Gene Deletion Contributes to Common Adult Brain Cancer
December 23, 2010 6:45 PM
Deletion of the gene NFKBIA helps cause tumor development and treatment resistance in those with glioblastoma
Researchers from the
Stanford University School of Medicine
have found a gene deletion in the most common adult brain cancer that aids in tumor development and therapy resistance.
Griffith Harsh, MD, lead author of the study and professor of neurosurgery at the Stanford University School of Medicine, along with Markus Bredel, MD, Ph.D., associate professor in Stanford's Department of Neurosurgery who is visiting from the University of Alabama-Birmingham, and Branimir Sikic, MD, professor of oncology and clinical pharmacology at Stanford, have discovered that a certain gene deletion is found in up to one of every four cases of a common adult brain cancer, encouraging tumor growth as well as therapy resistance.
The deletion occurs in a copy of
the gene NFKBIA
, which is normally found on chromosome 14 and in a variety of other cancers. Now, researchers have found that it provokes the development of tumors and resistance to therapy in individuals with glioblastoma, which is a common adult brain cancer with low survival rates. In fact, this gene deletion acts much like another "aberration" in glioblastoma, which is the alteration of the epidermal growth factor receptor (EGFR). Both produce the same outcome, but EGFR alteration is more well-known than the NFKBIA gene deletion, meaning that only one has been treated in the past. This may explain why previous treatments have failed.
"It's been known for 25 years that EGFR plays a role in glioblastoma as well as many
," said Bredel. "We asked ourselves, 'What causes the majority of glioblastomas that don't have this defect?'"
Researchers had an idea that NFKBIA may be linked to glioblastoma after a previous study indicated that glioblastoma patients with low NFKBIA expression were more resistant to temozolomide treatments.
To further investigate this finding, the researchers studied several hundred tumor samples from glioblastoma patients between 1989 and 2009. They grew glioblastoma cells in culture as well to heighten the activity of l-kappa-B, which is a protein that binds to NF-kappa-Band stops it from altering gene expression within the nucleus of a cell. By increasing the activity of these
proteins in cells
with EGFR hyperactivity or NFKBIA deficiency, cells restored normal behavior and appearance. They were also less resistant to temozolomide.
Out of all the samples, 25 percent contained NFKBIA deletions while one-third contained aberrations in the EGFR gene. In approximately five percent of the samples, both gene aberrations occurred. Researchers also found that patients with either aberration had a shorter survival rate than those who had neither, which was about 40 percent of patients.
"The way we identified this deletion for our study is not going to be efficient for general clinical-laboratory use," said Harsh. "But we're trying to develop an improved method - fast, cheap, reliable. That could happen within a year or so."
This sort of research could lead to improved treatments and therapies for those with glioblastoma, and possibly other cancers at some point.
was published in
The New England Journal of Medicine
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