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

Cooperativity of oncogenic K-ras and downregulated p16/INK4A in human pancreatic tumorigenesis.

PloS one - 1 Jan 2014

Chang Zhe, Ju Huaiqiang, Ling Jianhua, Zhuang Zhuonan, Li Zhongkui, Wang Huamin, Fleming Jason B, Freeman James W, Yu Dihua, Huang Peng, Chiao Paul J

Abstract excerpt

Activation of K-ras and inactivation of p16 are the most frequently identified genetic alterations in human pancreatic epithelial adenocarcinoma (PDAC). Mouse models engineered with mutant K-ras and deleted p16 recapitulate key pathological features of PDAC. However, a human cell culture transformation model that recapitulates the human pancreatic molecular carcinogenesis is lacking. In this study, we...

Read the complete abstract on PubMed

Topics

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

Share to Carcinogenesis
Share to Cellular Senescence

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

Share to Cyclin-Dependent Kinase Inhibitor p16

Share to Down-Regulation

Share to Gene Silencing

Share to Genes, ras

Share to Neoplasm Metastasis

Share to Pancreatic Neoplasms

Source

Open in PubMed Open full text

Identifiers

PMID: 25029561
DOI: 10.1371/journal.pone.0101452
PMCID: PMC4100754

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 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

Cooperativity of oncogenic K-ras and downregulated p16/INK4A in human pancreatic tumorigenesis.PMID 25029561Read ↗

In vitro Modeling of Human Pancreatic Duct Epithelial Cell Transformation Defines Gene Expression Changes Induced by K- ras Oncogenic Activation in Pancreatic CarcinogenesisSemantic proximity Read ↗

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

Antagonism between Prdm16 and Smad4 specifies the trajectory and progression of pancreatic cancerSemantic proximity Read ↗

Oncogenic K-Ras and Loss of Smad4 Mediate Invasion by Activating an EGFR/NF-κB Axis That Induces Expression of MMP9 and uPA in Human Pancreas Progenitor CellsSemantic proximity Read ↗

A human cancer xenograft model utilizing normal pancreatic duct epithelial cells conditionally transformed with defined oncogenes.Semantic proximity Read ↗

p53 and p16Ink4a/p19Arf Loss Promotes Different Pancreatic Tumor Types from PyMT-Expressing Progenitor Cells.Semantic proximity Read ↗

Recombinant expression of different mutant K-ras gene in pancreatic cancer Bxpc-3 cells and its effects on chemotherapy sensitivity.Semantic proximity Read ↗

Expression of oncogenic K-ras and loss of Smad4 cooperate to induce the expression of EGFR and to promote invasion of immortalized human pancreas ductal cells.Semantic proximity Read ↗

Pancreatic cell plasticity and cancer initiation induced by oncogenic Kras is completely dependent on wild-type PI 3-kinase p110α.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 ↗

Mutated K-ras activates CDK8 to stimulate the epithelial-to-mesenchymal transition in pancreatic cancer in part via the Wnt/β-catenin signaling pathway.Semantic proximity Read ↗

The activity of Gli transcription factors is essential for Kras-induced pancreatic tumorigenesisSemantic proximity Read ↗

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