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

Functional analysis of wild-type and malignant glioma derived CDKN2Abeta alleles: evidence for an RB-independent growth suppressive pathway.

Oncogene - 23 Oct 1997

Arap W, Knudsen E, Sewell D A, Sidransky D, Wang J Y, Huang H J, Cavenee W K

Abstract excerpt

The tumor suppressor gene CDKN2A (p16/MTS1/INK4A), which encodes the cyclin-dependent kinase inhibitor p16(INK4a), is a target of 9p21 deletions during the malignant progression of human gliomas. This gene also encodes a second protein product (human p16beta, murine p19ARF), which originates from an unrelated exon of CDKN2A (exon 1beta) spliced onto exon 2 in an alternate reading frame. Cell cycle arrest by...

Read the complete abstract on PubMed

Topics

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

Share to Alleles
Share to Cell Division
Share to Chromosome Deletion

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genetic Vectors

Share to Phosphorylation

Share to Point Mutation

Share to Transfection

Share to Tumor Cells, Cultured

Source

Identifiers

PMID: 9366518
DOI: 10.1038/sj.onc.1201389

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.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Functional analysis of wild-type and malignant glioma derived CDKN2Abeta alleles: evidence for an RB-independent growth suppressive pathway.PMID 9366518Read ↗

Point mutations can inactivate in vitro and in vivo activities of p16(INK4a)/CDKN2A in human glioma.Semantic proximity Read ↗

Functional evidence for a role of combined CDKN2A (p16-p14(ARF))/CDKN2B (p15) gene inactivation in malignant gliomas.Semantic proximity Read ↗

Hemizygous or homozygous deletion of the chromosomal region containing the p16INK4a gene is associated with amplification of the EGF receptor gene in glioblastomas.Semantic proximity Read ↗

Identification of p18 INK4c as a tumor suppressor gene in glioblastoma multiforme.Semantic proximity Read ↗

p16 Immunohistochemical Expression as a Surrogate Assessment of CDKN2A Alteration in Gliomas Leading to Prognostic SignificancesSemantic proximity Read ↗

The meaning of p16<sup>ink4a</sup>expression in tumorsSemantic proximity Read ↗

p16-Cdk4-Rb axis controls sensitivity to a cyclin-dependent kinase inhibitor PD0332991 in glioblastoma xenograft cellsSemantic proximity Read ↗

Transforming Growth Factor-β-mediated p15INK4BInduction and Growth Inhibition in Astrocytes Is SMAD3-dependent and a Pathway Prominently Altered in Human Glioma Cell LinesSemantic proximity Read ↗

Tumour-derived p16 alleles encoding proteins defective in cell-cycle inhibition.Semantic proximity Read ↗

Familial head and neck cancer: molecular analysis of a new clinical entity.Semantic proximity Read ↗

Expression of p19 INK4d, CDK4, CDK6 in glioblastoma multiformeSemantic proximity Read ↗

Loss of P16INK4 expression is frequent in high grade gliomas.Semantic proximity Read ↗

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