ArticleNature chemical biology2019
Combined chemosensitivity and chromatin profiling prioritizes drug combinations in CLL.
Article in Nature chemical biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Longitudinal omics data and preclinical treatment suggest the proteasome inhibitor carfilzomib as therapy for ibrutinib-resistant CLL.Nature communications · 2025Article
- Enhancer-driven gene regulatory networks inference from single-cell RNA-seq and ATAC-seq data.Briefings in bioinformatics · 2024Article
- Oncogenic MTOR Signaling Axis Compensates BTK Inhibition in a Chronic Lymphocytic Leukemia Patient with Richter Transformation: A Case Report and Review of the Literature.Acta haematologica · 2024Review
- Standardized assays to monitor drug sensitivity in hematologic cancers.Cell death discovery · 2023Article
- Advancing Targeted Protein Degradation via Multiomics Profiling and Artificial Intelligence.Journal of the American Chemical Society · 2023Review
- Influence of cryopreservation on drug responses and gene expression of AML cells: Implications for the use of biobanked tissues.British journal of haematology · 2023Article
- MiR-145 inhibits the differentiation and proliferation of bone marrow stromal mesenchymal stem cells by GABARAPL1 in steroid-induced femoral head necrosis.BMC musculoskeletal disorders · 2022Article
- Deep Morphology Learning Enhances Ex Vivo Drug Profiling-Based Precision Medicine.Blood cancer discovery · 2022Article
- Precision oncology using ex vivo technology: a step towards individualised cancer care?Expert reviews in molecular medicine · 2022Review
- Article
- Chromatin accessibility profiling by ATAC-seq.Nature protocols · 2022Review
- Functional Drug Screening in the Era of Precision Medicine.Frontiers in medicine · 2022Review
- A Novel Antagonistic CD73 Antibody for Inhibition of the Immunosuppressive Adenosine Pathway.Molecular cancer therapeutics · 2021Article
- Bruton's tyrosine kinase inhibition induces rewiring of proximal and distal B-cell receptor signaling in mice.European journal of immunology · 2021Article
- Overcoming resistance to targeted therapies in chronic lymphocytic leukemia.Blood advances · 2021Article
- Article
- Chromatin accessibility profiling methods.Nature reviews. Methods primers · 2021Article
- Survey of ex vivo drug combination effects in chronic lymphocytic leukemia reveals synergistic drug effects and genetic dependencies.Leukemia · 2020Article
- Genetic and Non-Genetic Mechanisms of Resistance to BCR Signaling Inhibitors in B Cell Malignancies.Frontiers in oncology · 2020Article
- In Human Visualization of Ibrutinib-Induced CLL Compartment Shift.Cancer immunology research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
26 authors at 5 institutions in 3 countries.
Funding
Abstract
The Bruton tyrosine kinase (BTK) inhibitor ibrutinib has substantially improved therapeutic options for chronic lymphocytic leukemia (CLL). Although ibrutinib is not curative, it has a profound effect on CLL cells and may create new pharmacologically exploitable vulnerabilities. To identify such vulnerabilities, we developed a systematic approach that combines epigenome profiling (charting the gene-regulatory basis of cell state) with single-cell chemosensitivity profiling (quantifying cell-type-specific drug response) and bioinformatic data integration. By applying our method to a cohort of matched patient samples collected before and during ibrutinib therapy, we identified characteristic ibrutinib-induced changes that provide a starting point for the rational design of ibrutinib combination therapies. Specifically, we observed and validated preferential sensitivity to proteasome, PLK1, and mTOR inhibitors during ibrutinib treatment. More generally, our study establishes a broadly applicable method for investigating treatment-specific vulnerabilities by integrating the complementary perspectives of epigenetic cell states and phenotypic drug responses in primary patient samples.
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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.