At a median follow-up of 14.1 months, the addition of tafasitamab to lenalidomide and rituximab resulted in a significant improvement in PFS compared with placebo (22.4 months versus 13.9 months; hazard ratio [HR] [95% CI], 0.43 [0.32, 0.58]; p<0.0001). In addition, tafasitamab demonstrated a higher ORR (83.5% versus 72.4%, p=0.0014) and PET-CR rate (49.4% versus 39.8%, p=0.029). Overall, these findings suggest that the addition of tafasitamab to lenalidomide and rituximab results in a clinically significant and durable improvement in PFS in patients with R/R FL.²

Timothy Fenske, MD, Medical College of Wisconsin, Milwaukee, WI, shared results from an initial report of this study, which was conducted through the U.S. National Clinical Trials Network (NCTN) and the Blood and Marrow Transplant Clinical Trials Network (BMT-CTN). Patients aged 18-70 with MCL and CR after induction therapy were eligible for inclusion. The primary and secondary endpoints were OS and PFS, respectively. Patients with uMRD at a sensitivity of 1 in 10^-6 were randomized to receive either autoSCT plus three years of maintenance rituximab (Arm A) or maintenance rituximab alone (Arm B). Patients with MRD-positive CR or MRD-indeterminate CR received autoSCT plus maintenance rituximab (Arms C and D, respectively).⁵

From August 2017 to July 2024, 650 patients were assigned to a treatment arm, with 257, 259, 49, and 85 patients enrolled on Arms A, B, C, and D, respectively. Results demonstrated that the three-year OS was 82.1% in Arm A and 82.7% in Arm B for all randomized patients and 86.2% and 84.8% in patients treated as assigned. The three-year PFS for Arms A and B were 76.6% and 77.4% in all randomized patients and 81.5% and 80.4% in patients treated as assigned. Results from this interim analysis suggest that in the current era of highly effective induction and maintenance regimens, patients with MCL in first CR and uMRD do not benefit from consolidative autoSCT, although further studies are warranted.⁵

Polycythemia vera (PV) and essential thrombocythemia (ET) are myeloproliferative neoplasms (MPNs) characterized by chronic inflammation and increased thrombotic risk.⁶ Recent studies have investigated the genetic factors that modulate the inflammatory pathways in these diseases, with a particular focus on the NF-κB pathway, which regulates pro-inflammatory cytokines.⁷

Josef Prchal, MD, Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, shared findings from a study investigating the genetic basis for elevated hemoglobin levels in Andean natives (Aymara) using granulocyte transcriptome data. Three novel, alternatively spliced NFKB1 transcripts (AS-NFKB1) were identified and found to be associated with inflammatory and HIF pathways. The study revealed that the Aymara-enriched NFKB1 rs230511 T allele is associated with reduced inflammation, lower expression of prothrombotic and HIF-targeted genes, and a better response to ropeginterferon alfa-2b.⁶ The novel insights from this study offer valuable implications for PV and ET treatment.

At years one and three, the alloSCT group reported better physical and school functioning, though no significant differences in ischemic lesions or cognitive performance were observed. Furthermore, at 10 years, sickle cell hemoglobin (HbS%), reticulocytes, bilirubin, and white blood cell (WBC) counts were lower in the alloSCT group (p<0.001). These results demonstrate that alloSCT provides sustained benefits over SoC in children with SCA, supporting alloSCT as the preferred treatment option for this patient population.¹⁰