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

FGFR2 Abrogation Intercepts Pancreatic Ductal Adenocarcinoma Development.

Cancer research - 2 Jun 2025

Tonelli Claudia, Deschênes Astrid, Gaeth Victoria A, Jensen Amanda, Vithlani Nandan, Yao Melissa A, Zhao Zhen, Park Youngkyu, Tuveson David A

Abstract excerpt

Activating KRAS mutations are a key feature of pancreatic ductal adenocarcinoma (PDAC) and drive tumor initiation and progression. However, mutant KRAS by itself is weakly oncogenic. Defining the pathways that cooperate with mutant KRAS to induce tumorigenesis could identify prevention and treatment strategies. Analyzing organoids and murine and human pancreatic specimens, we found that the receptor tyrosine...

Read the complete abstract on PubMed

Topics

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

Share to Carcinoma, Pancreatic Ductal
Share to Cell Proliferation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Transformation, Neoplastic

Share to ErbB Receptors

Share to Pancreatic Neoplasms

Share to Proto-Oncogene Proteins p21(ras)

Share to Receptor, Fibroblast Growth Factor, Type 2

Share to Signal Transduction

Source

Open in PubMed Open full text

Identifiers

PMID: 40170241
DOI: 10.1158/0008-5472.CAN-24-4576
PMCID: PMC12169444

Genes

FGFR2
KRAS
EGFR

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

FGFR2 Abrogation Intercepts Pancreatic Ductal Adenocarcinoma Development.PMID 40170241Read ↗

Ductal pancreatic cancer interception by FGFR2 abrogationSemantic proximity Read ↗

Loss of FGFR4 promotes the malignant phenotype of PDAC.Semantic proximity Read ↗

Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer.Semantic proximity Read ↗

Mutant KRAS in the initiation of pancreatic cancer.Semantic proximity Read ↗

An essential role for Argonaute 2 in EGFR-KRAS signaling in pancreatic cancer development.Semantic proximity Read ↗

An Essential Role for <i>Argonaute 2</i> in EGFR-KRAS Signaling in Pancreatic Cancer DevelopmentSemantic proximity Read ↗

AP1/Fra1 confers resistance to MAPK cascade inhibition in pancreatic cancer.Semantic proximity Read ↗

KRAS Loss of Heterozygosity Promotes MAPK-Dependent Pancreatic Ductal Adenocarcinoma Initiation and Induces Therapeutic Sensitivity to MEK Inhibition.Semantic proximity Read ↗

KRAS mutation and epithelial-macrophage interplay in pancreatic neoplastic transformation.Semantic proximity Read ↗

Hedgehog/Ras interactions regulate early stages of pancreatic cancer.Semantic proximity Read ↗

Organoid-based ex vivo reconstitution of Kras-driven pancreatic ductal carcinogenesisSemantic proximity Read ↗

Cancer interception with KRAS inhibitors in preclinical models of pancreatic ductal adenocarcinoma.Semantic proximity Read ↗

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