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

Direct reprogramming by oncogenic Ras and Myc.

Proceedings of the National Academy of Sciences of the United States of America - 5 Mar 2013

Ischenko Irene, Zhi Jizu, Moll Ute M, Nemajerova Alice, Petrenko Oleksi

Abstract excerpt

Genetically or epigenetically defined reprogramming is a hallmark of cancer cells. However, a causal association between genome reprogramming and cancer has not yet been conclusively established. In particular, little is known about the mechanisms that underlie metastasis of cancer, and even less is known about the identity of metastasizing cancer cells. In this study, we used a model of conditional expression of...

Read the complete abstract on PubMed

Topics

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

Share to Cell Transdifferentiation
Share to Cell Transformation, Neoplastic

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genes, myc

Share to Genes, p53

Share to Genes, ras

Share to Neoplasm Metastasis

Share to Neoplastic Stem Cells

Share to Pancreatic Neoplasms

Source

Open in PubMed Open full text

Identifiers

PMID: 23431158
DOI: 10.1073/pnas.1219592110
PMCID: PMC3593888

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Direct reprogramming by oncogenic Ras and Myc.PMID 23431158Read ↗

In vivo reprogramming drives Kras-induced cancer development.Semantic proximity Read ↗

Tumorigenic potential is restored during differentiation in fusion-reprogrammed cancer cells.Semantic proximity Read ↗

Molecular dynamics driving phenotypic divergence among KRAS mutants in pancreatic tumorigenesisSemantic proximity Read ↗

Mesenchymal tumor cells drive adaptive resistance of Trp53-/- breast tumor cells to inactivated mutant Kras.Semantic proximity Read ↗

Decoding cancer etiology with cellular reprogramming.Semantic proximity Read ↗

Reprogramming to developmental plasticity in cancer stem cells.Semantic proximity Read ↗

KRAS mutations take different trajectories to drive pancreatic transformation.Semantic proximity Read ↗

Behind the Wheel of Epithelial Plasticity in KRAS-Driven CancersSemantic proximity Read ↗

Analysis of the tumor-initiating and metastatic capacity of PDX1-positive cells from the adult pancreasSemantic proximity Read ↗

Dormant Cancer Cells Contribute to Residual Disease in a Model of Reversible Pancreatic CancerSemantic proximity Read ↗

Molecular dynamics driving phenotypic divergence among KRAS mutants in pancreatic tumorigenesis.Semantic proximity Read ↗

Evolutionary fingerprints of EMT in pancreatic cancersSemantic proximity Read ↗

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