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Review
. 2020 Sep:43:100650.
doi: 10.1016/j.blre.2019.100650. Epub 2019 Dec 20.

The minimal that kills: Why defining and targeting measurable residual disease is the "Sine Qua Non" for further progress in management of acute myeloid leukemia

Jan Philipp Bewersdorf  1 , Rory M Shallis  1 , Prajwal C Boddu  1 , Brent Wood  2 , Jerald Radich  3 , Stephanie Halene  4 , Amer M Zeidan  5
Affiliations
Review

The minimal that kills: Why defining and targeting measurable residual disease is the "Sine Qua Non" for further progress in management of acute myeloid leukemia

Jan Philipp Bewersdorf et al. Blood Rev. 2020 Sep.

Abstract

Patients with acute myeloid leukemia (AML) who achieve morphologic remission in the bone marrow after initial treatment often continue to harbor residual leukemic cells that can give rise to disease relapse. Achievement of a deeper remission has been associated with a reduced risk of relapse and improved event-free and overall survival in several studies. However, standardization of diagnostic techniques, sample acquisition and test timing are needed before minimal, also known as measurable, residual disease (MRD) quantification can be used to guide treatment decision making. Furthermore, clinical trial evidence that preemptive intervention at MRD level can alter the natural history of AML is required. Herein, we outline the current landscape of MRD assessment in AML, summarize the available evidence and challenges, and highlight the potential for MRD status to serve as a surrogate endpoint for hard clinical outcomes and as an approvable endpoint in clinical trials for regulatory purposes.

Keywords: Acute myeloid leukemia; Immune checkpoint; MRD; Minimal residual disease; Next generation sequencing.

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Conflict of interest statement

Declaration of Competing Interest A.M.Z. received research funding (institutional) from Celgene, Abbvie, Astex, Pfizer, Medimmune/AstraZeneca, Boehringer-Ingelheim, Trovagene, Incyte, Takeda, Novartis, Aprea, and ADC Therapeutics. A.M.Z had a consultancy with and received honoraria from AbbVie, Otsuka, Pfizer, Celgene, Jazz, Incyte, Agios, Boehringer-Ingelheim, Novartis, Acceleron, Astellas, Daiichi Sankyo, Cardinal Health, Taiho, Seattle Genetics, BeyondSpring, Trovagene, Takeda, Ionis, and Epizyme. A.M.Z received travel support for meetings from Pfizer, Novartis, and Trovagene. None of these relationships were related to the development of this manuscript. The other authors have no relevant conflicts of interest to declare.

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