Disruption of KMT2D perturbs germinal center B cell development and promotes lymphomagenesis. - Test2 - elhamkhani - TriplyDB

Disruption of KMT2D perturbs germinal center B cell development and promotes lymphomagenesis.

Disruption of KMT2D perturbs germinal center B cell development and promotes lymphomagenesis.

http://www.wikidata.org/entity/Q34494007

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New developments in the pathology of malignant lymphoma. A review of the literature published from September 2015–December 2015 Epigenetics in normal and malignant hematopoiesis: An overview and update 2017.Diffuse large B-cell lymphoma: can genomics improve treatment options for a curable cancer?ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia.KMT2D regulates specific programs in heart development via histone H3 lysine 4 di-methylation.H3K4 Methyltransferase Activity Is Required for MLL4 Protein Stability.PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D.Epigenetics of hematopoiesis and hematological malignancies.Dpy30 is critical for maintaining the identity and function of adult hematopoietic stem cells The mutational landscape of ocular marginal zone lymphoma identifies frequent alterations in TNFAIP3 followed by mutations in TBL1XR1 and CREBBP.Early loss of Crebbp confers malignant stem cell properties on lymphoid progenitors.The role of next-generation sequencing in understanding the genomic basis of diffuse large B cell lymphoma and advancing targeted therapies.Genetic landscape and deregulated pathways in B-cell lymphoid malignancies.Inactivation of CREBBP expands the germinal center B cell compartment, down-regulates MHCII expression and promotes DLBCL growth.Chronic lymphocytic leukemia: Time to go past genomics?Chromosomal abnormalities and molecular landscape of metastasizing mucinous salivary adenocarcinoma.Reduced Expression of Histone Methyltransferases KMT2C and KMT2D Correlates with Improved Outcome in Pancreatic Ductal Adenocarcinoma MLL3/MLL4/COMPASS Family on Epigenetic Regulation of Enhancer Function and Cancer.Oncogenic events rather than antigen selection pressure may be the main driving forces for relapse in diffuse large B-cell lymphomas.Enhancer deregulation in cancer and other diseases.Indications to Epigenetic Dysfunction in the Pathogenesis of Common Variable Immunodeficiency.ChIP-seq in studying epigenetic mechanisms of disease and promoting precision medicine: progresses and future directions.Epigenetic balance of gene expression by Polycomb and COMPASS families.Distinct functions of histone H3, lysine 4 methyltransferases in normal and malignant hematopoiesis.SET/MLL family proteins in hematopoiesis and leukemia.Frequently mutated genes/pathways and genomic instability as prevention targets in liver cancer.Small Cell Lung Cancer Exhibits Frequent Inactivating Mutations in the Histone Methyltransferase KMT2D/MLL2: CALGB 151111 (Alliance).Follicular lymphoma, a B cell malignancy addicted to epigenetic mutations.Murine models of germinal center derived-lymphomas.Follicular lymphoma: State-of-the-art ICML workshop in Lugano 2015.Histone H3 lysine 4 methyltransferase KMT2D.Epigenetic plasticity and the hallmarks of cancer.Targeting Gene Function in Germinal Center B Cells: A Practical Approach.Genome-wide analysis of pediatric-type follicular lymphoma reveals low genetic complexity and recurrent alterations of TNFRSF14 gene.A study of the mutational landscape of pediatric-type follicular lymphoma and pediatric nodal marginal zone lymphoma.Genetic and epigenetic inactivation of SESTRIN1 controls mTORC1 and response to EZH2 inhibition in follicular lymphoma.Genomic landscape characterization of large granular lymphocyte leukemia with a systems genetics approach CREBBP Inactivation Promotes the Development of HDAC3-Dependent Lymphomas.PTIP chromatin regulator controls development and activation of B cell subsets to license humoral immunity in mice.Chromatin modifying gene mutations in follicular lymphoma.

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Disruption of KMT2D perturbs germinal center B cell development and promotes lymphomagenesis.

http://www.wikidata.org/entity/Q34494007

description

2015 nî lūn-bûn

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2015 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

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2015 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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name

Disruption of KMT2D perturbs g ...... and promotes lymphomagenesis.

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Disruption of KMT2D perturbs g ...... and promotes lymphomagenesis.

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Disruption of KMT2D perturbs g ...... and promotes lymphomagenesis.

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Disruption of KMT2D perturbs g ...... and promotes lymphomagenesis.

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Disruption of KMT2D perturbs g ...... and promotes lymphomagenesis.

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Disruption of KMT2D perturbs g ...... and promotes lymphomagenesis.

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Disruption of KMT2D perturbs g ...... and promotes lymphomagenesis.

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Disruption of KMT2D perturbs g ...... and promotes lymphomagenesis.

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Disruption of KMT2D perturbs g ...... and promotes lymphomagenesis.

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Nature Medicine

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Disruption of KMT2D perturbs g ...... t and promotes lymphomagenesis

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Antony B Holmes

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David Dominguez-Sola

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Hongyan Tang

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Ji-Eun Lee

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Jiyuan Zhang

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Katia Basso

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Mukesh Bansal

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Riccardo Dalla-Favera

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Shafinaz Hussein

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Sofija Vlasevska

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Cloning and characterization of APS, an adaptor molecule containing PH and SH2 domains that is tyrosine phosphorylated upon B-cell receptor stimulation

The Saccharomyces cerevisiae Set1 complex includes an Ash2 homologue and methylates histone 3 lysine 4

Transcriptional analysis of the B cell germinal center reaction

Discovery and prioritization of somatic mutations in diffuse large B-cell lymphoma (DLBCL) by whole-exome sequencing

Exome sequencing identifies MLL2 mutations as a cause of Kabuki syndrome

Histone H3K27ac separates active from poised enhancers and predicts developmental state

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

Regulation of immune cell development through soluble inositol-1,3,4,5-tetrakisphosphate

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets

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10.1038/NM.3940

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10

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Laura Pasqualucci

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