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

Antagonism between Prdm16 and Smad4 specifies the trajectory and progression of pancreatic cancer

24 Jan 2023

Abstract excerpt

The transcription factor Prdm16 functions as a potent suppressor of transforming growth factor-beta (TGF-β) signaling, whose inactivation is deemed essential to the progression of pancreatic ductal adenocarcinoma (PDAC). Using the KrasG12D-based mouse model of human PDAC, we surprisingly found that ablating Prdm16 did not block but instead accelerated PDAC formation and progression, suggesting that Prdm16 might...

Read the complete abstract on PubMed

Topics

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

Share to Epigenetics and DNA Methylation
Share to Pancreatic and Hepatic Oncology Research
Share to TGF-β signaling in diseases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 36828547
DOI: 10.1083/jcb.202203036

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

Antagonism between Prdm16 and Smad4 specifies the trajectory and progression of pancreatic cancerPMID 36828547Read ↗

Inactivation of Smad4 Accelerates KrasG12D-Mediated Pancreatic NeoplasiaSemantic proximity Read ↗

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

Both p16 <sup>Ink4a</sup> and the p19 <sup>Arf</sup> -p53 pathway constrain progression of pancreatic adenocarcinoma in the mouseSemantic proximity Read ↗

SMAD4 and the TGFβ Pathway in Patients with Pancreatic Ductal AdenocarcinomaSemantic proximity Read ↗

The TGF-β/Smad4 Signaling Pathway in Pancreatic Carcinogenesis and Its Clinical SignificanceSemantic proximity Read ↗

METTL16 predicts a favorable outcome and primes antitumor immunity in pancreatic ductal adenocarcinomaSemantic proximity Read ↗

Aggressive pancreatic ductal adenocarcinoma in mice caused by pancreas-specific blockade of transforming growth factor-beta signaling in cooperation with active Kras expression.Semantic proximity Read ↗

Deciphering the mechanisms of tumorigenesis in human pancreatic ductal epithelial cells.Semantic proximity Read ↗

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

An update on molecular research of pancreatic adenocarcinoma.Semantic proximity Read ↗

Genetic Progression of Pancreatic CancerSemantic proximity Read ↗

The role of TGF-β/SMAD4 signaling in cancer.Semantic proximity Read ↗

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