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

SMAD4 induces opposite effects on metastatic growth from pancreatic tumors depending on the organ of residence.

Nature cancer - 1 Nov 2025

Tsanov Kaloyan M, Barriga Francisco M, Ho Yu-Jui, Alonso-Curbelo Direna, Livshits Geulah, Tian Sha, Koche Richard P, Baslan Timour, Simon Janelle, Wuest Alexandra N, Reyes José, Park Jin, Luan Wei, Wilkinson John E, Bhanot Umesh, Ray-Kirton Jordana, Masilionis Ignas, Dimitrova Nevenka, Iacobuzio-Donahue Christine A, Chaligné Ronan, Pe'er Dana, Massagué Joan, Lowe Scott W

Abstract excerpt

The role of driver gene mutations in sustaining tumor growth at metastatic sites is poorly understood. SMAD4 inactivation is a paradigm of such mutations and a hallmark of pancreatic ductal adenocarcinoma (PDAC). To determine whether metastatic tumors are dependent on SMAD4 inactivation, we developed a mouse model of PDAC that enables spatiotemporal control of Smad4 expression. While Smad4 inactivation in the...

Read the complete abstract on PubMed

Topics

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

Share to Carcinoma, Pancreatic Ductal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Gene Expression Regulation, Neoplastic

Share to Kruppel-Like Factor 4

Share to Kruppel-Like Transcription Factors

Share to Liver Neoplasms

Share to Neoplasm Metastasis

Share to Pancreatic Neoplasms

Share to Smad4 Protein

Source

Open in PubMed Open full text

Identifiers

PMID: 40999053
DOI: 10.1038/s43018-025-01047-5
PMCID: PMC12643927

Genes

SMAD4
KLF4
RUNX1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

SMAD4 induces opposite effects on metastatic growth from pancreatic tumors depending on the organ of residence.PMID 40999053Read ↗

Metastatic site influences driver gene function in pancreatic cancerSemantic proximity Read ↗

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

Two sides of the story? Smad4 loss in pancreatic cancer versus head‐and‐neck cancerSemantic proximity Read ↗

Loss of the transcriptional repressor TGIF1 results in enhanced Kras-driven development of pancreatic cancerSemantic proximity Read ↗

Molecular Pathogenesis of Pancreatic Cancer: Advances and ChallengesSemantic proximity Read ↗

Insertional mutagenesis defines drivers and evolutionary relationships in pancreatic cancer metastasisSemantic proximity Read ↗

A Genetically Engineered Human Organoid Model Reveals Distinct Genetic and Epigenetic Barriers of Lineage Plasticity in Early PDAC TransformationSemantic proximity Read ↗

Deregulation of Transcription Factor Networks Driving Cell Plasticity and Metastasis in Pancreatic CancerSemantic proximity Read ↗

A GATA6-centered gene regulatory network involving HNFs and ΔNp63 controls plasticity and immune escape in pancreatic cancerSemantic proximity Read ↗

Smad4 deficiency substitutes Cdkn2b but not Cdkn2a downregulation in pancreatic cancer following induction of genetic events in adult mice.Semantic proximity Read ↗

Loss of p53 and SMAD4 induces adenosquamous subtype pancreatic cancer in the absence of an oncogenic KRAS mutation.Semantic proximity Read ↗

Modeling pancreatic cancer in mice for experimental therapeutics.Semantic proximity Read ↗

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