ReviewHemaSphere2023
An Overview of Targeted Therapies in Acute Myeloid Leukemia.
Review in HemaSphere, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Antileukemic therapies for older adults with AML ineligible for conventional therapy: systematic review and meta-analysis.Blood advances · 2026Pooled it
- Targeting ACSF2 overcomes Ara-C resistance in acute myeloid leukemia via the cholesterol metabolism-ERK signaling axis.Leukemia · 2026Article
- N-3 PUFAs Enhancing Chemotherapy Efficacy in Acute Myeloid Leukemia While Safeguarding Healthy Cells.Biotechnology and applied biochemistry · 2026Article
- A rare case of acute basophilic leukemia transformed from high risk myelodysplastic syndrome.Annals of hematology · 2026Article
- Suppression of UCP2 alleviates leukemogenesis by enhancing branched-chain amino acids-induced oxidative stress via activating the PI3K/AKT/mTOR signaling pathway.Genes & diseases · 2026Article
- Diagnosis-Driven Targeted Therapy in Acute Myeloid Leukemia: Clinical Integration of Tyrosine Kinase, BCL-2, and CD33-Directed Strategies with Midostaurin, Venetoclax, and Gemtuzumab Ozogamicin.Journal of clinical medicine · 2026Review
- From complexity to clarity: aging bone marrow niche in bone and blood regeneration and malignancy.Bone research · 2026Review
- Advances in ligand-targeted nanodelivery systems for leukemia therapy: from single- to dual-ligand strategies.Journal of translational medicine · 2026Review
- Glutaredoxin 2 is essential for AML survival through mitochondrial permeability transition pore regulation.Blood · 2026Article
- Hijacking the helpers: platelet and neutrophil trafficking in AML and therapeutic exploitation.Experimental hematology & oncology · 2026Review
- Molecularly targeted therapy and immunotherapy in leukemias.Journal of hematology & oncology · 2026Review
- Deciphering Multitarget Mechanisms of Cardiac Glycosides in Acute Myeloid Leukemia Using a Network Pharmacology and Molecular Docking.Drug design, development and therapy · 2026Article
- Caspase 3-specific cleavage of ubiquitin-specific peptidase 48 enhances drug-induced apoptosis in AML.Cancer biology & therapy · 2025Article
- Article
- Targeting lipid metabolism in acute myeloid leukemia: biological insights and therapeutic opportunities.Leukemia · 2025Review
- Fitness assessment in acute myeloid leukemia: recommendations from an expert panel on behalf of the European LeukemiaNet.Blood advances · 2025Review
- Article
- Molecular principles underlying aggressive cancers.Signal transduction and targeted therapy · 2025Review
- Article
- Development and comparison of single FLT3-inhibitors to dual FLT3/TAF1-inhibitors as an anti-leukemic approach.PloS one · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Acute myeloid leukemia (AML) is the most aggressive adult leukemia, characterized by clonal differentiation arrest of progenitor or precursor hematopoietic cells. Intense preclinical and clinical research has led to regulatory approval of several targeted therapeutics, administered either as single agents or as combination therapies. However, the majority of patients still face a poor prognosis and disease relapse frequently occurs due to selection of therapy-resistant clones. Hence, more effective novel therapies, most likely as innovative, rational combination therapies, are urgently needed. Chromosomal aberrations, gene mutations, and epigenetic alterations drive AML pathogenesis but concurrently provide vulnerabilities to specifically target leukemic cells. Other molecules, either aberrantly active and/or overexpressed in leukemic stem cells, may also be leveraged for therapeutic benefit. This concise review of targeted therapies for AML treatment, which are either approved or are being actively investigated in clinical trials or recent preclinical studies, provides a flavor of the direction of travel, but also highlights the current challenges in AML treatment.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.