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Neuro-Oncology 2009 11(5):563-699; doi:10.1215/15228517-2009-034
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Copyright 2009 by the Society for Neuro-Oncology

Abstracts from the 2009 Joint Meeting of the Society for Neuro-Oncology (SNO) and the American Association of Neurological Surgeons/Congress of Neurological Surgeons (AANS/CNS) Section on Tumors

The first 150 words of the full text of this article appear below.


   CELL BIOLOGY/SIGNALING
 
1. JNK2ALPHA2 REGULATES GBM CELL SURVIVAL BY PHOSPHORYLATING BCL-2

Ryan Nitta; Albert J. Wong

INTRODUCTION: Activation of the JNK pathway has been implicated in glioblastoma multiforme (GBM). Expression and activity of a specific JNK isoform, JNK2{alpha}2, are increased in 86% of primary GBMs. Since we have shown JNK2{alpha}2 is constitutively active and induces glial tumor formation, we studied the connection between JNK2{alpha}2 and a proto-oncogene, BCL-2. BCL-2 was the first gene associated with regulating apoptosis and is important for GBM cell survival. The JNK family was shown to directly phosphorylate BCL-2 at Ser70, thereby regulating its antiapoptotic ability. Enhanced phosphorylation of Ser70 increased resistance to apoptosis and increased tumor formation. We hypothesized that JNK2{alpha}2-induced tumorigenesis may result from altered levels of BCL-2 Ser70 phosphorylation. METHODS: We used retrovirus to introduce shRNAs targeted to the JNK2{alpha} gene to reduce expression in two GBM cell lines, U87-MG and . . . [Full Text of this Article]


   EPIDEMIOLOGY
 

   EXPERIMENTAL THERAPEUTICS (PRECLINICAL)
 

   GENETICS/GENOMICS
 

   IMMUNOLOGY/IMMUNOTHERAPY
 

   MEDICAL ONCOLOGY
 

   MODELS (PRECLINICAL)
 

   NEUROCOGNITIVE
 

   PATHOLOGY/PROGNOSTIC MARKERS
 

   QUALITY OF LIFE/SYMPTOM MANAGEMENT
 

   RADIATION ONCOLOGY
 

   RADIOLOGY
 

   STEM CELLS
 

   SURGICAL ONCOLOGY
 

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