An important gene deletion in up to one of every four cases of glioblastoma, the most common adult brain cancer has been discovered by scineists.
This deletion contributes to tumor development, promotes resistance to therapy and considerably worsens a patient's survival prospects, according to researchers at the Stanford University School of Medicine.
The deletion of the gene, known as NFKBIA, triggers biochemical processes similar to those resulting from a better-known aberration common in glioblastomas: alteration of the epidermal growth factor receptor, or EGFR.
Aberrant EGF receptors continuously send out biochemical signals that direct cells to proliferate, igniting tumor development.
The investigators analyzed several hundred tumor samples collected from glioblastoma patients treated at several institutions between 1989 and 2009, and found NFKBIA deletions in a surprisingly high proportion, 25 percent, of the samples.
They also confirmed earlier findings about EGFR, identifying aberrations in that gene in about one-third of these samples. Interestingly, there were only a handful of instances where both gene aberrations occurred in the same sample.
Thus, the two defects taken together accounted for a majority of all glioblastomas examined.
Moreover, the authors learned, patients with either the NFKBIA or EGFR abnormality had a significantly shorter survival, despite maximal therapy, than the remaining patients whose tumors bore neither genetic defect.
The defects on NFKBIA and EGFR have a similar effect on an important molecule called NF-kappa-B, a "transcription factor" found in all cells, but they do this by different mechanisms.
The finding appeared online Dec. 22 in the New England Journal of Medicine.