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

LCK inhibition downregulates YAP activity and is therapeutic in patient-derived models of cholangiocarcinoma

24 Sept 2022

Abstract excerpt

BACKGROUND & AIMS: There is an unmet need to develop novel, effective medical therapies for cholangiocarcinoma (CCA). The Hippo pathway effector, Yes-associated protein (YAP), is oncogenic in CCA, but has historically been difficult to target therapeutically. Recently, we described a novel role for the LCK proto-oncogene, Src family tyrosine kinase (LCK) in activating YAP through tyrosine phosphorylation. This...

Read the complete abstract on PubMed

Topics

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

Share to Hippo pathway signaling and YAP/TAZ
Share to Liver physiology and pathology
Share to Proteoglycans and glycosaminoglycans research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 36162702
DOI: 10.1016/j.jhep.2022.09.014

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

LCK inhibition downregulates YAP activity and is therapeutic in patient-derived models of cholangiocarcinomaPMID 36162702Read ↗

Multiomics-driven discovery of predictive biomarkers and strategies to overcome resistance to SFK-YAP inhibition in cholangiocarcinomaSemantic proximity Read ↗

FGFR Inhibitors: Clinical Activity and Development in the Treatment of Cholangiocarcinoma.Semantic proximity Read ↗

YAP ‐ TEAD inhibition is associated with upregulation of an androgen receptor mediated transcription program providing therapeutic escapeSemantic proximity Read ↗

CLK1 Activates YAP to Promote Intrahepatic CholangiocarcinogenesisSemantic proximity Read ↗

The molecular interaction pattern of lenvatinib enables inhibition of wild-type or kinase-mutated FGFR2-driven cholangiocarcinomaSemantic proximity Read ↗

Autophagy suppression via SRC induction represents a therapeutic vulnerability for BAP1 -mutant cancersSemantic proximity Read ↗

RLY-4008, the First Highly Selective FGFR2 Inhibitor with Activity across FGFR2 Alterations and Resistance Mutations.Semantic proximity Read ↗

Derazantinib: an investigational drug for the treatment of cholangiocarcinoma.Semantic proximity Read ↗

Erdafitinib in Patients with FGFR-Altered Advanced or Metastatic Cholangiocarcinoma.Semantic proximity Read ↗

Past, present, and future of FGFR inhibitors in cholangiocarcinoma: from biological mechanisms to clinical applications.Semantic proximity Read ↗

The Co-mutational Spectrum Determines the Therapeutic Response in Murine FGFR2 Fusion-Driven Cholangiocarcinoma.Semantic proximity Read ↗

Serine/threonine kinase TBK1 promotes cholangiocarcinoma progression via direct regulation of β-cateninSemantic proximity Read ↗

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