How I treat AML relapse after allogeneic HSCT

M Mahasweta Gooptu (1Dana Farber Cancer Institute, Boston, United States) H H. Moses Murdock (1Dana-Farber Cancer Institute, Department of Medical Oncology, Boston, United States) R Robert J. Soiffer (Dana-Farber Cancer Institute)

Abstract

Abstract Allogeneic hematopoietic stem cell transplantation (HSCT) is one of the principal curative approaches in the treatment of acute myeloid leukemia (AML); however, relapse after transplantation remains a catastrophic event with poor prognosis. The incidence of relapse has remained unchanged over the last 3 decades despite an evolving understanding of the immunobiology of the graft-versus-leukemia effect and the immune escape mechanisms that lead to post-HSCT relapse. The approach to posttransplant relapse is highly individualized and is dictated both by disease biology and genomics as well as the patient's clinical status at the time of relapse and the interval between relapse and transplantation. With the help of 3 illustrative cases, we discuss our approach to early, late, and incipient relapse. Current therapeutic strategies incorporate immunosuppression taper when feasible, a variety of targeted and nontargeted chemotherapeutic agents, and consolidative cellular therapies including donor lymphocyte infusions or a second allogeneic transplant. We then summarize evolving frontiers in the treatment and prognostication of relapse, including the critical role of measurable residual disease. Finally, we emphasize enrollment on clinical trials and thoughtful discussions regarding goals of care and supporting frail patients as universal principles that should be incorporated in approaches to treatment of AML relapse after transplantation.

Article Details

Journal Blood
Volume / Issue Vol. 145, Issue 19
Published May 08, 2025
Pages 2128-2137
ISSN 0006-4971
Publisher Elsevier BV

Journal Info

Blood

Elsevier BV

ISSN: 0006-4971 Health Sciences

Authors (3)

M

Mahasweta Gooptu

1Dana Farber Cancer Institute, Boston, United States

H

H. Moses Murdock

1Dana-Farber Cancer Institute, Department of Medical Oncology, Boston, United States

R

Robert J. Soiffer

Dana-Farber Cancer Institute