Huntsville, Ala. -- A team including researchers at the HudsonAlpha Institute and Stanford University, together with colleagues from a number of other organizations, today publishes a comprehensive analysis of genomic variation in the brain cancer glioblastoma. These results are the first from the Cancer Genome Atlas (TCGA) research network, a collaborative effort funded by the National Cancer Institute and the National Human Genome Research Institute of the National Institutes of Health. Glioblastoma is the most common and most aggressive of the primary brain tumors: Notably, U.S. Senator Edward M. Kennedy was diagnosed with glioblastoma earlier this year.
Drs. Devin Absher and Rick Myers, with their labs at HudsonAlpha and Stanford, measured changes in the genetic code of both normal and cancer samples. They specifically looked at regions that either gained or lost large chunks of DNA, larger than 1000 bases, to determine the molecular differences between a normal and glioblastoma genome. The data were analyzed in collaboration with Drs. Gavin Sherlock and James Brooks at Stanford, and Dr. Jun Li at the University of Michigan.
Tumors generally accumulate gains and losses in DNA as they grow, and measuring these changes in a number of samples can illuminate which changes are necessary for tumor development. Targeting genes affected by these changes can lead to improved diagnosis and more specific therapies, with fewer side effects to normal cells in the brain.
The HudsonAlpha and Stanford data on genomic changes were integrated with data from institutions around the country measuring changes in other types of genomic variation and in epigenomic variation. Epigenomic variation refers to molecules that are added to our genome to regulate how genetic instructions are processed in the cell. We know these changes are important to cancer cells, but previous studies have not integrated genomic and epigenomic measurements on such a larg
|Contact: Holly Ralston McClain|
HudsonAlpha Institute for Biotechnology