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A new algorithm based on gene expression data for 151 DNA repair genes can identify outcomes and response to platinum-based chemotherapy in patients with epithelial ovarian cancer, researchers at the Dana-Farber Cancer Institute report.
A new algorithm based on gene expression data for 151 DNA repair genes can identify outcomes and response to platinum-based chemotherapy in patients with epithelial ovarian cancer, researchers at the Dana-Farber Cancer Institute (Boston, Massachusetts) report. If clinical trials bear out the initial data, this predictive tool would enable clinicians to identify the patients most likely to have a durable response to platinum-based therapy earlier in the course of treatment and to assign others to alternate therapies.
Epithelial ovarian cancer often is detected in late stages of the disease, and the standard treatment of surgical debulking followed by up to 8 cycles of platinum-based chemotherapy delivered concurrently with a taxane is highly toxic: 30% of patients will not respond to therapy, 42% will be unable to complete therapy, and 75 of those who do respond will relapse.
Researchers postulated that the tumors in non-responders to therapy have differential expression of 23 genes involved in repairing DNA damaged by platinum, and that by measuring the levels of gene expression, it would be possible to predict both response to initial platinum-based therapy and overall survival.
Improved survival could be predicted by a high score (high vs low 5-year overall survival, 40% vs 17%; P<0.001) and results were reproduced in 2 independent validation microarray datasets (P<0.05). The score was the only pretreatment factor that was statistically significantly associated with overall survival (P<0.001), and it outperformed all known predictive clinical factors. A positive association was seen between the score and complete response rate, recurrence-free survival, and progression-free survival.
Kang J, D'Andrea AD, Kozono D. Outcomes in ovarian cancer treated with platinum-based chemotherapy. J Natl Cancer Institute. 2012;104(9):670-681.