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

Inactivation of TIF1γ Cooperates with KrasG12D to Induce Cystic Tumors of the Pancreas

23 Jul 2009

Abstract excerpt

Inactivation of the Transforming Growth Factor Beta (TGFbeta) tumor suppressor pathway contributes to the progression of Pancreatic Ductal AdenoCarcinoma (PDAC) since it is inactivated in virtually all cases of this malignancy. Genetic lesions inactivating this pathway contribute to pancreatic tumor progression in mouse models. Transcriptional Intermediary Factor 1 gamma (TIF1gamma) has recently been proposed to...

Read the complete abstract on PubMed

Topics

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

Share to Pancreatic and Hepatic Oncology Research
Share to Renal and related cancers
Share to TGF-β signaling in diseases

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 19629168
DOI: 10.1371/journal.pgen.1000575

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 24 Oct 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Inactivation of TIF1γ Cooperates with KrasG12D to Induce Cystic Tumors of the PancreasPMID 19629168Read ↗

Tif1γ suppresses murine pancreatic tumoral transformation by a Smad4-independent pathway.Semantic proximity Read ↗

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

Loss of Trefoil Factor 2 From Pancreatic Duct Glands Promotes Formation of Intraductal Papillary Mucinous Neoplasms in Mice.Semantic proximity Read ↗

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 ↗

TGIF1-Twist1 axis 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 ↗

Loss of Jag1 cooperates with oncogenic Kras to induce pancreatic cystic neoplasms.Semantic proximity Read ↗

ID1 Mediates Escape from TGFβ Tumor Suppression in Pancreatic CancerSemantic proximity Read ↗

Concomitant pancreatic activation of Kras(G12D) and Tgfa results in cystic papillary neoplasms reminiscent of human IPMN.Semantic proximity Read ↗

Loss of Activin Receptor Type 1B Accelerates Development of Intraductal Papillary Mucinous Neoplasms in Mice With Activated KRAS.Semantic proximity Read ↗

Synergistic action of Smad4 and Pten in suppressing pancreatic ductal adenocarcinoma formation in mice.Semantic proximity Read ↗

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