Journal
MOLECULAR SYSTEMS BIOLOGY
Volume 4, Issue -, Pages -Publisher
WILEY
DOI: 10.1038/msb.2008.2
Keywords
B-cell lymphoma; drug mechanism-of-action (MOA); gene network; interactome; oncogene
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Funding
- NCI NIH HHS [R01 CA109755, R01CA109755, U54CA121852, U54 CA121852] Funding Source: Medline
- NIAID NIH HHS [R01 AI066116, R01AI066116] Funding Source: Medline
- NLM NIH HHS [5 T15 LM007079-15, T15 LM007079] Funding Source: Medline
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The computational identification of oncogenic lesions is still a key open problem in cancer biology. Although several methods have been proposed, they fail to model how such events are mediated by the network of molecular interactions in the cell. In this paper, we introduce a systems biology approach, based on the analysis of molecular interactions that become dysregulated in specific tumor phenotypes. Such a strategy provides important insights into tumorigenesis, effectively extending and complementing existing methods. Furthermore, we show that the same approach is highly effective in identifying the targets of molecular perturbations in a human cellular context, a task virtually unaddressed by existing computational methods. To identify interactions that are dysregulated in three distinct non-Hodgkin's lymphomas and in samples perturbed with CD40 ligand, we use the B-cell interactome (BCI), a genome-wide compendium of human B-cell molecular interactions, in combination with a large set of microarray expression profiles. The method consistently ranked the known gene in the top 20 (0.3%), outperforming conventional approaches in 3 of 4 cases.
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