromosomal instability and reduced fertility reminiscent of Fanconi anaemia

Germ cell defects and hematopoietic hypersensitivity to gamma-interferon in mice with a targeted disruption of the Fanconi anemia C gene

Excess of rare cancers in Werner syndrome (adult progeria)

Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells

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665-674

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scholarly article

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10.1016/J.EXPHEM.2013.04.008

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8

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41

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2013-04-30T00:00:00Z

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23643835

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3729593

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