# Landscape of Measurable Residual Disease in Acute Myeloid Leukemia: From Molecular Detection to Clinical Practice

**Authors:** Mohammad Shahzaib Qadir, Omer Jamy

PMC · DOI: 10.3390/medsci14010123 · Medical Sciences · 2026-03-05

## TL;DR

This paper reviews how detecting small amounts of remaining leukemia cells helps guide treatment decisions and improves outcomes in patients with acute myeloid leukemia.

## Contribution

The paper provides a comprehensive overview of MRD detection technologies and their clinical integration in AML management.

## Key findings

- MRD assessment is now aided by a wide range of technologies including next-generation sequencing and flow cytometry.
- MRD is increasingly used to inform therapeutic decisions in non-intensive treatment settings and peri-transplant care.
- Challenges remain regarding standardization and interpretation of MRD results across clinical scenarios.

## Abstract

Measurable residual disease (MRD) has become a central determinant of prognosis and treatment planning in acute myeloid leukemia (AML). MRD assessment is now aided by a wide range of technologies, including next-generation sequencing, PCR-based assays, multiparameter flow cytometry, and emerging approaches such as liquid biopsy platforms and imaging-based detection. These modalities differ in sensitivity, applicability, and interpretive framework, yet each offers distinct advantages in specific disease contexts. Beyond technical issues, MRD is becoming increasingly integrated into clinical practice. In non-intensive treatment settings, where targeted and low-intensity regimens rely on dynamic disease monitoring to guide ongoing management, MRD is increasingly being used to inform therapeutic decisions. In the peri-transplant setting, MRD status influences conditioning strategies, donor selection, and the use of post-transplant interventions. Despite the growing evidence supporting the clinical relevance of MRD across these scenarios, challenges remain regarding standardization, optimal timing of assessment, and the interpretation of discordant results. This review summarizes the full landscape of MRD detection methods and examines the evolving role of MRD in contemporary AML management, emphasizing current applications and areas requiring further refinement.

## Linked entities

- **Diseases:** acute myeloid leukemia (MONDO:0015667), AML (MONDO:0018874)

## Full-text entities

- **Genes:** CLEC12A (C-type lectin domain family 12 member A) [NCBI Gene 160364] {aka CD371, CLL-1, CLL1, DCAL-2, MICL, hKLRL1}, DNMT3A (DNA methyltransferase 3 alpha) [NCBI Gene 1788] {aka DNMT3A2, HESJAS, M.HsaIIIA, TBRS}, ANPEP (alanyl aminopeptidase, membrane) [NCBI Gene 290] {aka AP-M, AP-N, APN, CD13, GP150, LAP1}, CEBPZ (CCAAT enhancer binding protein zeta) [NCBI Gene 10153] {aka CBF, CBF2, HSP-CBF, NOC1}, IDH2 (isocitrate dehydrogenase (NADP(+)) 2) [NCBI Gene 3418] {aka D2HGA2, ICD-M, IDH, IDH-2, IDHM, IDP}, ABL1 (ABL proto-oncogene 1, non-receptor tyrosine kinase) [NCBI Gene 25] {aka ABL, BCR-ABL, CHDSKM, JTK7, bcr/abl, c-ABL}, CD7 (CD7 molecule) [NCBI Gene 924] {aka GP40, LEU-9, TP41, Tp40}, CD34 (CD34 molecule) [NCBI Gene 947], CD38 (CD38 molecule) [NCBI Gene 952] {aka ADPRC 1, ADPRC1, cADPR1}, FLT3 (fms related receptor tyrosine kinase 3) [NCBI Gene 2322] {aka CD135, FLK-2, FLK2, STK1}, KIT (KIT proto-oncogene, receptor tyrosine kinase) [NCBI Gene 3815] {aka C-Kit, CD117, MASTC, PBT, SCFR}, ASXL1 (ASXL transcriptional regulator 1) [NCBI Gene 171023] {aka BOPS, MDS}, NCAM1 (neural cell adhesion molecule 1) [NCBI Gene 4684] {aka CD56, MSK39, NCAM}, CD33 (CD33 molecule) [NCBI Gene 945] {aka CD33rSiglec, SIGLEC-3, SIGLEC3, p67}, WT1 (WT1 transcription factor) [NCBI Gene 7490] {aka AWT1, GUD, NPHS4, WAGR, WIT-2, WT-1}, IL3RA (interleukin 3 receptor subunit alpha) [NCBI Gene 3563] {aka CD123, IL-3R-alpha, IL3R, IL3RAY, IL3RX, IL3RY}, PTPRC (protein tyrosine phosphatase receptor type C) [NCBI Gene 5788] {aka B220, CD45, CD45R, GP180, IMD105, L-CA}, MECOM (MDS1 and EVI1 complex locus) [NCBI Gene 2122] {aka AML1-EVI-1, EVI1, KMT8E, MDS1, MDS1-EVI1, PRDM3}, NPM1 (nucleophosmin 1) [NCBI Gene 4869] {aka B23, NPM}, TK1 (thymidine kinase 1) [NCBI Gene 7083], TET2 (tet methylcytosine dioxygenase 2) [NCBI Gene 54790] {aka IMD75, KIAA1546, MDS}, SRSF2 (serine and arginine rich splicing factor 2) [NCBI Gene 6427] {aka PR264, SC-35, SC35, SFRS2, SFRS2A, SRp30b}, IDH1 (isocitrate dehydrogenase (NADP(+)) 1) [NCBI Gene 3417] {aka HEL-216, HEL-S-26, IDCD, IDH, IDP, IDPC}
- **Diseases:** minimal residual disease (MESH:D018365), APL (MESH:D015473), cancerous (MESH:D009369), CR (MESH:D012075), ALL (MESH:D054198), hematological malignancies (MESH:D019337), CML (MESH:D015464), extramedullary disease (MESH:D023981), injury to (MESH:D014947), AML (MESH:D015470), disease (MESH:D004194), CBF leukemias (MESH:D007938), MFC (MESH:D054318), toxicity (MESH:D064420), hematologic (MESH:D006402)
- **Chemicals:** decitabine (MESH:D000077209), quizartinib (MESH:C544967), blinatumomab (MESH:C510808), sorafenib (MESH:D000077157), glucose (MESH:D005947), VEN (MESH:C579720), cytarabine (MESH:D003561), HMA (-), CPX-351 (MESH:C000629812), 18FFDG (MESH:D019788), AZA (MESH:D001374), 3'-deoxy-3'-18Ffluorothymidine (MESH:C002854), gilteritinib (MESH:C000609080)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

103 references — full list in the complete paper: https://tomesphere.com/paper/PMC13028118/full.md

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Source: https://tomesphere.com/paper/PMC13028118