ArticleBiomarker research2020
Longitudinal CITE-Seq profiling of chronic lymphocytic leukemia during ibrutinib treatment: evolution of leukemic and immune cells at relapse.
Article in Biomarker research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 30 citations in OpenAlex.
- Immunophenotyping by Single-Cell CITE-Seq.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Single-cell sequencing reveals transcriptional and immunogenetic diversity in stereotyped chronic lymphocytic leukemia.Blood neoplasia · 2026Article
- 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
- Data driven network inference and longitudinal transcriptomics unveil dynamic regulation in Chronic Lymphocytic Leukaemia models.NPJ systems biology and applications · 2026Article
- Tumor heterogeneity as a driver of drug resistance and its implications for personalized therapy.Cancer drug resistance (Alhambra, Calif.) · 2026Review
- Single Cell RNA Sequencing in Colorectal Cancer Immunology: Recent Updates, Application, and Emerging Challenges.Current molecular medicine · 2026Review
- Advances in Microfluidic Single-Cell RNA Sequencing and Spatial Transcriptomics.Micromachines · 2025Review
- Co-expression of CD69, CD49d, CD279 and CD20 in chronic lymphocytic leukemia cells is a new biomarker of active disease before or under therapy.Haematologica · 2025Article
- Article
- Early reappearance of intraclonal proliferative subpopulations in ibrutinib-resistant chronic lymphocytic leukemia.Leukemia · 2024Article
- Characterization and decontamination of background noise in droplet-based single-cell protein expression data with DecontPro.Nucleic acids research · 2024Article
- A multi-omics strategy to understand PASC through the RECOVER cohorts: a paradigm for a systems biology approach to the study of chronic conditions.Frontiers in systems biology · 2024Review
- Systems immunology spanning tumors, lymph nodes, and periphery.Cell reports methods · 2023Review
- Single-cell dissection of tumor microenvironmental response and resistance to cancer therapy.Trends in genetics : TIG · 2023Review
- Dynamic thresholding and tissue dissociation optimization for CITE-seq identifies differential surface protein abundance in metastatic melanoma.Communications biology · 2023Article
- Cytotoxicity of the CD3×CD20 bispecific antibody epcoritamab in CLL is increased by concurrent BTK or BCL-2 targeting.Blood advances · 2023Article
- An agent-based model of monocyte differentiation into tumour-associated macrophages in chronic lymphocytic leukemia.iScience · 2023Article
- Article
- Comparison of the blood immune repertoire with clinical features in chronic lymphocytic leukemia patients treated with chemoimmunotherapy or ibrutinib.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIbrutinib, an irreversible Bruton Tyrosine Kinase (BTK) inhibitor, has revolutionized Chronic Lymphocytic Leukemia (CLL) treatment, but resistances to ibrutinib have emerged, whether related or not to BTK mutations. Patterns of CLL evolution under ibrutinib therapy are well characterized for the leukemic cells but not for their microenvironment.
methodsHere, we addressed this question at the single cell level of both transcriptome and immune-phenotype. The PBMCs from a CLL patient were monitored during ibrutinib treatment using Cellular Indexing of Transcriptomes and Epitopes by sequencing (CITE-Seq) technology.
resultsThis unveiled that the short clinical relapse of this patient driven by BTK mutation is associated with intraclonal heterogeneity in B leukemic cells and up-regulation of common signaling pathways induced by ibrutinib in both B leukemic cells and immune cells. This approach also pinpointed a subset of leukemic cells present before treatment and highly enriched during progression under ibrutinib. These latter exhibit an original gene signature including up-regulated BCR, MYC-activated, and other targetable pathways. Meanwhile, although ibrutinib differentially affected the exhaustion of T lymphocytes, this treatment enhanced the T cell cytotoxicity even during disease progression.
conclusionsThese results could open new alternative of therapeutic strategies for ibrutinib-refractory CLL patients, based on immunotherapy or targeting B leukemic cells themselves.
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