The Cancer Genome Atlas (TCGA), a project to catalogue genetic mutations in cancer, reported the new findings about genetic abnormalities that drive glioblastoma multiforme (GBM). In the U.S., about 23,000 new cases of GBM are expected in 2013, and most patients die within 15 months of diagnosis. As a result of this study, the research team at team at TCGA, with more than 100 scientists from 14 institutions, specifically targeted the disease as part of their overarching project to create a genetic roadmap of cancer. This five-year scientific and clinical sojourn, which was recently detailed in the October 10th edition of Cell, provides the most complete genetic profiles of glioblastoma multiforme to date.
Lynda Chin, M.D., professor and chair of Genomic Medicine and scientific director of the Institute for Applied Cancer Science at The University of Texas MD Anderson Cancer Center, helps put the findings in context, commenting: “The first paper in 2008 characterized glioblastoma in important new ways and illuminated the path for all TCGA organ studies that have followed. Information generated by this unbiased, data-driven analysis presents new opportunities to discover genomics-based biomarkers, understand disease mechanisms and generate new hypotheses to develop better, targeted therapies.”
The Cell paper outlines an analysis of tumor samples and molecular data from 599 patients at 17 study sites, all of which provides a wealth of new findings. The new information included in the TCGA report includes a comprehensive array of data and information on genetic mutations, deletions, amplifications; gene expression and epigenetic regulation; structural changes due to chromosomal alterations, proteomic effects and molecular networks that enhance GBM progression — all of which will prove vital to developing new treatment modalities and, someday, a potential cure for the disease.
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Researchers confirmed mutated genes discovered before — such as the tumor suppressors TP53, PTEN and RB1, and the oncogene PIK3CA — and also identified 61 new mutated genes. Common amplification events were found at the epidermal growth factor receptor (EGFR) on chromosome 7. The EGFR gene was mutated in 57% of tumors and increased EGFR protein levels were observed in GBM cells.
Roeland Verhaak, Ph.D., assistant professor of Bioinformatics and Computational Biology at MD Anderson, and other researchers have begun to classify GBM tumors by gene expression and subgroups. Understanding the subgroups could establish biomarkers to guide treatment and identify new therapeutic targets.