No ING1 mutations in human brain tumours but reduced expression in high malignancy grades of astrocytoma
✍ Scribed by Gesche Tallen; Ines Kaiser; Sonja Krabbe; Ulrike Lass; Christian Hartmann; Günter Henze; Karl Riabowol; Andreas von Deimling
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- French
- Weight
- 102 KB
- Volume
- 109
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
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 p33^ING1b^ 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 p47^ING1a^, p33^ING1b^ and p24^ING1c^ 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. © 2004 Wiley‐Liss, Inc.