PMID- 21143702
OWN - NLM
STAT- MEDLINE
DCOM- 20110311
LR  - 20210102
IS  - 1349-7006 (Electronic)
IS  - 1347-9032 (Linking)
VI  - 102
IP  - 2
DP  - 2011 Feb
TI  - Expression of nuclear receptor corepressors and class I histone deacetylases in 
      astrocytic gliomas.
PG  - 387-92
LID - 10.1111/j.1349-7006.2010.01792.x [doi]
AB  - Transcriptional repressors such as nuclear receptor corepressors (NCORs) and 
      class I histone deacetylases (HDACs) are considered potential therapeutic targets 
      in various human malignancies. In astrocytic gliomas, however, there is still a 
      need to understand the role of these transcriptional repressors in tumor 
      proliferation, tumor differentiation, and patient survival. We 
      immunohistochemically analyzed the expression of NCOR1 and 2 as well as HDAC1, 2, 
      and 3 on a tissue microarray comprising tumor samples from 283 astrocytic gliomas 
      and correlated the expression levels with tumor differentiation, tumor 
      proliferation, and patient survival. Strong nuclear expression was found in 
      glioma cells for HDAC1, HDAC2, and NCOR2. In contrast, weak expression of NCOR1 
      and HDAC3 was detected in the cytoplasm and nuclei of tumor cells. HDAC3 
      expression was inversely associated with tumor grade. Consequently, increased 
      HDAC3 expression was associated with better patient survival in univariate 
      regression. Expression of HDAC1 and HDAC2 increased during tumor recurrence and 
      malignant tumor progression, respectively, whereas expression of the remaining 
      antigens did not seem to depend on tumor grade and was comparable to expression 
      levels found in non-neoplastic brain tissues. Finally, we detected a positive 
      association between HDAC2 expression and tumor proliferation as well as between 
      NCOR1 and expression of the stem cell-associated intermediate filament protein 
      nestin. Our findings suggest that "classical" transcriptional repressors are 
      expressed in astrocytic tumors and that the roles of HDAC2 and HDAC3 in these 
      tumors deserve further investigation.
CI  - (c) 2010 Japanese Cancer Association.
FAU - Campos, Benito
AU  - Campos B
AD  - Division of Neurosurgical Research, Department of Neurosurgery, University of 
      Heidelberg, Heidelberg, Germany.
FAU - Bermejo, Justo Lorenzo
AU  - Bermejo JL
FAU - Han, Lin
AU  - Han L
FAU - Felsberg, Jorg
AU  - Felsberg J
FAU - Ahmadi, Rezvan
AU  - Ahmadi R
FAU - Grabe, Niels
AU  - Grabe N
FAU - Reifenberger, Guido
AU  - Reifenberger G
FAU - Unterberg, Andreas
AU  - Unterberg A
FAU - Herold-Mende, Christel
AU  - Herold-Mende C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20101210
PL  - England
TA  - Cancer Sci
JT  - Cancer science
JID - 101168776
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Co-Repressor Proteins)
RN  - 0 (NCOR1 protein, human)
RN  - 0 (NCOR2 protein, human)
RN  - 0 (Nuclear Receptor Co-Repressor 1)
RN  - 0 (Nuclear Receptor Co-Repressor 2)
RN  - EC 3.5.1.98 (HDAC1 protein, human)
RN  - EC 3.5.1.98 (Histone Deacetylase 1)
RN  - EC 3.5.1.98 (Histone Deacetylase 2)
RN  - EC 3.5.1.98 (Histone Deacetylases)
RN  - EC 3.5.1.98 (histone deacetylase 3)
SB  - IM
MH  - Adult
MH  - Astrocytoma/*metabolism/pathology
MH  - Biomarkers, Tumor/*analysis
MH  - Brain Neoplasms/*metabolism/pathology
MH  - Co-Repressor Proteins/*biosynthesis
MH  - Female
MH  - Histone Deacetylase 1/biosynthesis
MH  - Histone Deacetylase 2/biosynthesis
MH  - Histone Deacetylases/*biosynthesis
MH  - Humans
MH  - Immunohistochemistry
MH  - Male
MH  - Middle Aged
MH  - Nuclear Receptor Co-Repressor 1/biosynthesis
MH  - Nuclear Receptor Co-Repressor 2/biosynthesis
MH  - Tissue Array Analysis
EDAT- 2010/12/15 06:00
MHDA- 2011/03/12 06:00
CRDT- 2010/12/15 06:00
PHST- 2010/12/15 06:00 [entrez]
PHST- 2010/12/15 06:00 [pubmed]
PHST- 2011/03/12 06:00 [medline]
AID - 10.1111/j.1349-7006.2010.01792.x [doi]
PST - ppublish
SO  - Cancer Sci. 2011 Feb;102(2):387-92. doi: 10.1111/j.1349-7006.2010.01792.x. Epub 
      2010 Dec 10.