ReviewCell death & disease2024
Venetoclax therapy and emerging resistance mechanisms in acute myeloid leukaemia.
Review in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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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
59 citing papers in PubMed.
- Dose-Adjusted Treatment With 7-Day Venetoclax Plus Azacitidine or Decitabine in Patients With Acute Myeloid Leukaemia.European journal of haematology · 2026Article
- ROCKing resistance: cytoskeletal mitochondrial synergy in acute myeloid leukemia.Haematologica · 2026Article
- Venetoclax for elderly patients with acute myeloid leukaemia unfit for intensive chemotherapy: Prospects, resistance mechanisms and management strategies.Clinical and translational medicine · 2026Review
- RNA terminal uridylyl transferases are druggable vulnerabilities in AML but are dispensable for normal hematopoiesis.Science advances · 2026Article
- Molecular Docking and Simulation-Based Exploration of Niclosamide as a Potential Inhibitor of the p62 ZZ Domain.Biology · 2026Article
- The Natural Quassinoid Brusatol Enhances Venetoclax Efficacy and Overcomes Resistance in Myeloid Leukemias.Cancer science · 2026Article
- Validation of ELN 2024 genetic classification in patients with AML treated with HMA-based regimens: PETHEMA registry study.Blood neoplasia · 2026Article
- Inflammatory immune modulators of AML lung infiltration and respiratory failure.Nature immunology · 2026Article
- RBM15 and ZMYND8 shape acute myeloid leukemia response to BCL2 inhibitors.Haematologica · 2026Article
- Cancer-Associated BCL-2 Mutants Reveal Mechanisms Towards Venetoclax Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Premature senescence impairs hematopoietic stem cell function during sickle cell disease in mice and humans.Science translational medicine · 2026Article
- Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- 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
- A Nomogram Prediction Model and Scoring System for Resistance in Acute Myeloid Leukemia Patients Treated with Venetoclax Combined with Hypomethylating Agents.Current oncology (Toronto, Ont.) · 2026Article
- Article
- HDAC8 inhibition targets STAT3-MYC axis and synergizes with Venetoclax in KMT2A-rearranged acute myeloid leukemia.Leukemia · 2026Article
- SEMA4A promotes acute myeloid leukemia progression through inhibiting apoptosis.Genes & genomics · 2026Article
- Apoptosis signaling and cancer targeted therapy: from bench to bespoke.Translational cancer research · 2026Review
- Re-evaluating the rationale for targeting oxidative phosphorylation in acute myeloid leukemia.The Biochemical journal · 2026Review
- AcTor, a novel mTOR stimulator, potentiates ixazomib for the treatment of acute myeloid leukemia.Molecular cancer · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Acute myeloid leukaemia (AML) is a highly aggressive and devastating malignancy of the bone marrow and blood. For decades, intensive chemotherapy has been the frontline treatment for AML but has yielded only poor patient outcomes as exemplified by a 5-year survival rate of < 30%, even in younger adults. As knowledge of the molecular underpinnings of AML has advanced, so too has the development new strategies with potential to improve the treatment of AML patients. To date the most promising of these targeted agents is the BH3-mimetic venetoclax which in combination with standard of care therapies, has manageable non-haematological toxicity and exhibits impressive efficacy. However, approximately 30% of AML patients fail to respond to venetoclax-based regimens and almost all treatment responders eventually relapse. Here, we review the emerging mechanisms of intrinsic and acquired venetoclax resistance in AML and highlight recent efforts to identify novel strategies to overcome resistance to venetoclax.
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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.