ArticleBlood2025
How I treat acute myeloid leukemia with differentiation therapy.
Article in Blood, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- A phase 1/2 study of DS-1594 menin inhibitor in relapsed/refractory acute leukemias.Journal of hematology & oncology · 2025Trial
- Synergistic immune interactions between T cells and natural killer cells in allogeneic haematopoietic stem cell transplantation for acute myeloid leukaemia: current status and future directions.Annals of medicine · 2026Review
- Menin Inhibitors in Acute Myeloid Leukemia: Clinical Integration, Resistance, and the Path Beyond Monotherapy.Cancers · 2026Review
- Exploring the landscape of targetable alterations in patients with glioblastoma.Nature reviews. Clinical oncology · 2026Review
- A New Paradigm for Pediatric AML: Improving the Pipeline for Treatments Targeting Cytogenetic and Molecular Alterations.Cancers · 2026Review
- Controversies in the Management of AML in Older Patients: A Canadian Perspective.Current oncology (Toronto, Ont.) · 2026Review
- Electrical stimulation induces differentiation onset consistent with a therapeutic approach in neuroblastoma cells.Scientific reports · 2026Article
- Identification and Management of Differentiation Syndrome in Emergency Settings: A Narrative Review.Cancers · 2026Review
- Cytoplasmic retention of IRF3 binding Vimentin competitively with ERK1/2 mitigates acute myeloid leukemia through TFEB nuclear translocation.Cell communication and signaling : CCS · 2026Article
- Preliminary Effects of Benralizumab in an AML Cell Model with Promyelocytic Features Expressing IL-5R: An Exploratory Proof-of-Concept Study.Biomedicines · 2026Article
- Acute Myeloid Leukemia with an FMS-like Tyrosine Kinase 3-tyrosine Kinase Domain Mutation Developing Gilteritinib-induced Differentiation Syndrome.Internal medicine (Tokyo, Japan) · 2026Article
- Genome Agnostic Reprogramming of Acute Myelocytic Leukemia Hallmarks by Targeting Non-Oncogene Addictions with Azacitidine Plus Pioglitazone and All-Trans Retinoic Acid.International journal of molecular sciences · 2026Review
- Exudative Retinal Detachment During Induction Therapy for Acute Promyelocytic Leukemia: A Manifestation of Differentiation Syndrome.International medical case reports journal · 2026Article
- Analysis of risk factors for differentiation syndrome in patients with acute promyelocytic leukemia.Medicine · 2025Observational
- Atypical acute promyelocytic leukemia with tripartite fusion geneHaematologica · 2025Article
- Optimizing lower intensity triplet therapy in acute myeloid leukemia: a practical guide.Blood cancer journal · 2025Review
- lncRNA TMEM147-AS1 promotes acute myeloid leukemia development by regulating miR-873-3p/ZFX axis.Journal of molecular histology · 2025Article
- Catalytic Inhibition of KAT6/KAT7 Enhances the Efficacy and Overcomes Primary and Acquired Resistance to Menin Inhibitors in MLL Leukemia.Cancer discovery · 2025Article
- "Dexamethasing" acute myeloid leukemia: new opportunities for an "old" drug.Haematologica · 2025Article
- Enasidenib as treatment for AML with IDH2 mutation: multicenter real-life study of the early-access program in Spain.Annals of hematology · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
abstractAn increasing number of acute myeloid leukemia (AML) therapeutics have been developed, not as cytotoxic therapies but rather as targeted agents able to restore the aberrant and leukemogenic "block" in normal differentiation. All-trans retinoic acid and arsenic trioxide are classic examples of differentiating agents for treatment of acute promyelocytic leukemia (APL); newer therapies functioning through differentiation include isocitrate dehydrogenase 1 and 2 inhibitors, FMS-like tyrosine kinase 3 inhibitors, and menin inhibitors. The terminal differentiation of leukemic blasts via differentiating-agent therapy can lead to a constellation of signs and symptoms, originally referred to as "retinoic acid syndrome" and now termed "differentiation syndrome" (DS), characterized predominantly by systemic inflammatory response system-like features of dyspnea, pulmonary infiltrates, pleural and pericardial effusions, unexplained fevers, hypotension, edema, and renal insufficiency. DS in patients with newly diagnosed APL is generally straightforward to identify; however, DS in patients with multiply relapsed AML can be more challenging to diagnose, due to nonspecific signs and symptoms that can be mistakenly attributed to infectious etiologies or the underlying refractory leukemia itself. Prompt consideration of DS, rapid initiation of systemic corticosteroids, and early cytoreduction in the setting of concomitant hyperleukocytosis are essential for optimal management.
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