Memorial Sloan Kettering Cancer Center

Our hypothesis is that unraveling the genomic alterations of diffuse infiltrating pontine gliomas or DIPGs will lead to improved understanding of the biology of such tumors and improved therapeutic options.

Genomic alterations of diffuse infiltrating pontine gliomas (DIPGs) are understudied, as these tumors are not routinely resected or biopsied.   In contrast, the genomic alterations of adult gliomas have been analyzed extensively and these tumors harbor a large number of Copy Number Variations (CNVs) such as amplifications and deletions of oncogenes and tumor suppressor genes respectively, that drive gliomagenesis.  Evaluation for such alterations may reveal which signaling pathways drive the growth of DIPGs as well as allow us to unravel the heterogeneity of these tumors. In particular we have developed a mouse model for DIPGs by overexpressing the PDGF signaling pathway in progenitor cells that reside at the brainstem.  We would like to know if components of the PDGF pathway are amplified in the genomic level of DIPGs providing further validation for this DIPG mouse model.  Alternatively, we may determine that other CNVs drive DIPGs and so we can develop an improved mouse model.  Therefore we propose to use array CGH technology from Agilent to analyze the Copy Number Variations of DIPGs. 

We are currently collecting additional tumor tissue, so please ask your physician if tumor tissue is available (paraffin tissue or frozen tissue).  Analysis will commence pending funding.

Contact: 
Oren Becher, M.D
Memorial Sloan Kettering Cancer Center
1275 York Avenue
New York, NY 10065
Phone- 212-639-2152
Email- bechero@mskcc.org

Last update July 30, 2009