ArticleCell reports2017
BET-Bromodomain Inhibitors Engage the Host Immune System and Regulate Expression of the Immune Checkpoint Ligand PD-L1.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
197 citing papers in PubMed, 1 synthesis or guideline pooled it, 296 citations in OpenAlex.
- PD-1/PD-L1 immune checkpoint blockade in breast cancer: research insights and sensitization strategies.Molecular cancer · 2024Pooled it
- Pleiotropic effects of BET inhibition broadly boost tumor immunogenicity to CD8Oncoimmunology · 2026Article
- BET Inhibition Synergizes with RLR Signaling to Enhance Tumor Immunogenicity and T-cell Recognition.Cancer immunology research · 2026Article
- In Situ Bioorthogonal Synthesis of PROTACs via Dual-Responsive Cleavage for Synergistic Photo-Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Bridging BET bromodomain and immune checkpoint inhibitors through generative bioorganic frameworks for next-generation cancer immunotherapy.RSC medicinal chemistry · 2026Review
- Review
- Regulation of immune checkpoint molecules in cancer immune evasion and therapy.Nature reviews. Cancer · 2026Review
- Self-assembled nano-PROTACs potentiate colorectal cancer immunotherapy via downregulating PD-L1 and GPX4 expression.Materials today. Bio · 2026Article
- Cancer stem cell plasticity: mechanisms, immune microenvironment crosstalk, and therapeutic implications.Journal of hematology & oncology · 2026Review
- Insight of immune checkpoint blockades in melanoma: mechanism and clinical translation.Molecular cancer · 2026Review
- Bi-directional regulation between NAD/NAMPT and IFN-γ/PD-L1 axes via BRD4/IRF1 and mitochondrial respiration in metastatic cutaneous melanoma.Journal of experimental & clinical cancer research : CR · 2026Article
- Breast cancer immunotherapy: mechanisms of immune evasion, biomarkers, and emerging therapeutic strategies.Molecular cancer · 2026Review
- International guidelines on the diagnosis and treatment of NUT carcinoma.Innovation (Cambridge (Mass.)) · 2026Review
- Overcoming immunotherapy barriers in pediatric brain tumors: epigenetic strategies.Frontiers in oncology · 2026Review
- Epigenetic Modulators and Immunotherapy in Malignant Melanoma.Oncology research · 2026Review
- BET Protein Degrader ZBC260 Induces Tumor Vascular Reprogramming Through Endothelial Cell Remodeling.Breast cancer (Dove Medical Press) · 2026Article
- Towards epigenetically informed and biobank-driven precision immunotherapy in melanoma.Frontiers in immunology · 2026Review
- Epigenetic drugs in cancer therapy: mechanisms, immune modulation, and therapeutic applications.Molecular biomedicine · 2025Review
- Hypoxia-activated paclitaxel prodrugs enable PD-L1 degradation to potentiate cancer chemo-immunotherapy.Journal of nanobiotechnology · 2025Article
- BRD4 inhibition leads to MDSC apoptosis and enhances checkpoint blockade therapy.The Journal of clinical investigation · 2025Article
137 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
18 authors at 9 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BET inhibitors (BETi) target bromodomain-containing proteins and are currently being evaluated as anti-cancer agents. We find that maximal therapeutic effects of BETi in a Myc-driven B cell lymphoma model required an intact host immune system. Genome-wide analysis of the BETi-induced transcriptional response identified the immune checkpoint ligand Cd274 (Pd-l1) as a Myc-independent, BETi target-gene. BETi directly repressed constitutively expressed and interferon-gamma (IFN-γ) induced CD274 expression across different human and mouse tumor cell lines and primary patient samples. Mechanistically, BETi decreased Brd4 occupancy at the Cd274 locus without any change in Myc occupancy, resulting in transcriptional pausing and rapid loss of Cd274 mRNA production. Finally, targeted inhibition of the PD-1/PD-L1 axis by combining anti-PD-1 antibodies and the BETi JQ1 caused synergistic responses in mice bearing Myc-driven lymphomas. Our data uncover an interaction between BETi and the PD-1/PD-L1 immune-checkpoint and provide mechanistic insight into the transcriptional regulation of CD274.
Indexed as
Identifiers
What OpenQuestion holds
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.