Discover Community Create You

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

Article

Recurrent chromosomal rearrangements of ROS1, FRK and IL6 activating JAK/STAT pathway in inflammatory hepatocellular adenomas.

Gut - 1 Sept 2020

Bayard Quentin, Caruso Stefano, Couchy Gabrielle, Rebouissou Sandra, Bioulac Sage Paulette, Balabaud Charles, Paradis Valerie, Sturm Nathalie, de Muret Anne, Guettier Catherine, Bonsang Benjamin, Copie Christiane, Letouzé Eric, Calderaro Julien, Imbeaud Sandrine, Nault Jean-Charles, Zucman-Rossi Jessica

Abstract excerpt

BACKGROUND: Inflammatory hepatocellular adenomas (IHCAs) are benign liver tumours characterised by an activation of the janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway caused by oncogenic activating mutations. However, a subset of IHCA lacks of identified mutation explaining the inflammatory phenotype. METHODS: 657 hepatocellular adenomas developed in 504 patients were...

Read the complete abstract on PubMed

Topics

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

Share to Adenoma, Liver Cell
Share to Cytokine Receptor gp130

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Rearrangement

Share to Inflammation

Share to Janus Kinases

Share to Liver Neoplasms

Share to Protein-Tyrosine Kinases

Share to STAT Transcription Factors

Source

Identifiers

PMID: 31907296
DOI: 10.1136/gutjnl-2019-319790

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Recurrent chromosomal rearrangements of ROS1, FRK and IL6 activating JAK/STAT pathway in inflammatory hepatocellular adenomas.PMID 31907296Read ↗

Mutations leading to constitutive active gp130/JAK1/STAT3 pathway.Semantic proximity Read ↗

Somatic mutations activating STAT3 in human inflammatory hepatocellular adenomas.Semantic proximity Read ↗

Biochemical and functional analyses of gp130 mutants unveil JAK1 as a novel therapeutic target in human inflammatory hepatocellular adenomaSemantic proximity Read ↗

Genomic profiling of hepatocellular adenomas reveals recurrent FRK-activating mutations and the mechanisms of malignant transformation.Semantic proximity Read ↗

Molecular Classification of Hepatocellular Adenoma Associates With Risk Factors, Bleeding, and Malignant Transformation.Semantic proximity Read ↗

Molecular Characterization of Inflammatory Myofibroblastic Tumors With Frequent ALK and ROS1 Gene Fusions and Rare Novel RET RearrangementSemantic proximity Read ↗

Inflammatory Myofibroblastic Tumors Harbor Multiple Potentially Actionable Kinase FusionsSemantic proximity Read ↗

Inflammatory hepatocellular adenomas developed in the setting of chronic liver disease and cirrhosis.Semantic proximity Read ↗

<i>ROS1</i> Fusions in Cancer: A ReviewSemantic proximity Read ↗

Gene rearrangements in consecutive series of pediatric inflammatory myofibroblastic tumorsSemantic proximity Read ↗

GNAS-activating mutations define a rare subgroup of inflammatory liver tumors characterized by STAT3 activation.Semantic proximity Read ↗

ETV6-NTRK3 Is Expressed in a Subset of ALK-Negative Inflammatory Myofibroblastic TumorsSemantic proximity Read ↗

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