ArticleNature medicine2016
Eradication of large established tumors in mice by combination immunotherapy that engages innate and adaptive immune responses.
Article in Nature medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 342 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
342 citing papers in PubMed, 1 synthesis or guideline pooled it, 529 citations in OpenAlex.
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- Intratumoral TIGIT blockade augments antitumor responses and bypasses increased functionality of peripheral TIGIT+ NK cells in mouse and human models of bone and soft tissue sarcoma.Journal for immunotherapy of cancer · 2026Article
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- Reversing enhancer RNA-mediated IKBKE gene repression enables synthetic anticancer immunity in prostate cancer models.The Journal of clinical investigation · 2026Article
- PD-1 suppresses CAR signaling by forming the inhibitory signalosome colocalizing to CAR microclusters.Communications biology · 2026Article
- Research Progress of Nanodelivery Platforms in the Diagnosis and Treatment of Esophageal Cancer.International journal of nanomedicine · 2026Review
- Humanization of Drug Metabolism in theACS infectious diseases · 2025Article
- A versatile silica nanoparticle platform for induction of T cell responses - applied for therapeutic vaccination against HPV16 E6/E7-positive tumors in MHC-humanized mice.Oncoimmunology · 2025Article
282 more citing papers are in PubMed but not listed here.
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Authors and funding
22 authors at 5 institutions in 1 country.
Funding
Abstract
Checkpoint blockade with antibodies specific for cytotoxic T lymphocyte-associated protein (CTLA)-4 or programmed cell death 1 (PDCD1; also known as PD-1) elicits durable tumor regression in metastatic cancer, but these dramatic responses are confined to a minority of patients. This suboptimal outcome is probably due in part to the complex network of immunosuppressive pathways present in advanced tumors, which are unlikely to be overcome by intervention at a single signaling checkpoint. Here we describe a combination immunotherapy that recruits a variety of innate and adaptive immune cells to eliminate large tumor burdens in syngeneic tumor models and a genetically engineered mouse model of melanoma; to our knowledge tumors of this size have not previously been curable by treatments relying on endogenous immunity. Maximal antitumor efficacy required four components: a tumor-antigen-targeting antibody, a recombinant interleukin-2 with an extended half-life, anti-PD-1 and a powerful T cell vaccine. Depletion experiments revealed that CD8
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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.