Methylation, expression, and mutation analysis of the cell cycle control genes in human brain tumors (Q46071071)

19 December 2017

title

Methylation, expression, and mutation analysis of the cell cycle control genes in human brain tumors (English)

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19 December 2017

author name string

Dong Yin

1

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19 December 2017

Dong Xie

2

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19 December 2017

Wolf-Karsten Hofmann

3

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19 December 2017

Carl W Miller

4

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19 December 2017

Keith L Black

5

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19 December 2017

H Phillip Koeffler

6

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19 December 2017

language of work or name

English

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publication date

1 November 2002

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19 December 2017

published in

Oncogene

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19 December 2017

volume

21

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19 December 2017

page(s)

8372-8378

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19 December 2017

issue

54

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19 December 2017

https://scigraph.springernature.com/pub.10.1038/sj.onc.1206031

exact match

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cites work

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Frequency of homozygous deletion at p16/CDKN2 in primary human tumours

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Frequent somatic mutations and homozygous deletions of the p16 (MTS1) gene in pancreatic adenocarcinoma

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PTEN mutations in gliomas and glioneuronal tumors.

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Frequency and parental origin of hypermethylated RB1 alleles in retinoblastoma

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Growth suppression by p18, a p16INK4/MTS1- and p14INK4B/MTS2-related CDK6 inhibitor, correlates with wild-type pRb function

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Database of p53 gene somatic mutations in human tumors and cell lines: updated compilation and future prospects

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p15INK4B is a potential effector of TGF-beta-induced cell cycle arrest

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Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands

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Germline p16 mutations in familial melanoma

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Highly frequent homozygous deletion of the p16 gene in esophageal cancer cell lines

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

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Analysis of the p16 gene (CDKN2) as a candidate for the chromosome 9p melanoma susceptibility locus

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Functional and physical interactions of the ARF tumor suppressor with p53 and Mdm2

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Tumour-derived p16 alleles encoding proteins defective in cell-cycle inhibition

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Retinoblastoma-protein-dependent cell-cycle inhibition by the tumour suppressor p16

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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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p14ARF deletion and methylation in genetic pathways to glioblastomas.

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

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Hypermethylation in the retinoblastoma gene is associated with unilateral, sporadic retinoblastoma

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The Ink4a tumor suppressor gene product, p19Arf, interacts with MDM2 and neutralizes MDM2's inhibition of p53

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Alternative reading frames of the INK4a tumor suppressor gene encode two unrelated proteins capable of inducing cell cycle arrest

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Mutations associated with familial melanoma impair p16INK4 function.

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The human ARF cell cycle regulatory gene promoter is a CpG island which can be silenced by DNA methylation and down-regulated by wild-type p53.

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Infrequent methylation of CDKN2A(MTS1/p16) and rare mutation of both CDKN2A and CDKN2B(MTS2/p15) in primary astrocytic tumours

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

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

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The alternative product from the human CDKN2A locus, p14(ARF), participates in a regulatory feedback loop with p53 and MDM2.

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P19(ARF) stabilizes p53 by blocking nucleo-cytoplasmic shuttling of Mdm2

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Promoter hypermethylation and homozygous deletion of the p14ARF and p16INK4a genes in oligodendrogliomas.

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ARF promotes MDM2 degradation and stabilizes p53: ARF-INK4a locus deletion impairs both the Rb and p53 tumor suppression pathways

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7 January 2021

Identifiers

DOI

10.1038/SJ.ONC.1206031

1 reference

19 December 2017

PubMed ID

12447702

1 reference

19 December 2017