title: Correlation of chromosomal imbalances by comparative genomic hybridization and expression of EGFR, PTEN, p53, and MIB-1 in diffuse gliomas.
abstract: The histological subclassification of gliomas is increasingly assisted by the underlying molecular genetics which has major importance in guiding clinical management of the disease. However, the assessment of several molecular events for improving clinical care remains a challenge. Herein, we report on comparative genomic hybridization (CGH) and immunohistochemical (IHC) assessment of EGFR, PTEN, p53, and MIB-1 expression in 13 oligodendrogliomas (10 WHO grade II, 3 WHO grade III), one oligoastrocytoma (WHO grade III) and 23 high-grade astrocytomas (3 WHO grade III, 20 glioblastoma multiforme). The most frequent imbalances in oligodendroglial tumors including the oligoastrocytic case were, in decreasing order of frequency, +7q, -1p, and -4q and in astrocytomas +7q, -10q, +7p, -9p, -10p, +20q, and +20p. Some individual imbalances were associated with increasing numbers of chromosomal changes, that were +7q in both oligodendrogliomas and astrocytomas, and -9p, -10q, +20p, and +20q in astrocytomas. The markers p53 and MIB-1 were significantly higher expressed in astrocytomas than in oligodendrogliomas and expression levels of p53 and EGFR were inversely associated within the astrocytic group. In addition, p53 overexpression correlated positively with +7q and negatively with -1p in the oligodendroglial group whereas EGFR overexpression correlated positively with -1p in the oligodendroglial and positively with +7p and -10p in the astrocytic group. Short overall survival was significantly associated with +7p and -10q in astrocytomas. Collectively, these results contribute to the increasing clinical relevance of assessing tumor biological markers in gliomas.
authors: Medical Genetics Department, Faculty of Medicine, Uludag University, 16059 Bursa, Turkey. tyakut@uludag.edu.tr
authors: Tahsin
authors: T
authors: Yakut
authors: Angelika
authors: A
authors: Gutenberg
authors: Ahmet
authors: A
authors: Bekar
authors: Unal
authors: U
authors: Egeli
authors: Bastian
authors: B
authors: Gunawan
authors: Ilker
authors: I
authors: Ercan
authors: Sahsene
authors: S
authors: Tolunay
authors: Muammer
authors: M
authors: Doygun
authors: Hans-Jurgen
authors: HJ
authors: Schulten
mesh_terms: D000328:Adult; D000368:Aged; D002648:Child; D002675:Child, Preschool; D002869:Chromosome Aberrations; D066246:ErbB Receptors / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D005910:Glioma / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D008297:Male; D008875:Middle Aged; D009693:Nucleic Acid Hybridization / Q000379:methods; D051059:PTEN Phosphohydrolase / Q000096:biosynthesis* / Q000235:genetics; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis* / Q000235:genetics; D044767:Ubiquitin-Protein Ligases / Q000096:biosynthesis* / Q000235:genetics
chemical_list: D016159:Tumor Suppressor Protein p53; C513496:MIB1 ligase, human; D044767:Ubiquitin-Protein Ligases; C512478:EGFR protein, human; D066246:ErbB Receptors; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human