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 p53 Concurrent with RAS and TERT Activation Induces Glioma Formation.

Molecular neurobiology - 1 Jun 2023

Gong Meiting, Fan Xiaoqing, Yu Huihan, Niu Wanxiang, Sun Suling, Wang Hongzhi, Chen Xueran

Abstract excerpt

There is an ongoing debate regarding whether gliomas originate due to functional or genetic changes in neural stem cells (NSCs). Genetic engineering has made it possible to use NSCs to establish glioma models with the pathological features of human tumors. Here, we found that RAS, TERT, and p53 mutations or abnormal expression were associated with the occurrence of glioma in the mouse tumor transplantation model....

Read the complete abstract on PubMed

Topics

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

Share to Neural Stem Cells
Share to ras Proteins
Share to Brain Neoplasms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cell Transformation, Neoplastic

Share to Glioma

Share to MicroRNAs

Share to Telomerase

Share to Tumor Suppressor Protein p53

Source

Identifiers

PMID: 36867344
DOI: 10.1007/s12035-023-03288-w

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 p53 Concurrent with RAS and TERT Activation Induces Glioma Formation.PMID 36867344Read ↗

EZH2 Palmitoylation Mediated by ZDHHC5 in p53-Mutant Glioma Drives Malignant Development and Progression.Semantic proximity Read ↗

H3.3K27M Cooperates with Trp53 Loss and PDGFRA Gain in Mouse Embryonic Neural Progenitor Cells to Induce Invasive High-Grade Gliomas.Semantic proximity Read ↗

Mouse Models to Interrogate the Implications of the Differentiation Status in the Ontogeny of GliomasSemantic proximity Read ↗

Gliomagenesis Arising from Pten- and Ink4a/Arf-Deficient Neural Progenitor Cells Is Mediated by the p53-Fbxw7/Cdc4 Pathway, Which Controls c-MycSemantic proximity Read ↗

Combinations of genetic mutations in the adult neural stem cell compartment determine brain tumour phenotypes.Semantic proximity Read ↗

The Nuclear Receptor TLX Is Required for Gliomagenesis within the Adult Neurogenic NicheSemantic proximity Read ↗

Expression of mutant p53 proteins implicates a lineage relationship between neural stem cells and malignant astrocytic glioma in a murine model.Semantic proximity Read ↗

Olig1/2-Expressing Intermediate Lineage Progenitors Are Predisposed to PTEN/p53-Loss–Induced Gliomagenesis and Harbor Specific Therapeutic VulnerabilitiesSemantic proximity Read ↗

Neural and cancer stem cells in tumor suppressor mouse models of malignant astrocytoma.Semantic proximity Read ↗

Novel Perspectives on p53 Function in Neural Stem Cells and Brain TumorsSemantic proximity Read ↗

Beyond Conventional Models: Recreating the Initiation, Evolution, and Genome of GBMSemantic proximity Read ↗

Transposon mutagenesis identifies genes that transform neural stem cells into glioma-initiating cellsSemantic proximity Read ↗

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