PMID- 17202312
OWN - NLM
STAT- MEDLINE
DCOM- 20070424
LR  - 20070126
IS  - 1078-0432 (Print)
IS  - 1078-0432 (Linking)
VI  - 13
IP  - 2 Pt 1
DP  - 2007 Jan 15
TI  - Microarray-based identification of tenascin C and tenascin XB, genes possibly 
      involved in tumorigenesis associated with neurofibromatosis type 1.
PG  - 398-407
AB  - PURPOSE: Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder with a 
      complex variety of clinical manifestations. The hallmark of NF1 is the onset of 
      heterogeneous (dermal or plexiform) benign neurofibromas. Plexiform neurofibromas 
      can give rise to malignant peripheral nerve sheath tumors, which are resistant to 
      conventional therapies. EXPERIMENTAL DESIGN: To identify new signaling pathways 
      involved in the malignant transformation of plexiform neurofibromas, we applied a 
      22,000-oligonucleotide microarray approach to a series of plexiform neurofibromas 
      and malignant peripheral nerve sheath tumors. Changes in the expression of 
      selected genes were then confirmed by real-time quantitative reverse 
      transcription-PCR. RESULTS: We identified two tenascin gene family members that 
      were significantly deregulated in both human NF1-associated tumors and 
      NF1-deficient primary cells: Tenascin C (TNC) was up-regulated whereas tenascin 
      XB (TNXB) was down-regulated during tumor progression. TNC activation is mainly 
      due to the up-regulation of large TNC splice variants. Immunohistochemical 
      studies showed that TNC transcripts are translated into TNC protein in 
      TNC-overexpressing tumors. Aberrant transcriptional activation of TNC seems to be 
      principally mediated by activator protein transcription factor complexes. 
      CONCLUSION: TNXB and TNC may be involved in the malignant transformation of 
      plexiform neurofibromas. Anti-TNC antibodies, already used successfully in 
      clinical trials to treat malignant human gliomas, may be an appropriate new 
      therapeutic strategy for NF1.
FAU - Levy, Pascale
AU  - Levy P
AD  - Laboratoire de Genetique Moleculaire-Institut National de la Sante et de la 
      Recherche Medicale U745, Faculte des Sciences Pharmaceutiques et Biologiques, 
      Universite Paris V, 4 avenue de l'Observatoire, Paris, France.
FAU - Ripoche, Hugues
AU  - Ripoche H
FAU - Laurendeau, Ingrid
AU  - Laurendeau I
FAU - Lazar, Vladimir
AU  - Lazar V
FAU - Ortonne, Nicolas
AU  - Ortonne N
FAU - Parfait, Beatrice
AU  - Parfait B
FAU - Leroy, Karen
AU  - Leroy K
FAU - Wechsler, Janine
AU  - Wechsler J
FAU - Salmon, Isabelle
AU  - Salmon I
FAU - Wolkenstein, Pierre
AU  - Wolkenstein P
FAU - Dessen, Philippe
AU  - Dessen P
FAU - Vidaud, Michel
AU  - Vidaud M
FAU - Vidaud, Dominique
AU  - Vidaud D
FAU - Bieche, Ivan
AU  - Bieche I
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070103
PL  - United States
TA  - Clin Cancer Res
JT  - Clinical cancer research : an official journal of the American Association for 
      Cancer Research
JID - 9502500
RN  - 0 (Tenascin)
RN  - 0 (tenascin X)
SB  - IM
MH  - Alternative Splicing
MH  - Cell Differentiation
MH  - Cluster Analysis
MH  - Fibroblasts/metabolism
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Neurofibromatosis 1/*genetics/*pathology
MH  - Oligonucleotide Array Sequence Analysis/*methods
MH  - Signal Transduction
MH  - Tenascin/*biosynthesis
MH  - Treatment Outcome
EDAT- 2007/01/05 09:00
MHDA- 2007/04/25 09:00
CRDT- 2007/01/05 09:00
PHST- 2007/01/05 09:00 [pubmed]
PHST- 2007/04/25 09:00 [medline]
PHST- 2007/01/05 09:00 [entrez]
AID - 1078-0432.CCR-06-0182 [pii]
AID - 10.1158/1078-0432.CCR-06-0182 [doi]
PST - ppublish
SO  - Clin Cancer Res. 2007 Jan 15;13(2 Pt 1):398-407. doi: 
      10.1158/1078-0432.CCR-06-0182. Epub 2007 Jan 3.