ArticleCancer discovery2020
Monocytic Subclones Confer Resistance to Venetoclax-Based Therapy in Patients with Acute Myeloid Leukemia.
Article in Cancer discovery, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 372 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
372 citing papers in PubMed, 1 synthesis or guideline pooled it, 533 citations in OpenAlex.
- Venetoclax-Based Regimens in Chronic Myelomonocytic Leukemia: A Systematic Review and Meta-Analysis.Acta haematologica · 2026Pooled it
- Results of a phase 1 trial testing ruxolitinib plus venetoclax in patients with relapsed/refractory acute myeloid leukemia.Blood neoplasia · 2026Trial
- A phase 1 study of IO-202, an anti-LILRB4 antibody, in chronic myelomonocytic leukemia and acute myeloid leukemia.Blood neoplasia · 2025Trial
- Trial
- A phase 1/1b study of the all-oral regimen CC-486 and venetoclax in acute myeloid leukemia.Blood advances · 2026Article
- 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
- TIM3-targeted delivery of venetoclax overcomes drug resistance and reinvigorates NK cell activity in acute myeloid leukemia.Nature cancer · 2026Article
- The Pretherapy Endothelial Activation and Stress Index (EASIX) in Patients with Newly Diagnosed Acute Myeloid Leukemia: A Pilot Study.Diagnostics (Basel, Switzerland) · 2026Article
- 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
- Non-genetic remodeling drives leukemia propagation and reveals actionable vulnerabilities in acute myeloid leukemia.Cell reports. Medicine · 2026Article
- From pumps to networks: ABC transporters in leukemia resistance and microenvironmental adaptation.Medical oncology (Northwood, London, England) · 2026Review
- Brusatol Triggers Cell Cycle Arrest and Apoptosis, Disrupts Sterol Biosynthesis, and Enhances the Anti-Leukemic Activity of Venetoclax in AML Cells.Cell biochemistry and biophysics · 2026Article
- CD84 expression stratifies venetoclax response and reveals a targetable vulnerability in resistant acute myeloid leukemia.Experimental hematology & oncology · 2026Article
- Venetoclax and azacitidine for younger acute myeloid leukemia patients independent of fitness for intensive chemotherapy.Haematologica · 2026Article
- Putting the I in AML: Artificial Intelligence and Machine Learning in Acute Myeloid Leukemia.Cells · 2026Review
- Myeloid differentiation-associated autophagy drives venetoclax resistance in AML.Research square · 2026Article
- Chidamide plus venetoclax as effective and safe maintenance therapy in high-risk acute myeloid leukemia and myelodysplastic syndrome post-transplantation.Annals of hematology · 2026Article
- m6A and NuRD complexes regulate monocytic differentiation and resistance to BCL2/BCL2L1 inhibitors in acute myeloid leukemia.Haematologica · 2026Article
312 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
32 authors at 5 institutions in 1 country.
Funding
Abstract
Venetoclax-based therapy can induce responses in approximately 70% of older previously untreated patients with acute myeloid leukemia (AML). However, up-front resistance as well as relapse following initial response demonstrates the need for a deeper understanding of resistance mechanisms. In the present study, we report that responses to venetoclax +azacitidine in patients with AML correlate closely with developmental stage, where phenotypically primitive AML is sensitive, but monocytic AML is more resistant. Mechanistically, resistant monocytic AML has a distinct transcriptomic profile, loses expression of venetoclax target BCL2, and relies on MCL1 to mediate oxidative phosphorylation and survival. This differential sensitivity drives a selective process in patients which favors the outgrowth of monocytic subpopulations at relapse. Based on these findings, we conclude that resistance to venetoclax + azacitidine can arise due to biological properties intrinsic to monocytic differentiation. We propose that optimal AML therapies should be designed so as to independently target AML subclones that may arise at differing stages of pathogenesis. SIGNIFICANCE: Identifying characteristics of patients who respond poorly to venetoclax-based therapy and devising alternative therapeutic strategies for such patients are important topics in AML. We show that venetoclax resistance can arise due to intrinsic molecular/metabolic properties of monocytic AML cells and that such properties can potentially be targeted with alternative strategies.
Indexed as
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.