Loss of TNFAIP3 enhances MYD88-driven signaling in non-Hodgkin lymphoma

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Loss of TNFAIP3 enhances MYD88-driven signaling in non-Hodgkin lymphoma

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im Oktober 2018 veröffentlichter wissenschaftlicher Artikel

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scientific article published on 09 October 2018

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wetenschappelijk artikel

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наукова стаття, опублікована в жовтні 2018

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Loss of TNFAIP3 enhances MYD88-driven signaling in non-Hodgkin lymphoma

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Loss of TNFAIP3 enhances MYD88-driven signaling in non-Hodgkin lymphoma

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Loss of TNFAIP3 enhances MYD88-driven signaling in non-Hodgkin lymphoma

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Loss of TNFAIP3 enhances MYD88-driven signaling in non-Hodgkin lymphoma

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Loss of TNFAIP3 enhances MYD88-driven signaling in non-Hodgkin lymphoma

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Loss of TNFAIP3 enhances MYD88-driven signaling in non-Hodgkin lymphoma

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P1476

Loss of TNFAIP3 enhances MYD88L265P-driven signaling in non-Hodgkin lymphoma

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P2093

Anne J Novak

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Esteban Braggio

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Hanna R Schoon

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Kerstin Wenzl

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Michelle K Manske

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Patricia T Greipp

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Stephen M Ansell

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Susan L Slager

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Thomas E Witzig

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Vivekananda Sarangi

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P2860

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

A gene expression-based method to diagnose clinically distinct subgroups of diffuse large B cell lymphoma

MYD88 L265P somatic mutation in Waldenström's macroglobulinemia.

Resistance mechanisms for the Bruton's tyrosine kinase inhibitor ibrutinib

Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray

Identification of copy number abnormalities and inactivating mutations in two negative regulators of nuclear factor-kappaB signaling pathways in Waldenstrom's macroglobulinemia

Gene-expression profiling of Waldenstrom macroglobulinemia reveals a phenotype more similar to chronic lymphocytic leukemia than multiple myeloma

Oncogenically active MYD88 mutations in human lymphoma

The genomic landscape of Waldenstrom macroglobulinemia is characterized by highly recurring MYD88 and WHIM-like CXCR4 mutations, and small somatic deletions associated with B-cell lymphomagenesis

B cells lacking the tumor suppressor TNFAIP3/A20 display impaired differentiation and hyperactivation and cause inflammation and autoimmunity in aged mice

P2888

s41408-018-0130-3

P304

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P31

scholarly article

P356

10.1038/S41408-018-0130-3

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P407

English

P433

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P478

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P50

Andrew L Feldman

James R Cerhan

Matthew J Maurer

P577

2018-10-09T00:00:00Z

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P6179

1107500024

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P698

30301877

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P921

hematology

P932

6177394

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