ArticleNature communications2025
Reprogramming the tumor microenvironment with c-MYC-based gene circuit platform to enhance specific cancer immunotherapy.
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 9 papers.
What it found
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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.
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Who cites it
9 citing papers in PubMed.
- Immunotherapy 3.0: Breakthroughs Steering the Next Generation of Cancer Control.Cancer reports (Hoboken, N.J.) · 2026Review
- Targeting TPX2-dependent lineage plasticity by CDK4/6 inhibition reverses therapy resistance in neuroendocrine bladder carcinoma.Cell reports. Medicine · 2026Article
- Article
- Nuclear hexokinase 2 couples hyperglycemia to MYC-driven glycolytic and stemness programs in bladder cancer.Cell death & disease · 2026Article
- Miniature and versatile genome regulation TnpB-ωRNA toolkits facilitate cancer immunotherapy.Nature communications · 2026Article
- A smart gene circuit for precise regulation of tumor cell behavior.Synthetic and systems biotechnology · 2026Article
- Polyarginine Peptide R11-Actin Interaction Induces a Domino Effect on Cytoskeleton Remodeling to Suppress Bladder Cancer Metastasis.Research (Washington, D.C.) · 2026Article
- Field cancerization in urothelial carcinoma: molecular alterations and clinical implications.Journal of Cancer · 2026Review
- The international and domestic research trends of targeted therapy in bladder cancer: a bibliometric analysis of the past three decades.Frontiers in oncology · 2026Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intratumor heterogeneity (ITH) is associated with anti-tumoral immune response and with the efficiency of cancer immunotherapy, yet overcoming ITH remains a significant challenge. Notably, cellular MYC (c-MYC) has been shown to be a pivotal orchestrator of this ITH progression. Here, we develop a c-MYC-based sensing circuit (cMSC) that is activated exclusively by aberrant c-MYC levels, along with an exosome-based cell-to-cell (CtC) system that augments communication among tumor cells, effectively targeting all cells in tumors circumventing the limitations imposed by ITH. Further expression of multifunctional immunostimulatory agents in these cMSC-reprogrammed cancer cells remodels the tumor microenvironment, enhancing selective T-cell-mediated oncolysis. Our cMSC/CtC platform specifically senses aberrant c-MYC expression and subsequently triggers a robust cancer immunotherapeutic response. These findings offer a promising avenue for targeting cancers via precisely sensing c-MYC, overcoming the limitations of ITH.
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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.