Advertisement


Eunice S. Wang, MD, on AML: Gemtuzumab Ozogamicin Plus Standard Induction Chemotherapy Improves Outcomes

2022 ASH Annual Meeting and Exposition

Advertisement

Eunice S. Wang, MD, of Roswell Park Comprehensive Cancer Center, discusses the outcomes of patients newly diagnosed with acute myeloid leukemia (AML) who were treated with cytarabine plus daunorubicin plus gemtuzumab ozogamicin (GO). These patients experienced higher rates of measurable residual disease–negative complete remission and complete remission with incomplete count recovery, compared to those treated with cytarabine plus idarubicin daunorubicin alone. Although adding GO was not associated with improved overall survival, longer follow-up is warranted to determine an absolute survival advantage of this regimen (Abstract 58).



Related Videos

Lymphoma

Eva Hoster, PhD, on Mantle Cell Lymphoma: Predictive Value of Minimal Residual Disease on Efficacy of Rituximab Maintenance

Eva Hoster, PhD, of Munich University, discusses results from the European MCL Elderly Trial, which confirmed the strong efficacy of rituximab maintenance in minimal residual disease (MRD)-negative patients with mantle cell lymphoma (MCL) after induction. Omitting maintenance based on MRD-negativity is thus discouraged. Considering the short time to progression, more effective treatment strategies should be explored in MRD-positive patients to improve long-term prognosis (Abstract 544).

Lymphoma

Jia Ruan, MD, PhD, on Mantle Cell Lymphoma: Phase II Findings on Acalabrutinib/Lenalidomide/Rituximab

Jia Ruan, MD, PhD, of Meyer Cancer Center, Weill Cornell Medicine, and NewYork-Presbyterian Hospital, discusses trial results demonstrating that the triple chemotherapy-free combination of acalabrutinib, lenalidomide, and rituximab is well tolerated, highly effective, and produces high rates of minimal residual disease (MRD)-negative complete response as an initial treatment for patients with mantle cell lymphoma, including those with TP53 mutations. Real-time MRD analysis may enable treatment de-escalation during maintenance to minimize toxicity, which warrants further evaluation. An expansion cohort of acalabrutinib/lenalidomide/obinutuzumab is being launched (Abstract 73).

Lymphoma

Tomohiro Aoki, MD, PhD, on the Spatial Tumor Microenvironment and Outcome of Relapsed/Refractory Classical Hodgkin Lymphoma

Tomohiro Aoki, MD, PhD, of the University of British Columbia and the Centre for Lymphoid Cancer at BC Cancer, discusses a novel prognostic model applicable to patients with relapsed or refractory classical Hodgkin lymphoma who were treated with autologous stem cell transplantation. The model has shown the interaction between the biomarker CXCR5 on HRS cells (Hodgkin and Reed/Sternberg cells, hallmarks of Hodgkin lymphoma) with specific follicular T helper cells and macrophages, a prominent crosstalk axis in relapsed disease. This insight opens new avenues to developing predictive biomarkers (Abstract 71).

 

Leukemia
Lymphoma

Jennifer R. Brown, MD, PhD, on CLL/SLL: New Findings on Zanubrutinib vs Ibrutinib for Relapsed or Refractory Disease

Jennifer R. Brown, MD, PhD, of Dana-Farber Cancer Institute, discusses phase III findings of the ALPINE study, which showed that zanubrutinib is more efficacious and better tolerated than ibrutinib as a treatment for patients with relapsed or refractory chronic lymphocytic leukemia (CLL) and small lymphocytic lymphoma (SLL). In this first head-to-head comparison of the two BTK inhibitors, the superior progression-free survival of zanubrutinib was observed across all major subgroups, including high-risk patients (Abstract LBA-6).

Leukemia
Genomics/Genetics

Irene Roberts, MD, on Leukemogenesis in Infants With Trisomy 21

Irene Roberts, MD, of Oxford’s Weatherall Institute of Molecular Medicine, discusses children with Down syndrome, who have a more than 100-fold increased risk of developing acute myeloid leukemia before their fourth birthday compared to children without Down syndrome. Their risk of acute lymphoblastic leukemia is also increased by around 30-fold. Dr. Roberts details current knowledge about the biologic and molecular basis of this relationship between leukemia and Down syndrome, the role of trisomy 21 in leukemogenesis, and the clinical implications of these findings.

Advertisement

Advertisement




Advertisement