CDKN2/p16 predicts survival in oligodendrogliomas: comparison with astrocytomas. (Q48192705)

9 February 2018

title

CDKN2/p16 predicts survival in oligodendrogliomas: comparison with astrocytomas. (English)

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9 February 2018

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H Miettinen

1

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9 February 2018

J Kononen

2

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P Sallinen

3

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H Alho

4

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P Helen

5

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H Helin

6

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H Kalimo

7

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L Paljärvi

8

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J Isola

9

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H Haapasalo

10

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publication date

1 February 1999

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9 February 2018

Journal of Neuro-Oncology

published in

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9 February 2018

volume

41

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issue

3

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9 February 2018

page(s)

205-211

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9 February 2018

https://scigraph.springernature.com/pub.10.1023/a:1006185220369

exact match

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cites work

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Silencing of p16/CDKN2 expression in human gliomas by methylation and chromatin condensation.

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Differential expression and cell cycle regulation of the cyclin-dependent kinase 4 inhibitor p16Ink4.

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CDKN2 (p16/MTS1) gene deletion or CDK4 amplification occurs in the majority of glioblastomas.

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Mutational analysis of CDKN2 (MTS1/p16ink4) in human breast carcinomas

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Homozygous deletions of the multiple tumor suppressor gene 1 in the progression of human astrocytomas.

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Malignant astrocytomas with homozygous CDKN2/p16 gene deletions have higher Ki-67 proliferation indices.

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The retinoblastoma protein and cell cycle control

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Molecular analysis of deletions of the short arm of chromosome 9 in human gliomas.

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Human glioblastomas with no alterations of the CDKN2A (p16INK4A, MTS1) and CDK4 genes have frequent mutations of the retinoblastoma gene.

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Adenovirus-mediated p16/CDKN2 gene transfer induces growth arrest and modifies the transformed phenotype of glioma cells.

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Deletions of the cyclin-dependent kinase-4 inhibitor gene in multiple human cancers

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CDKN2/p16 inactivation and p16 immunohistochemistry in astrocytic gliomas.

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Determination of p53 mutations, EGFR overexpression, and loss of p16 expression in pediatric glioblastomas.

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Infrequent alterations of the p15, p16, CDK4 and cyclin D1 genes in non-astrocytic human brain tumors.

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Prognostication of astrocytoma patient survival by Ki-67 (MIB-1), PCNA, and S-phase fraction using archival paraffin-embedded samples

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Mutations of the p16 gene in gliomas.

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A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4

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Homozygous deletion of the MTS1/p16 and MTS2/p15 genes and amplification of the CDK4 gene in glioma.

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Immunohistochemical detection of the cyclin-dependent kinase inhibitor 2/multiple tumor suppressor gene 1 (CDKN2/MTS1) product p16INK4A in archival human solid tumors: correlation with retinoblastoma protein expression

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P16 deletion and mutation analysis in human brain tumors

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Loss of expression of the p16INK4/CDKN2 gene in cutaneous malignant melanoma correlates with tumor cell proliferation and invasive stage.

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5′ CpG island methylation is associated with transcriptional silencing of the tumour suppressor p16/CDKN2/MTS1 in human cancers

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Hypermethylation of the CpG island of p16/CDKN2 correlates with gene inactivation in gliomas.

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Replacement of the p16/CDKN2 gene suppresses human glioma cell growth

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Loss of P16INK4 expression is frequent in high grade gliomas.

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CDK4 amplification is an alternative mechanism to p16 gene homozygous deletion in glioma cell lines

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12 December 2020

Frequent loss of heterozygosity on chromosome 9, and low incidence of mutations of cyclin-dependent kinase inhibitors p15 (MTS2) and p16 (MTS1) genes in gliomas.

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MTS1/p16/CDKN2 lesions in primary glioblastoma multiforme.

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A cell cycle regulator potentially involved in genesis of many tumor types

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12 December 2020

Identifiers

DOI

10.1023/A:1006185220369

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9 February 2018

Dimensions Publication ID

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9 February 2018