Premium
No ING1 mutations in human brain tumours but reduced expression in high malignancy grades of astrocytoma
Author(s) -
Tallen Gesche,
Kaiser Ines,
Krabbe Sonja,
Lass Ulrike,
Hartmann Christian,
Henze Günter,
Riabowol Karl,
von Deimling Andreas
Publication year - 2004
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.11715
Subject(s) - astrocytoma , malignancy , pathology , medicine , cancer research , oncology , biology , glioma
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.