Somatic IL4R mutations in primary mediastinal large B-cell lymphoma lead to constitutive JAK-STAT signaling activation.

doi:10.1182/blood-2017-09-808907

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

Somatic IL4R mutations in primary mediastinal large B-cell lymphoma lead to constitutive JAK-STAT signaling activation.

Blood - 3 May 2018

Viganò Elena, Gunawardana Jay, Mottok Anja, Van Tol Tessa, Mak Katina, Chan Fong Chun, Chong Lauren, Chavez Elizabeth, Woolcock Bruce, Takata Katsuyoshi, Twa David, Shulha Hennady P, Telenius Adèle, Kutovaya Olga, Hung Stacy S, Healy Shannon, Ben-Neriah Susana, Leroy Karen, Gaulard Philippe, Diepstra Arjan, Kridel Robert, Savage Kerry J, Rimsza Lisa, Gascoyne Randy, Steidl Christian

Abstract excerpt

Primary mediastinal large B-cell lymphoma (PMBCL) is a distinct subtype of diffuse large B-cell lymphoma thought to arise from thymic medullary B cells. Gene mutations underlying the molecular pathogenesis of the disease are incompletely characterized. Here, we describe novel somatic IL4R mutations in 15 of 62 primary cases of PMBCL (24.2%) and in all PMBCL-derived cell lines tested. The majority of mutations...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Line, Tumor

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Disease Models, Animal

Share to Interleukin-4 Receptor alpha Subunit

Share to Janus Kinases

Share to Lymphoma, Large B-Cell, Diffuse

Share to Mediastinal Neoplasms

Share to Phosphorylation

Share to STAT Transcription Factors

Source

Open in PubMed

Identifiers

PMID: 29467182
DOI: 10.1182/blood-2017-09-808907

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Somatic IL4R mutations in primary mediastinal large B-cell lymphoma lead to constitutive JAK-STAT signaling activation.PMID 29467182Read ↗

Integrative genomic analysis identifies key pathogenic mechanisms in primary mediastinal large B-cell lymphomaSemantic proximity Read ↗

The molecular pathogenesis of primary mediastinal large B-cell lymphomaSemantic proximity Read ↗

Structural genomic alterations in primary mediastinal large B-cell lymphoma.Semantic proximity Read ↗

Primary mediastinal large B-cell lymphomaSemantic proximity Read ↗

Genomic Alterations in CIITA Are Frequent in Primary Mediastinal Large B Cell Lymphoma and Are Associated with Diminished MHC Class II Expression.Semantic proximity Read ↗

Genomic rearrangements involving programmed death ligands are recurrent in primary mediastinal large B-cell lymphoma.Semantic proximity Read ↗

Recurrent somatic mutations of PTPN1 in primary mediastinal B cell lymphoma and Hodgkin lymphoma.Semantic proximity Read ↗

STAT6 mutations enriched at diffuse large B-cell lymphoma relapse reshape the tumor microenvironment.Semantic proximity Read ↗

Recurrent mutations of the STAT6 DNA binding domain in primary mediastinal B-cell lymphoma.Semantic proximity Read ↗

The T-cell leukemia-associated ribosomal RPL10 R98S mutation enhances JAK-STAT signaling.Semantic proximity Read ↗

A Novel Missense (M206K) STAT3 Mutation in Diffuse Large B Cell Lymphoma Deregulates STAT3 SignalingSemantic proximity Read ↗

The Interleukin-7 Receptor Signaling Pathway and Its Perturbation in Immunodeficiency, Autoimmune Disease and Lymphoid Malignancy.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.