title: Amplification and overexpression of epidermal growth factor receptor gene in glioblastomas of Chinese patients correlates with patient's age but not with tumor's clinicopathological pathway.
abstract: It is believed that there are two distinct pathological pathways leading to the development of human glioblastomas (GBM) in Caucasian populations. Primary (de novo) GBM most often occurs in older individuals, and is characterized by the overexpression/amplification of epidermal growth factor receptor gene (EGFR), whereas secondary GBM, which progresses from a low-grade astrocytoma, often affects younger individuals and frequently contains the TP53 mutation. We and others have previously found that the age of onset of GBM in Chinese patients tends to be younger than that in Caucasian patients. To identify whether GBMs from Chinese patients share this common pattern of genetic alterations, expression levels of EGFR and TP53 and TP53 mutation were analyzed in 56 randomly selected Chinese GBMs (30 primary and 26 secondary), including 47 adult-onset and 9 pediatric GBMs. Consistent with other studies, overexpression/mutation of TP53 and aneuploid DNA content were more frequently detected in secondary GBMs of Chinese adult patients. In contrast to that observed in Caucasian patients, no significant difference was observed in the age distribution and the frequency of EGFR overexpression/amplification between primary and secondary GBMs in adult Chinese patients. Furthermore, the overexpression of EGFR was much higher in late-onset (age >45 years) GBMs (73%) than that in both early-onset (age 18-45 years) (17%) and pediatric (age <18 years) GBMs (11%), suggesting that overexpression of EGFR in Chinese GBMs may be associated closely with the patients age but not with the tumors' pathological pathway.
authors.affiliation: State Key Laboratory of Oncology in Southern China, Cancer Center, Sun Yat-Sen University, Guangzhou, China.
authors.forename: Dan
authors.initials: D
authors.lastname: Xie
authors.forename: Yi Xin
authors.initials: YX
authors.lastname: Zeng
authors.forename: Hai Jun
authors.initials: HJ
authors.lastname: Wang
authors.forename: Lai Shan
authors.initials: LS
authors.lastname: Tai
authors.forename: Jian Ming
authors.initials: JM
authors.lastname: Wen
authors.forename: Yu
authors.initials: Y
authors.lastname: Tao
authors.forename: Ning Fang
authors.initials: NF
authors.lastname: Ma
authors.forename: Liang
authors.initials: L
authors.lastname: Hu
authors.forename: Jonathan S T
authors.initials: JS
authors.lastname: Sham
authors.forename: Xin Yuan
authors.initials: XY
authors.lastname: Guan
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000375:Aging / Q000235:genetics*; D044466:Asian People / Q000235:genetics; D001932:Brain Neoplasms / Q000737:chemistry / Q000235:genetics* / Q000503:physiopathology; D002648:Child; D002681:China; D004273:DNA, Neoplasm / Q000032:analysis / Q000235:genetics; D066246:ErbB Receptors / Q000032:analysis / Q000235:genetics*; D005260:Female; D005784:Gene Amplification; D015972:Gene Expression Regulation, Neoplastic; D016158:Genes, p53; D005909:Glioblastoma / Q000737:chemistry / Q000235:genetics* / Q000503:physiopathology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009154:Mutation; D011003:Ploidies; D016159:Tumor Suppressor Protein p53 / Q000032:analysis / Q000235:genetics / Q000502:physiology; D044465:White People / Q000235:genetics
chemical_list: D004273:DNA, Neoplasm; D016159:Tumor Suppressor Protein p53; D066246:ErbB Receptors