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The formation of human tumors is a complex process involving the accumulation of genetic lesions in genes that normally regulate cell proliferation, differentiation and cell death. For glioblastoma (GBM), the most frequent CNS tumor in adults, these genetic lesions occur in a relatively defined order and include loss of heterozygosity for chromosome 17p, mutation of the p53 gene, overexpression of the platelet derived growth factor receptor (PDGFA receptor), allelic losses of chromosome 22q, 13q (inclusive of the RB1 locus), and 19q, deletion of the interferon alpha and beta and INK4a and 4b loci on chromosome 9p, losses of heterozygosity for chromosome 10 for which the phosphatase and tensin (PTEN) homology gene, located at 10q23.3 is a frequent target, and gene amplification of EGFR. Data from many studies, including the recent Cancer Genome Atlas (TCGA) initiative of the NCI, show that both PTEN mutation and EGFR amplification are the most frequent of the genetic lesions found in GBMs. The focus of my research group is to investigate the role of these two genetic lesions in the genesis of GBM and how they cooperate to promote therapeutic resistance commonly associated with this tumor type.

Track(s):
Genetics
MCB

BMS Focus Areas:
Cancer Biology