title: Higher pAkt expression predicts a significant worse prognosis in glioblastomas.
abstract: phosphorylated-Akt (pAkt) plays an important role in tumorigenesis through promotion of cell survival by inhibiting apoptosis and mediating cell proliferation. Higher expression of pAkt has been reported to be associated with an unfavorable prognosis in several malignant tumors. In this study, the prognostic value of pAkt expression was investigated in glioblastomas by using immunohistochemical methods. Tissue sections obtained from 64 patients with glioblastoma were evaluated. The mean and median follow-up period was 16.2 +/- 12.4 and 12 months, respectively (range: from 1 to 62 months). pAkt expression levels were determined by immunohistochemical staining and evaluated for cell positivity. Positive staining was defined when more than 50% of the tumor cells were stained in each section. The correlation between expression of pAkt and overall survival rate was assessed. Glioblastomas showed either or both cytoplasmic and nuclear positive findings for pAkt. A total of 29.7% (19/64) of tissue specimens had greater than 50% positivity. The median survival periods of the patients with pAkt positive and negative tumor were 10 and 14 months, respectively. Two years overall survival rate of the pAkt positive and negative patients were 0% and 24.4%, respectively. Survival rate of the patients with pAkt positive tumor was significantly lower than that of the patients with pAkt negative tumors (p = 0.004). Multivariate analysis showed that extent of surgery was the strongest factor for survival (p = 0.01) and the pAkt expression was the secondly strongest factor (p = 0.06). These results suggest that the higher expression of pAkt the poorer prognosis in patients with glioblastoma.
authors.affiliation: Department of Radiation Oncology, Gunma University Graduate School of Medicine, Maebashi 371-8511, Japan. syoshi@med.gunma-u.ac.jp
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Shirai
authors.forename: Kuniyuki
authors.initials: K
authors.lastname: Oka
authors.forename: Abdulelah
authors.initials: A
authors.lastname: Mobaraki
authors.forename: Yukari
authors.initials: Y
authors.lastname: Yoshida
authors.forename: Shin-ei
authors.initials: SE
authors.lastname: Noda
authors.forename: Masahiko
authors.initials: M
authors.lastname: Okamoto
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Jun
authors.initials: J
authors.lastname: Itoh
authors.forename: Hideaki
authors.initials: H
authors.lastname: Itoh
authors.forename: Shogo
authors.initials: S
authors.lastname: Ishiuchi
authors.forename: Takashi
authors.initials: T
authors.lastname: Nakano
mesh_terms: D000368:Aged; D017209:Apoptosis; D001932:Brain Neoplasms / Q000175:diagnosis* / Q000378:metabolism*; D002470:Cell Survival; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D005909:Glioblastoma / Q000175:diagnosis* / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010766:Phosphorylation; D011379:Prognosis; D051057:Proto-Oncogene Proteins c-akt / Q000096:biosynthesis*; D016896:Treatment Outcome
chemical_list: D051057:Proto-Oncogene Proteins c-akt