Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway.
- Author:
Lun DONG
1
;
Pei-yu PU
;
Hu WANG
;
Guang-xiu WANG
;
Chun-sheng KANG
;
De-rang JIAO
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Aged; Astrocytoma; genetics; metabolism; pathology; Base Sequence; Brain Neoplasms; genetics; metabolism; pathology; DNA Mutational Analysis; Female; Gene Expression Regulation, Neoplastic; Glioblastoma; genetics; metabolism; pathology; Humans; Immunohistochemistry; Male; Middle Aged; Molecular Sequence Data; Mutation; Polymerase Chain Reaction; Polymorphism, Single-Stranded Conformational; RNA, Messenger; biosynthesis; genetics; Receptor, Epidermal Growth Factor; biosynthesis; genetics; Reverse Transcriptase Polymerase Chain Reaction; Tumor Suppressor Protein p53; biosynthesis; genetics
- From: Chinese Journal of Pathology 2006;35(4):232-236
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study further the most important and frequent genetic alterations of p53 and epidermal growth factor receptor (EGFR) in astrocytic gliomas.
METHODS(1) EGFR expression was examined in samples collected from 37 astrocytic gliomas and 6 normal brain tissue using reverse transcriptase polymerase chain reaction and immunohistochemical staining. (2) p53 gene mutation and accumulation were detected simultaneously in the same specimens using PCR-SSCP, DNA sequencing and immunohistochemical staining.
RESULTSThe frequency of p53 mutation in diffuse astrocytomas, anaplastic astrocytomas, primary glioblastomas and secondary glioblastomas was 1/10, 4/19 (21.1%), 4/6 and 2/2, respectively and the frequency of EGFR overexpression was 5/10, 10/19 (52.6%), 5/6 and 2/2, respectively. Both p53 accumulation and EGFR overexpression increased accompanied by a successive increase of degree of the glioma malignancy.
CONCLUSIONSEGFR overexpression is not infrequently seen, however, p53 mutation is rarely seen in the low grade gliomas. Both p53 gene mutation and EGFR overexpression are often associated with primary and secondary glioblastoma. Consequently, EGFR overexpression and p53 gene mutation are not mutually exclusive in astrocytic gliomagenesis but synergistically to promote the glioma progression.