Expert Point of View: David Steensma, MD and Bob Löwenberg, MD


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Bob Löwenberg, MD

Acute myeloid leukemia has a dazzling amount of abnormalities, even in individual patients. Each patient has a unique configuration of genetic abnormalities, and these variations undergo dynamic changes over time.

—Bob Löwenberg, MD

Commenting on this study, David Steensma, MD, of Dana-Farber Cancer Institute and Harvard Medical School in Boston, said that longer follow-up is needed, especially in light of the lack of overall survival benefit, which may have been due to salvage therapy.

“Sorafenib clearly has activity in acute myeloid leukemia. While there have been small nonrandomized trials and case series reported before, this is the first randomized study to show a benefit in this setting. It is also the first time a tyrosine kinase inhibitor combined with chemotherapy has shown benefit in acute myeloid leukemia. At our center, we are using sorafenib [Nexavar] off-label in relapsed/refractory acute myeloid leukemia with FLT3 mutations, but this study suggests there may be a broader benefit that includes patients without FLT3 mutations,” Dr. Steensma continued. “With these data, I hope that more payers will approve it [for acute myeloid leukemia].”

“The fact that sorafenib is a ‘messy’ tyrosine kinase inhibitor may not be bad [ie, having several targets],” he said. “I’ve treated acute myeloid leukemia patients with sorafenib and observed decreased blasts and increased blood counts. When community physicians see these data, I think that uptake of sorafenib will increase, but this is an uncommon disease,” he said.

Bob Löwenberg, MD, of Erasmus University Medical Center, Rotterdam, The Netherlands, who introduced this talk at the plenary session, commented on the “open-minded approach” of enrolling all newly diagnosed patients with acute myeloid leukemia under age 60 and not focusing on one subset.

He too suggested that sorafenib’s ability to block so many targets may account for the positive showing in this study, since no other tyrosine kinase inhibitor has shown enough of an effect to move forward in this disease.

“Acute myeloid leukemia has a dazzling amount of abnormalities, even in individual patients. Each patient has a unique configuration of genetic abnormalities, and these variations undergo dynamic changes over time. This may explain why a drug specifically targeted to one molecular abnormality won’t work,” Dr. Löwenberg commented. ■

Disclosure: Drs. Steensma and Löwenberg reported no potential conflicts of interest.

 


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