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Article

Combinatorial BTK and MALT1 inhibition augments killing of CD79 mutant diffuse large B cell lymphoma.

Oncotarget - 8 Dec 2015

Nagel Daniel, Bognar Miriam, Eitelhuber Andrea C, Kutzner Kerstin, Vincendeau Michelle, Krappmann Daniel

Abstract excerpt

Survival of activated B cell-subtype (ABC) of diffuse large B cell lymphoma (DLBCL) is driven by chronic B cell receptor (BCR) signaling that activates the canonical NF-κB pathway. Inhibition of BTK by Ibrutinib has been shown to kill ABC DLBCL cells that carry activating mutations in the BCR adaptor CD79. However, mutations in BTK or in downstream components such as CARMA1/CARD11 can render lymphomas Ibrutinib...

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Topics

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Share to Agammaglobulinaemia Tyrosine Kinase
Share to CARD Signaling Adaptor Proteins

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to CD79 Antigens

Share to Guanylate Cyclase

Share to Jurkat Cells

Share to Lymphoma, Large B-Cell, Diffuse

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Share to Stereoisomerism

Source

Open in PubMed Open full text

Identifiers

PMID: 26540570
DOI: 10.18632/oncotarget.6273
PMCID: PMC4747221

Genes

BTK
MALT1
BCR
CARD11

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

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Combinatorial BTK and MALT1 inhibition augments killing of CD79 mutant diffuse large B cell lymphoma.PMID 26540570Read ↗

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