CDK4 Amplification Is an Alternative Mechanism to p16 Gene Homozygous Deletion in Glioma Cell Lines

Ju He, James R. Allen, C. David James, V. Peter Collins, M. Joan Allalunis-Turner, Roseline Godbout, Rufus S. Day

Research output: Contribution to journalArticlepeer-review

245 Scopus citations

Abstract

Recently, it has been shown that a gene encoding the cyclin-dependent kinase 4 inhibitory protein, p16, is frequently targeted for homozygous deletions in several types of tumor cell lines, including those established from malignant gliomas. Here we have examined 32 glioma cell lines for amplification-associated overexpression of the CDK4 gene as an alternative mechanism for abrogating the growth-regulatory effects of pl6. Two of the cell lines revealed high-level expression of CDK4 in association with gene amplification, and this alteration was observed among the 10 cases having intact p16 genes. Consequently, 24 of 32 glioma cell lines revealed one of two alternative genetic alterations, each of which indicates that increased cdk4 kinase activity is important to glial tumor development.

Original languageEnglish (US)
Pages (from-to)5804-5807
Number of pages4
JournalCancer Research
Volume54
Issue number22
StatePublished - Jul 1 1994

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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