A Network Model of a Cooperative Genetic Landscape in Brain Tumors

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Abstract
Malignant gliomas, with disproportionately high morbidity and mortality,1 are among the most devastating of human tumors. Particular genomic alterations are fundamental to both their formation and their malignant progression.2,3 Although genomic instability (Box) lends a dynamic character to the human glioma genome, gliomas harbor recurrent chromosomal alterations (Box).2,4,5 Chromosomal alterations presumably exert their tumor-promoting effect on glioma cells by modifying the expression or function of distinct genes, which map to those alterations,6 so as to deregulate growth factor signaling and survival pathways. For many chromosomal alterations, the biologically relevant target genes remain to be discovered.