No ING1 mutations in human brain tumours but reduced expression in high malignancy grades of astrocytoma

Int J Cancer. 2004 Apr 10;109(3):476-9. doi: 10.1002/ijc.11715.

Abstract

The ING1 family of proteins has been shown to have regulatory functions in oncogenesis, apoptosis, DNA repair and cell cycle regulation. Here we present the first report on LOH analysis of the ING1 locus, mutation analysis of the complete coding sequence including intron-exon boundaries and expression analysis of the different ING1 splice products and protein isoforms in primary brain tumours. No somatic ING1 mutations were detected. Semi-quantitative analysis revealed higher levels of p33ING1b RNA in benign than in malignant lesions. This correlation was significant in a subset of 37 astrocytic tumours WHO grades I to IV. ING1 protein isoforms p47ING1a, p33ING1b and p24ING1c were found to be expressed variably in this series. Our findings support a regulatory contribution of ING1 to the development or progression of brain tumours.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Astrocytoma / genetics*
  • Brain Neoplasms / genetics*
  • Cell Cycle Proteins
  • DNA, Neoplasm / genetics
  • DNA-Binding Proteins
  • Down-Regulation*
  • Exons
  • Gene Expression Regulation, Neoplastic
  • Genes, Tumor Suppressor
  • Humans
  • Inhibitor of Growth Protein 1
  • Intracellular Signaling Peptides and Proteins
  • Introns
  • Loss of Heterozygosity
  • Mutation*
  • Neoplasm Staging
  • Nuclear Proteins
  • Protein Isoforms
  • Proteins / genetics*
  • Proteins / metabolism
  • RNA, Messenger / genetics
  • RNA, Neoplasm / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Suppressor Proteins

Substances

  • Cell Cycle Proteins
  • DNA, Neoplasm
  • DNA-Binding Proteins
  • ING1 protein, human
  • Inhibitor of Growth Protein 1
  • Intracellular Signaling Peptides and Proteins
  • Nuclear Proteins
  • Protein Isoforms
  • Proteins
  • RNA, Messenger
  • RNA, Neoplasm
  • Tumor Suppressor Proteins