PMID- 27553586
OWN - NLM
STAT- MEDLINE
DCOM- 20170314
LR  - 20181202
IS  - 1423-0291 (Electronic)
IS  - 1015-2008 (Linking)
VI  - 84
IP  - 2
DP  - 2017
TI  - Multicentric Glioma Develops via a Mutant IDH1-Independent Pathway: 
      Immunohistochemical Study of Multicentric Glioma.
PG  - 99-107
LID - 10.1159/000447951 [doi]
AB  - Multicentric gliomas are very rare. Due to differences in their tumor types they 
      remain enigmatic. We focused on the pathogenesis of multicentric gliomas and 
      compared their immunoprofile with that of solitary gliomas. This retrospective 
      study included 6 males and 8 females with multicentric glioma (8 glioblastomas, 2 
      anaplastic astrocytomas, 4 diffuse astrocytomas). Their age ranged from 27 to 75 
      years and all were treated between 2004 and June 2015. The expression of mutant 
      isocitrate dehydrogenase 1 (IDH1), alpha-thalassemia X-linked intellectual disability 
      (ATRX), p53, phosphatase and tensin homolog (PTEN), and epidermal growth factor 
      receptor (EGFR) was examined immunohistochemically; for 1p19q analysis we used 
      fluorescence in situ hybridization (FISH). In all patients, immunohistochemical 
      staining was negative for mutant IDH1 and cytoplasmic PTEN; only 1 patient (7.1%) 
      manifested nuclear PTEN positivity. FISH for 1p19q codeletion was negative in all 
      9 examined samples; 5 of 14 specimens (35.7%) were p53-positive, 9 (64.3%) were 
      EGFR-positive, and 4 (28.6%) were ATRX-negative. The MIB-1 labeling index was 
      0.9-15.6% for grades II and III, and ranged between 17.3 and 52.4% for 
      glioblastoma. Our results suggest that the pathogenesis of multicentric gliomas 
      is different from the mutant IDH1-R132H pathogenesis of lower-grade glioma and 
      secondary glioblastomas. More studies are needed to confirm the molecular 
      mechanisms underlying the pathogenesis of multicentric glioma.
CI  - (c) 2016 S. Karger AG, Basel.
FAU - Karlowee, Vega
AU  - Karlowee V
AD  - Department of Neurosurgery, Graduate School of Biomedical and Health Sciences, 
      Hiroshima University, Hiroshima, Japan.
FAU - Amatya, Vishwa Jeet
AU  - Amatya VJ
FAU - Hirano, Hirofumi
AU  - Hirano H
FAU - Takayasu, Takeshi
AU  - Takayasu T
FAU - Nosaka, Ryo
AU  - Nosaka R
FAU - Kolakshyapati, Manish
AU  - Kolakshyapati M
FAU - Yoshihiro, Masako
AU  - Yoshihiro M
FAU - Takeshima, Yukio
AU  - Takeshima Y
FAU - Sugiyama, Kazuhiko
AU  - Sugiyama K
FAU - Arita, Kazunori
AU  - Arita K
FAU - Kurisu, Kaoru
AU  - Kurisu K
FAU - Yamasaki, Fumiyuki
AU  - Yamasaki F
LA  - eng
PT  - Journal Article
DEP - 20160824
PL  - Switzerland
TA  - Pathobiology
JT  - Pathobiology : journal of immunopathology, molecular and cellular biology
JID - 9007504
RN  - 0 (Nuclear Proteins)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - EC 1.1.1.41 (Isocitrate Dehydrogenase)
RN  - EC 1.1.1.42. (IDH1 protein, human)
RN  - EC 2.7.10.1 (EGFR protein, human)
RN  - EC 2.7.10.1 (ErbB Receptors)
RN  - EC 3.1.3.67 (PTEN Phosphohydrolase)
RN  - EC 3.6.4.- (DNA Helicases)
RN  - EC 3.6.4.12 (ATRX protein, human)
RN  - EC 3.6.4.12 (X-linked Nuclear Protein)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Astrocytoma/*metabolism/pathology
MH  - Brain Neoplasms/*metabolism/pathology
MH  - DNA Helicases/metabolism
MH  - ErbB Receptors/metabolism
MH  - Female
MH  - Glioblastoma/*metabolism/pathology
MH  - Humans
MH  - Immunohistochemistry
MH  - Isocitrate Dehydrogenase/*metabolism
MH  - Male
MH  - Middle Aged
MH  - Nuclear Proteins/metabolism
MH  - PTEN Phosphohydrolase/metabolism
MH  - Tumor Suppressor Protein p53/metabolism
MH  - X-linked Nuclear Protein
EDAT- 2016/08/25 06:00
MHDA- 2017/03/16 06:00
CRDT- 2016/08/25 06:00
PHST- 2016/02/24 00:00 [received]
PHST- 2016/06/22 00:00 [accepted]
PHST- 2016/08/25 06:00 [pubmed]
PHST- 2017/03/16 06:00 [medline]
PHST- 2016/08/25 06:00 [entrez]
AID - 000447951 [pii]
AID - 10.1159/000447951 [doi]
PST - ppublish
SO  - Pathobiology. 2017;84(2):99-107. doi: 10.1159/000447951. Epub 2016 Aug 24.