PMID- 21298772
OWN - NLM
STAT- MEDLINE
DCOM- 20120103
LR  - 20151119
IS  - 1545-5017 (Electronic)
IS  - 1545-5009 (Linking)
VI  - 57
IP  - 7
DP  - 2011 Dec 15
TI  - Shared molecular targets in pediatric gliomas and ependymomas.
PG  - 1117-23
LID - 10.1002/pbc.23009 [doi]
AB  - BACKGROUND: Recent advances in multidisciplinary treatment approaches have 
      improved the overall prognosis of pediatric brain tumors, but some patients 
      remain refractory to treatment and do poorly. Several molecularly targeted 
      therapies are under development for the treatment of brain tumors, and high-grade 
      gliomas in adults are a particular area of study. PROCEDURE: To better understand 
      if these new therapies can be used in pediatric populations, we examined the 
      expression of the following seven marker genes involved in signaling pathways 
      targeted by new therapies: beta-catenin, suppressor of fused (SUFU), erythroblastic 
      leukemia viral oncogene homolog (ERBB) 2, platelet-derived growth factor 
      receptoralpha (PDGFRalpha), proliferating cell nuclear antigen (PCNA), secreted protein 
      acid and rich in cysteine (SPARC), and granulocyte colony-stimulating factor 
      receptor (G-CSFR). Samples from 27 patients with the primitive neuroectodermal 
      tumor (PNET)/medulloblastomas (MBs) (n = 8), ependymomas (n = 5), or gliomas (n = 
      14) were assessed by quantitative real-time PCR. [Correction made here after 
      initial online publication]. We assigned an EXP score to compare across samples 
      and determined the levels of gene expression among tumor cell types. RESULTS: 
      Gene expression varied among the different tumors, but, within a tumor type, 
      clear expression patterns were seen. The expression of SUFU, ERBB2, and PCNA in 
      metastatic MBs were greater than that seen in non-metastatic MBs. Most glioma 
      cases highly expressed PDGFRalpha and G-CSFR. Additionally, the expression patterns 
      of gliomas and ependymomas were similar (r = 0.77, P = 0.04), but PNET/MBs 
      substantially differed from gliomas (r = -0.37, P = 0.41) or ependymomas (r = 
      0.23, P = 0.62). CONCLUSIONS: The development of new drugs targeting up-regulated 
      pathways may be useful for the treatment of pediatric brain tumors. As new drugs 
      are developed, gliomas and ependymomas may be treated with similar compounds.
CI  - Copyright (c) 2011 Wiley Periodicals, Inc.
FAU - Tsuruta, Toshihisa
AU  - Tsuruta T
AD  - Department of Clinical Examination, National Hospital Organization Kumamoto 
      Medical Center, Kumamoto, Japan. ttsuruta@kumamoto2.hosp.go.jp
FAU - Aihara, Yasuo
AU  - Aihara Y
FAU - Kanno, Hitoshi
AU  - Kanno H
FAU - Funase, Masakazu
AU  - Funase M
FAU - Murayama, Toshihiko
AU  - Murayama T
FAU - Osawa, Makiko
AU  - Osawa M
FAU - Fujii, Hisaichi
AU  - Fujii H
FAU - Kubo, Osami
AU  - Kubo O
FAU - Okada, Yoshikazu
AU  - Okada Y
LA  - eng
PT  - Journal Article
DEP - 20110204
PL  - United States
TA  - Pediatr Blood Cancer
JT  - Pediatric blood & cancer
JID - 101186624
RN  - 0 (Biomarkers, Tumor)
SB  - IM
MH  - Biomarkers, Tumor/*genetics
MH  - Brain Neoplasms/*genetics/metabolism/pathology
MH  - Child
MH  - Ependymoma/*genetics/metabolism/pathology
MH  - Female
MH  - Gene Expression
MH  - Gene Expression Profiling
MH  - Glioma/*genetics/metabolism/pathology
MH  - Humans
MH  - Immunohistochemistry
MH  - Male
MH  - Real-Time Polymerase Chain Reaction
MH  - Signal Transduction/*physiology
EDAT- 2011/02/08 06:00
MHDA- 2012/01/04 06:00
CRDT- 2011/02/08 06:00
PHST- 2010/10/04 00:00 [received]
PHST- 2010/12/08 00:00 [accepted]
PHST- 2011/02/08 06:00 [entrez]
PHST- 2011/02/08 06:00 [pubmed]
PHST- 2012/01/04 06:00 [medline]
AID - 10.1002/pbc.23009 [doi]
PST - ppublish
SO  - Pediatr Blood Cancer. 2011 Dec 15;57(7):1117-23. doi: 10.1002/pbc.23009. Epub 
      2011 Feb 4.