ArticleNature communications2025
Cellular interactions within the immune microenvironment underpins resistance to cell cycle inhibition in breast cancers.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- CDK4/6 inhibitors as conditional immune-priming agents in breast cancer: therapeutic windows, sequencing strategies, and rational combinations with immunotherapy, radiotherapy, and antibody-drug conjugates.Frontiers in immunology · 2026Pooled it
- Palbociclib and endocrine therapy diminish adaptive anti-tumor immunity in early breast cancer: The NeoRHEA phase 2 study.Nature communications · 2025Trial
- Lactobacillus salivarius potentiates gastrointestinal cancer immunotherapy through its metabolite chenodeoxycholic acid.Cell reports. Medicine · 2026Article
- Knowledge-guided contextual gene set analysis with large language models.Bioinformatics (Oxford, England) · 2026Article
- Targeting IL27RA Enhances Immunotherapy in Triple-Negative Breast Cancer by Modulating Tumor Cells and the Tumor Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Pretreatment tumor infiltrating lymphocytes and outcome in patients with HR+/HER2- advanced breast cancer treated with CDK4/6 inhibitors.Scientific reports · 2026Article
- GNAL-driven calcium signaling reshapes the spatiotemporal immune landscape in ERTranslational cancer research · 2026Article
- Peptide Arrays as Tools for Unraveling Tumor Microenvironments and Drug Discovery in Oncology.Cells · 2026Review
- Recent advances in dissolving microneedles for breast cancer immunotherapy: local delivery and tumor microenvironment remodeling.Frontiers in immunology · 2026Review
- Cyclin-dependent kinase 4 and 6 inhibitors and the breast cancer immune ecosystem: immune remodeling, resistance, and therapeutic reprogramming.Frontiers in immunology · 2026Review
- Reprogramming the immunosuppressive breast cancer microenvironment: integrating cellular, metabolic, and stromal targets for rational immunotherapy.Frontiers in immunology · 2026Review
- The Dual Effects of CDK4/6 Inhibitors on Tumor Immunity.Cancers · 2025Review
- Inferring causal trajectories from spatial transcriptomics using CASCAT.Nucleic acids research · 2025Article
- Review
- Single-cell ligand-receptor profiling reveals an immunotherapy-responsive subtype and prognostic signature in triple-negative breast cancer.Frontiers in immunology · 2025Article
- Exploring the Role of Immune Cells in Glioma: Causal Associations and Clinical Implications.International journal of medical sciences · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Immune evasion by cancer cells involves reshaping the tumor microenvironment (TME) via communication with non-malignant cells. However, resistance-promoting interactions during treatment remain lesser known. Here we examine the composition, communication, and phenotypes of tumor-associated cells in serial biopsies from stage II and III high-risk estrogen receptor positive (ER+ ) breast cancers of patients receiving endocrine therapy (letrozole) as single agent or in combination with ribociclib, a CDK4/6-targeting cell cycle inhibitor. Single-cell RNA sequencing analyses on longitudinally collected samples show that in tumors overcoming the growth suppressive effects of ribociclib, first cancer cells upregulate cytokines and growth factors that stimulate immune-suppressive myeloid differentiation, resulting in reduced myeloid cell- CD8 + T-cell crosstalk via IL-15/18 signaling. Subsequently, tumors growing during treatment show diminished T-cell activation and recruitment. In vitro, ribociclib does not only inhibit cancer cell growth but also T cell proliferation and activation upon co-culturing. Exogenous IL-15 improves CDK4/6 inhibitor efficacy by augmenting T-cell proliferation and cancer cell killing by T cells. In summary, response to ribociclib in stage II and III high-risk ER + breast cancer depends on the composition, activation phenotypes and communication network of immune cells.
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