REMBRANDT Project
The REpository of Molecular BRAin Neoplasia DaTa (REMBRANDT) project, run by the Glioma Molecular Diagnosis Initiative, is focused on uncovering the underlying causes of glioblastoma multiforme (GBM) cancer. More specifically, the REMBRANDT project seeks to characterize a large number of adult and pediatric primary brain tumors and identify biomarkers by correlating molecular data with extensive retrospective and prospective clinical data.
REMBRANDT provides a bioinformatics framework and Web portal that allows researchers to integrate clinical and functional genomics data from clinical trials involving patients suffering from Gliomas. The portal is enabled by caIntegrator and leverages the caBIG® Clinical Genomics Object Model (CGOM) to provide Web-based and programmatic access to the data.
REMBRANDT currently houses two sets of data:
- The first comes from the NCI-sponsored Glioma Molecular Diagnostic Initiative, the largest genetic/clinical corollary study ever conducted on Gliomas
- The second comprises a wide array of molecular and genetic data regarding all types of primary brain tumors
Researchers can query across these data sets and identify relationships between gene expression and clinical outcomes. The program has collected data from more than 550 patients as of 2009. Almost 1300 researchers from more than 500 organizations have registered for access to the data.
In 2009, caBIG® community members published a paper profiling REMBRANDT in the peer-reviewed journal Molecular Cancer Research. It explains how: 1) Access to large sample sets and inconsistent collection and annotation methods can be barriers to productive research; and 2) caBIG® addresses these challenges by allowing the easy integration, redistribution, and analysis of data within and across functional domains.
- Additional recent publications making use of the data from REMBRANDT include:
- Madhavan S, Zenklusen JC, Kotliarov Y, Sahni H, Fine HA, Buetow K. Rembrandt: helping personalized medicine become a reality through integrative translational research. Mol Cancer Res. 2009 Feb;7(2):157-67. Epub 2009 Feb 10.
- Schmidt N, Windmann S, Reifenberger G, Riemenschneider MJ. DNA hypermethylation and histone modifications downregulate the candidate tumor suppressor gene RRP22 on 22q12 in human gliomas. Brain Pathol. 2011 Jun 2. doi: 10.1111/j.1750-3639.2011.00507.x. [Epub ahead of print]
- Cogdell D, Chung W, Liu Y, McDonald JM, Aldape K, Issa JP, Fuller GN, Zhang W. Tumor-associated methylation of the putative tumor suppressor AJAP1 gene and association between decreased AJAP1 expression and shorter survival in patients with glioma. Chin J Cancer. 2011 Apr;30(4):247-53.
- Beckner ME, Fellows-Mayle W, Zhang Z, Agostino NR, Kant JA, Day BW, Pollack IF.Identification of ATP citrate lyase as a positive regulator of glycolytic function in glioblastomas.Int J Cancer. 2010 May 15;126(10):2282-95.
View the REMBRANDT Data Portal for access to clinical and functional genomics data from clinical trials of patients with Glioblastoma multiforme.
Read the REMBRANDT paper caBIG® community members published in Molecular Cancer Research.
