ArticleProceedings of the National Academy of Sciences of the United States of America2018
Modeling combination therapy for breast cancer with BET and immune checkpoint inhibitors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 108 citations in OpenAlex.
- Bridging BET bromodomain and immune checkpoint inhibitors through generative bioorganic frameworks for next-generation cancer immunotherapy.RSC medicinal chemistry · 2026Review
- Review
- Multiscale modeling reveals synergy between CCL19 and PD-1 blockade in reshaping the TNBC microenvironment.NPJ systems biology and applications · 2026Article
- Immunotherapy rechallenge after progression in non-small cell lung cancer: A systematic review and network meta-analysis.iScience · 2026Article
- BRD4 inhibition leads to MDSC apoptosis and enhances checkpoint blockade therapy.The Journal of clinical investigation · 2025Article
- A Systematic Computational Framework for Practical Identifiability Analysis in Mathematical Models Arising from Biology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Modeling combination chemo-immunotherapy for heterogeneous tumors.Quantitative biology (Beijing, China) · 2025Article
- Multiscale mathematical model-informed reinforcement learning optimizes combination treatment scheduling in glioblastoma evolution.Science advances · 2025Article
- Article
- Quantitative cancer-immunity cycle modeling for predicting disease progression in advanced metastatic colorectal cancer.NPJ systems biology and applications · 2025Article
- Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Mathematical models of intercellular signaling in breast cancer.Seminars in cancer biology · 2025Review
- Mathematical model of tumor immune microenvironment with application to the combined therapy targeting the PD-1/PD-L1 pathway and IL-10 cytokine antibody.Theory in biosciences = Theorie in den Biowissenschaften · 2025Article
- Bromodomain and extra-terminal proteins in solid tumors: regulators of immune microenvironment and emerging therapeutic targets.Frontiers in immunology · 2025Review
- Alterations of ceramide synthesis induce PD-L1 internalization and signaling to regulate tumor metastasis and immunotherapy response.Cell reports · 2024Article
- Modeling of Mouse Experiments Suggests that Optimal Anti-Hormonal Treatment for Breast Cancer is Diet-Dependent.Bulletin of mathematical biology · 2024Article
- Polydopamine-Based Nanoparticles for Synergistic Chemotherapy of Prostate Cancer.International journal of nanomedicine · 2024Article
- Global stability and parameter analysis reinforce therapeutic targets of PD-L1-PD-1 and MDSCs for glioblastoma.Journal of mathematical biology · 2023Article
- Bromodomain and extraterminal (BET) proteins: biological functions, diseases, and targeted therapy.Signal transduction and targeted therapy · 2023Review
- BET in hematologic tumors: Immunity, pathogenesis, clinical trials and drug combinations.Genes & diseases · 2023Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
CTLA-4 is an immune checkpoint expressed on active anticancer T cells. When it combines with its ligand B7 on dendritic cells, it inhibits the activity of the T cells. The Bromo- and Extra-Terminal (BET) protein family includes proteins that regulate the expression of key oncogenes and antiapoptotic proteins. BET inhibitor (BETi) has been shown to reduce the expression of MYC by suppressing its transcription factors and to down-regulate the hypoxic transcriptome response to VEGF-A. This paper develops a mathematical model of the treatment of cancer by combination therapy of BETi and CTLA-4 inhibitor. The model shows that the two drugs are positively correlated in the sense that the tumor volume decreases as the dose of each of the drugs is increased. The model also considers the effect of the combined therapy on levels of myeloid-derived suppressor cells (MDSCs) and the overexpression of TNF-α, which may predict gastrointestinal side effects of the combination.
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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.