According to Bredel, up to 50 percent of the 30,000 to 40,000 genes in the human genome may be altered in glioblastoma.
The key is discovering which changes are actually important.
"Many of those changes will be just passengers or bystanders," Bredel said. "We tried to count up and prioritize the genes that are potentially the most important in glioblastoma disease and as a means to develop future therapy."
Starting with a genome-wide approach, using tissue from 501 people with this type of tumor, the researchers whittled their way down to 31 genes that appear to be the captains or godfathers of the complex genetic changes leading to glioblastoma.
These 31 genes were altered in up to 75 percent of glioblastomas, forming a landscape common to about three-quarters of all cases of glioblastoma, the study found.
And within those 31 genes, a subset of seven genes allowed the researchers to group the disease into low, intermediate and high risk in terms of outcome, a tool that may be useful for prognosis, they said.
Not only the genes were important, but the relationships between them were also critical, the researchers found.
In their second study, the researchers delved deeper into the mechanisms driving two of the 31 genes -- one so-called hub of genes and one gene that interacted with that hub, meaning those that have a high level of connectivity with the other genes.
The hub gene is the EGFR (epidermal growth factor receptor) oncogene on chromosome 7, according to the study. It is amplified in about 45 percent of glioblastoma cases, Bredel said. Oncogenes are genes that drive cancer growth.
The amplification seems to happen in parallel with a decrease in function in another gene, ANXA7, located on chromosome 10, the researchers reported. A decrease in the function of ANXA7 shoots the EGFR oncogene into overdrive, contributing to the development and
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