ArticleNature communications2024
Single-cell landscape of innate and acquired drug resistance in acute myeloid leukemia.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Deep learning in single-cell and spatial transcriptomics data analysis: advances and challenges from a data science perspective.Briefings in bioinformatics · 2025Pooled it
- From Cluster to Claim: Calibrating Interpretation in Single-Cell Transcriptomics.Advanced genetics (Hoboken, N.J.) · 2026Article
- Data-centric feedback loops for next-generation immunotherapy development.Nature biomedical engineering · 2026Review
- Integration and validation of complementary ex vivo assays for functional precision oncology.NPJ precision oncology · 2026Article
- p97 Inhibition Synergistically Enhances Hypomethylating Therapy through Targeting of PLK1 in Acute Myeloid Leukemia.Cancer research communications · 2026Article
- Re-evaluating the rationale for targeting oxidative phosphorylation in acute myeloid leukemia.The Biochemical journal · 2026Review
- CHRNB4-Mediated Neuroactive Signaling Rewiring Drives Adaptive Resistance to BCL-2 Inhibition in Acute Myeloid Leukemia.Cancers · 2026Article
- Molecular Oncodiagnostics in Precision Oncology: Integrating Tumor Transcriptomics, Patient Pharmacogenetics, and Ex Vivo Chemoresistance Testing to Improve Individual Chemotherapy Response.Journal of personalized medicine · 2026Review
- Studying clonal heterogeneity of acute myeloid leukemia under nutrient and chemotherapy stress.Blood advances · 2026Article
- Decoding the archipelago: single-cell biomarkers rechart the molecular geography of acute myeloid leukemia.Cell communication and signaling : CCS · 2026Review
- Ex vivo drug sensitivity testing predicts treatment outcomes in advanced ovarian cancer.NPJ precision oncology · 2026Article
- Hijacking the helpers: platelet and neutrophil trafficking in AML and therapeutic exploitation.Experimental hematology & oncology · 2026Review
- Rewired Neuroactive Ligand-Receptor Signaling Confers Adaptive Resistance to BCL-2 Inhibition in AML.Research square · 2026Article
- VARIDT 4.0: distribution variability of drug transporters.Nucleic acids research · 2026Article
- Drivers of clinical resistance to venetoclax and hypomethylating agents in acute myeloid leukemia and strategies for improving efficacy.HemaSphere · 2026Article
- Genes-first and phenotypes-first paths to treatment resistance in hematological malignancies.Cell death & disease · 2025Review
- Unveiling CrypticInternational journal of molecular sciences · 2025Article
- Targeting lipid metabolism in acute myeloid leukemia: biological insights and therapeutic opportunities.Leukemia · 2025Review
- Acquired resistance in cancer: towards targeted therapeutic strategies.Nature reviews. Cancer · 2025Review
- Dominant TET2 mutations predict adverse prognosis in cytogenetically normal acute myeloid leukemia patients.Frontiers in oncology · 2025Article
Corrections and comments
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Authors and funding
42 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deep single-cell multi-omic profiling offers a promising approach to understand and overcome drug resistance in relapsed or refractory (rr) acute myeloid leukemia (AML). Here, we combine single-cell ex vivo drug profiling (pharmacoscopy) with single-cell and bulk DNA, RNA, and protein analyses, alongside clinical data from 21 rrAML patients. Unsupervised data integration reveals reduced ex vivo response to the Bcl-2 inhibitor venetoclax (VEN) in patients treated with both a hypomethylating agent (HMA) and VEN, compared to those pre-exposed to chemotherapy or HMA alone. Integrative analysis identifies both known and unreported mechanisms of innate and treatment-related VEN resistance and suggests alternative treatments, like targeting increased proliferation with the PLK inhibitor volasertib. Additionally, high CD36 expression in VEN-resistant blasts associates with sensitivity to CD36-targeted antibody treatment ex vivo. This study demonstrates how single-cell multi-omic profiling can uncover drug resistance mechanisms and treatment vulnerabilities, providing a valuable resource for future AML research.
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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.