ASH Clinical News February 2015 | Page 23

CLINICAL NEWS Time to Reconsider Allogeneic SCT in NPM1Mutant AML? TABLE. Allogeneic stem cell transplantation (SCT) significantly improved rates of relapse-free survival (RFS), but not overall survival (OS), in patients with acute myeloid leukemia (AML) who also harbored a mutated nucleophosmin-1 gene (NPM1), according to results recently reported in the Journal of Clinical Oncology. NPM1 mutations, which are present in a large percentage of patients with AML who have a normal karyotype, are considered a favorable prognostic marker and are associated with improved outcomes and remission rates. While patients with high-risk profiles are typically referred for transplantation, patients with more favorable risk profiles, such as those with NPM1-mutant AML, are more likely to receive chemotherapy alone. So, should NPM1-mutant AML patients be referred for allogeneic SCT or chemotherapy alone as post-remission therapy? In this donor versus no-donor analysis, lead author Christopher Röllig, MD, from University Hospital Dresden in Germany, and colleagues compared the clinical courses of patients with NPM1mutant AML who were eligible for allogeneic SCT to assess its predictive value. ing clinically relevant bleeding, versus 8 percent (6 of 72 patients) of the enoxaparin group. “Our observation that the 300-mg dose regimen of FXI-ASO markedly reduced the rate of venous thrombosis, as compared with enoxaparin, and that any clots that formed were small, raises the possibility that factor XI may be involved not only in the propagation of thrombosis, but also in its initiation,” researchers wrote in their NEJM paper. These findings challenge “the concept that tissue factor is the main driver of thrombosis among patients undergoing surgery.” The ability to dissociate thrombosis and hemostasis is “the Holy Grail” of anticoagulant therapy, Dr. Büller said, and has the opportunity to revolutionize surgical care and reduce medical costs. ● References • Büller HR, Bethune C, Bhanot S, et al. Factor XI antisense oligonucleotid