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

DPC4/SMAD4 mediated tumor suppression of colon carcinoma cells is associated with reduced urokinase expression.

Oncogene - 20 May 1999

Schwarte-Waldhoff I, Klein S, Blass-Kampmann S, Hintelmann A, Eilert C, Dreschers S, Kalthoff H, Hahn S A, Schmiegel W

Abstract excerpt

We recently identified DPC4/Smad4 as a candidate tumor suppressor gene mutated or lost in one half of pancreatic carcinomas and in a subset of colon and biliary tract carcinomas. DPC4 plays a key role in signal transduction of the TGF-beta superfamily of molecules and inactivation of TGF-beta med...

Read the complete abstract on PubMed

Topics

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

Share to Cell Adhesion
Share to Colonic Neoplasms
Share to Mice, Nude

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Plasminogen Activator Inhibitor 1

Share to Smad4 Protein

Share to Trans-Activators

Share to Transforming Growth Factor beta

Share to Urokinase-Type Plasminogen Activator

Source

Identifiers

PMID: 10340387
DOI: 10.1038/sj.onc.1202641

Genes

SMAD4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-10340387-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

DPC4/SMAD4 mediated tumor suppression of colon carcinoma cells is associated with reduced urokinase expression.PMID 10340387Read ↗

Smad4/DPC4 silencing and hyperactive Ras jointly disrupt transforming growth factor-beta antiproliferative responses in colon cancer cells.Semantic proximity Read ↗

Smad4/DPC4-mediated tumor suppression through suppression of angiogenesisSemantic proximity Read ↗

Transforming growth factor-beta responsiveness in DPC4/SMAD4-null cancer cells.Semantic proximity Read ↗

SMAD4 loss triggers the phenotypic changes of pancreatic ductal adenocarcinoma cells.Semantic proximity Read ↗

Dpc4 transcriptional activation and dysfunction in cancer cells.Semantic proximity Read ↗

Smad4 Inactivation Promotes Malignancy and Drug Resistance of Colon CancerSemantic proximity Read ↗

The tumor suppressor Smad4/DPC 4 as a central mediator of Smad functionSemantic proximity Read ↗

Differential proteome analysis of conditioned media to detect Smad4 regulated secreted biomarkers in colon cancerSemantic proximity Read ↗

Restoration of SMAD4 by gene therapy reverses the invasive phenotype in pancreatic adenocarcinoma cells.Semantic proximity Read ↗

Functional blockade of Smad4 leads to a decrease in β-catenin levels and signaling activity in human pancreatic carcinoma cellsSemantic proximity Read ↗

C4.4A gene ablation is compatible with normal epidermal development and causes modest overt phenotypes.Semantic proximity Read ↗

Smad4 Loss Correlates With Higher Rates of Local and Distant Failure in Pancreatic Adenocarcinoma Patients Receiving Adjuvant Chemoradiation.Semantic proximity Read ↗

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