ArticleBlood2020
Molecular patterns of response and treatment failure after frontline venetoclax combinations in older patients with AML.
Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 446 papers, 4 of them syntheses that pooled it.
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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
446 citing papers in PubMed, 4 syntheses or guidelines pooled it, 633 citations in OpenAlex.
- Antileukemic therapies for older adults with AML ineligible for conventional therapy: systematic review and meta-analysis.Blood advances · 2026Pooled it
- American Society of Hematology 2025 guidelines for treating newly diagnosed acute myeloid leukemia in older adults.Blood advances · 2026Guideline
- Efficacy and safety of venetoclax plus azacitidine based regimens in the treatment of relapsed or refractory acute myeloid leukemia: a systematic review and meta-analysis.Annals of hematology · 2025Pooled it
- Pooled it
- Long-term outcomes of azacitidine, venetoclax, and gilteritinib in newly diagnosed FLT3-mutated AML.Blood advances · 2026Trial
- Results of a phase 1 trial testing ruxolitinib plus venetoclax in patients with relapsed/refractory acute myeloid leukemia.Blood neoplasia · 2026Trial
- Trial
- Real-world outcomes of newly diagnosed AML treated with venetoclax and azacitidine or low-dose cytarabine in the UK NHS.Blood neoplasia · 2024Trial
- Azacitidine, Venetoclax, and Gilteritinib in Newly Diagnosed and Relapsed or RefractoryJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2024Trial
- Oral decitabine and cedazuridine plus venetoclax for older or unfit patients with acute myeloid leukaemia: a phase 2 study.The Lancet. Haematology · 2024Trial
- Reduced dose azacitidine plus venetoclax as maintenance therapy in acute myeloid leukaemia following intensive or low-intensity induction: a single-centre, single-arm, phase 2 trial.The Lancet. Haematology · 2024Trial
- KRAS Mutations Predict Inferior Post-Remission Outcomes in Newly Diagnosed Acute Myeloid Leukemia With MAPK Pathway Mutations.European journal of haematology · 2026Article
- Article
- Current and future therapies for acute myeloblastic leukemia.Journal of hematology & oncology · 2026Review
- G3BP2 confers venetoclax resistance by stabilizing ELF1-mediated MCL1 transcription in acute myeloid leukemia.Leukemia · 2026Article
- Very Long Chain Fatty Acid Synthesis is a Targetable Dependency in RAS Pathway Mutant Leukemia.Blood cancer discovery · 2026Article
- Two Decades ofCancers · 2026Review
- Dynamic genetic and nongenetic RAS-pathway activation drives resistance to FLT3 and BCL2 inhibitor therapy.Blood · 2026Article
- Wired to Survive: How AML Cytogenetics Shape Apoptotic Dependence and Venetoclax Resistance.Genes · 2026Review
- AI-enabled multi-omics pharmacogenomic modeling guides resistance-aware multitarget optimization of venetoclax therapy in acute myeloid leukemia.NPJ precision oncology · 2026Article
386 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
29 authors at 6 institutions in 2 countries.
Funding
Abstract
The BCL-2 inhibitor venetoclax combined with hypomethylating agents or low-dose cytarabine represents an important new therapy for older or unfit patients with acute myeloid leukemia (AML). We analyzed 81 patients receiving these venetoclax-based combinations to identify molecular correlates of durable remission, response followed by relapse (adaptive resistance), or refractory disease (primary resistance). High response rates and durable remissions were typically associated with NPM1 or IDH2 mutations, with prolonged molecular remissions prevalent for NPM1 mutations. Primary and adaptive resistance to venetoclax-based combinations was most commonly characterized by acquisition or enrichment of clones activating signaling pathways such as FLT3 or RAS or biallelically perturbing TP53. Single-cell studies highlighted the polyclonal nature of intratumoral resistance mechanisms in some cases. Among cases that were primary refractory, we identified heterogeneous and sometimes divergent interval changes in leukemic clones within a single cycle of therapy, highlighting the dynamic and rapid occurrence of therapeutic selection in AML. In functional studies, FLT3 internal tandem duplication gain or TP53 loss conferred cross-resistance to both venetoclax and cytotoxic-based therapies. Collectively, we highlight molecular determinants of outcome with clinical relevance to patients with AML receiving venetoclax-based combination therapies.
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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.