ArticleNature communications2020
Chromatin mapping and single-cell immune profiling define the temporal dynamics of ibrutinib response in CLL.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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.
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Who cites it
66 citing papers in PubMed, 93 citations in OpenAlex.
- Trial
- Single-cell sequencing reveals transcriptional and immunogenetic diversity in stereotyped chronic lymphocytic leukemia.Blood neoplasia · 2026Article
- Article
- scRADAR: Dissecting intratumoral drug response heterogeneity at single-cell resolution via mechanism-guided prototype routing.PLoS computational biology · 2026Article
- Upregulation of TCF1 and BCL11B in CD8+ effector T cells predicts favorable response to ibrutinib in patients with chronic lymphocytic leukemia.Communications biology · 2026Article
- Co-mapping clonal and transcriptional heterogeneity in somatic evolution via GoT-Multi.Cell genomics · 2026Article
- Single-cell insights into the role of T cells in B-cell malignancies.FEBS letters · 2025Review
- Bruton tyrosine kinase covalent inhibition shapes the immune microenvironment in chronic lymphocytic leukemia.Haematologica · 2025Article
- Expression of Aldehyde Dehydrogenase 1A1 in Relapse-Associated Cells in Acute Myeloid Leukemia.Cells · 2025Review
- Leveraging the Immunomodulatory Potential of Ibrutinib for Improved Outcomes of T Cell-Mediated Therapies of B Cell Malignancies: A Narrative Review.Targeted oncology · 2025Review
- Aberrant heterochromatin silences immune response genes in chronic lymphocytic leukemia.Blood neoplasia · 2025Article
- Pan-cancer secreted proteome and skeletal muscle regulation: insight from a proteogenomic data-driven knowledge base.Functional & integrative genomics · 2025Review
- MYC target gene activation in chronic lymphocytic leukemia and richter transformation: links to aggressiveness and tumor microenvironment interactions.Frontiers in pharmacology · 2025Article
- Single-cell transcriptomic and spatial analysis reveal the immunosuppressive microenvironment in relapsed/refractory angioimmunoblastic T-cell lymphoma.Blood cancer journal · 2024Article
- Molecular Composition and Kinetics of B Cells During Ibrutinib Treatment in Patients with Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2024Article
- Early reappearance of intraclonal proliferative subpopulations in ibrutinib-resistant chronic lymphocytic leukemia.Leukemia · 2024Article
- Basal-epithelial subpopulations underlie and predict chemotherapy resistance in triple-negative breast cancer.EMBO molecular medicine · 2024Article
- The molecular map of CLL and Richter's syndrome.Seminars in hematology · 2024Review
- Lymphocyte migration and retention properties affected by ibrutinib in chronic lymphocytic leukemia.Haematologica · 2024Article
- Decoding leukemia at the single-cell level: clonal architecture, classification, microenvironment, and drug resistance.Experimental hematology & oncology · 2024Review
6 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
15 authors at 3 institutions in 3 countries.
Funding
Abstract
The Bruton tyrosine kinase (BTK) inhibitor ibrutinib provides effective treatment for patients with chronic lymphocytic leukemia (CLL), despite extensive heterogeneity in this disease. To define the underlining regulatory dynamics, we analyze high-resolution time courses of ibrutinib treatment in patients with CLL, combining immune-phenotyping, single-cell transcriptome profiling, and chromatin mapping. We identify a consistent regulatory program starting with a sharp decrease of NF-κB binding in CLL cells, which is followed by reduced activity of lineage-defining transcription factors, erosion of CLL cell identity, and acquisition of a quiescence-like gene signature. We observe patient-to-patient variation in the speed of execution of this program, which we exploit to predict patient-specific dynamics in the response to ibrutinib based on the pre-treatment patient samples. In aggregate, our study describes time-dependent cellular, molecular, and regulatory effects for therapeutic inhibition of B cell receptor signaling in CLL, and it establishes a broadly applicable method for epigenome/transcriptome-based treatment monitoring.
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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.