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Restoration of NFKBIA gene inhibited tumor growth, increased chemosensitivity in glioblastoma multiforme

Bredel M. N Engl J Med. 2010;doi:10.1056/NEJMoa1006312.

Issue: February 10, 2011

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Increased expression of the NFKBIA gene inhibited cell growth in glioblastoma tumors with epidermal growth factor receptor amplification and normal NFKBIA expression, and significantly improved outcomes for patients.

“We show that NFKBIA status may be an independent predictor of survival in certain patients with glioblastoma,” Arnab Chakravarti, MD, co-director of the Brain Tumor Program at The Ohio State University Comprehensive Cancer Center and one of the study’s investigators, said in a press release. “We also show that this gene plays a key role in glioblastoma behavior, and that it could be useful for predicting treatment outcomes.”

Researchers segregated 790 patients treated from July 1989 to August 2009 into 10 sets and used glioblastoma cell lines and tumor cells to assess the role of the NFKBIA gene on tumor-cell growth and sensitivity to temozolomide (Temodar, Schering). They then compared those molecular results with outcomes for 570 patients with glioblastoma multiforme.

Researchers found that retrovirally mediated re-expression of NFKBIA in established glioblastoma cell lines with heterozygous NFKBIA deletions inhibited cell-cycle transition, growth, migration and colony formation. Re-expression also reduced cell viability and induced cellular senescence. Additionally, the process increased tumor cells’ sensitivity to temozolomide.

Regression analysis of the 188 glioblastomas in study set one, in which data on gene copy number and survival were available, showed that patients with two copies of NFKBIA survived 131 weeks compared with 57 weeks for patients with tumors harboring a deletion (HR=0.45; 95% CI, 0.23-0.89). Multivariate analysis showed that there is an independent association between survival (HR=0.40; 95% CI, 0.20-0.78) and normal dosage of NFKBIA (HR=0.39; 95% CI, 0.20-0.77).

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