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

Loss of p16 pathways stabilizes EWS/FLI1 expression and complements EWS/FLI1 mediated transformation.

Oncogene - 11 Oct 2001

Deneen B, Denny C T

Abstract excerpt

Ewings sarcoma and primitive neuroectodermal tumors (ES/PNET) are characterized by the fusion of the N-terminus of the EWS gene to the C-terminus of a member of the ETS family of transcription factors. While such fusion proteins are thought to play dominant oncogenic roles, it is unlikely that a single genetic alteration by itself will support cellular transformation. Given that EWS/FLI1 is only able to transform...

Read the complete abstract on PubMed

Topics

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

Share to 3T3 Cells
Share to Cyclin-Dependent Kinase Inhibitor p16
Share to Oncogene Proteins, Fusion

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Proto-Oncogene Protein c-fli-1

Share to Retroviridae

Share to RNA-Binding Protein EWS

Share to Transduction, Genetic

Share to Tumor Suppressor Protein p14ARF

Source

Identifiers

PMID: 11709708
DOI: 10.1038/sj.onc.1204875

Genes

FLI1

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

Loss of p16 pathways stabilizes EWS/FLI1 expression and complements EWS/FLI1 mediated transformation.PMID 11709708Read ↗

EWS/FLI1 suppresses retinoblastoma protein function and senescence in Ewing's sarcoma cells.Semantic proximity Read ↗

Expression of the <i>EWS/FLI-1</i> Oncogene in Murine Primary Bone-Derived Cells Results in EWS/FLI-1–Dependent, Ewing Sarcoma–Like TumorsSemantic proximity Read ↗

GLI1 is a central mediator of EWS/FLI1 signaling in Ewing tumors.Semantic proximity Read ↗

Proto-oncogene FBI-1 Represses Transcription of p21CIP1 by Inhibition of Transcription Activation by p53 and Sp1Semantic proximity Read ↗

Interference with the constitutive activation of ERK1 and ERK2 impairs EWS/FLI-1-dependent transformation.Semantic proximity Read ↗

Stress-Regulated Transcription Factor ATF4 Promotes Neoplastic Transformation by Suppressing Expression of the INK4a/ARF Cell Senescence FactorsSemantic proximity Read ↗

EWS-FLI1 Suppresses NOTCH-Activated p53 in Ewing's SarcomaSemantic proximity Read ↗

Transformation induced by Ewing's sarcoma associated EWS/FLI-1 is suppressed by KRAB/FLI-1.Semantic proximity Read ↗

Development of Ewing's sarcoma from primary bone marrow-derived mesenchymal progenitor cells.Semantic proximity Read ↗

The Ewing's sarcoma oncoprotein EWS/FLI induces a p53-dependent growth arrest in primary human fibroblasts.Semantic proximity Read ↗

The EWS/FLI1 oncogenic transcription factor deregulates GLI1.Semantic proximity Read ↗

FOXM1 Is an Oncogenic Mediator in Ewing SarcomaSemantic proximity Read ↗

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