ArticleThe Journal of clinical investigation2018
Dinaciclib induces immunogenic cell death and enhances anti-PD1-mediated tumor suppression.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
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Who cites it
120 citing papers in PubMed.
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- Lenalidomide promotes melarsoprol-activated cGAS-STING-mediated immunotherapy for hepatocellular carcinomaFundamental research · 2025Article
- Targeting KIF18A triggers antitumor immunity and enhances efficiency of PD-1 blockade in colorectal cancer with chromosomal instability phenotype.Cell death discovery · 2025Article
- Metabolic Inhibition Induces Pyroptosis in Uveal Melanoma.Molecular cancer research : MCR · 2025Article
- The CDK12-BRCA1 signaling axis mediates dinaciclib-associated radiosensitivity through p53-mediated cellular senescence.Molecular oncology · 2025Article
- Establishing a cryopreserved biobank of living tumor tissues for drug sensitivity testing.Bioactive materials · 2025Article
- Oxygen-delivery nanoparticles enhanced immunotherapy efficacy monitored by granzyme B PET imaging in malignant tumors.Journal of nanobiotechnology · 2025Article
- Targeting the mevalonate pathway potentiates NUAK1 inhibition-induced immunogenic cell death and antitumor immunity.Cell reports. Medicine · 2025Article
60 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blockade of the checkpoint inhibitor programmed death 1 (PD1) has demonstrated remarkable success in the clinic for the treatment of cancer; however, a majority of tumors are resistant to anti-PD1 monotherapy. Numerous ongoing clinical combination therapy studies will likely reveal additional therapeutics that complement anti-PD1 blockade. Recent studies found that immunogenic cell death (ICD) improves T cell responses against different tumors, thus indicating that ICD may further augment antitumor immunity elicited by anti-PD1. Here, we observed antitumor activity following combinatorial therapy with anti-PD1 Ab and the cyclin-dependent kinase inhibitor dinaciclib in immunocompetent mouse tumor models. Dinaciclib induced a type I IFN gene signature within the tumor, leading us to hypothesize that dinaciclib potentiates the effects of anti-PD1 by eliciting ICD. Indeed, tumor cells treated with dinaciclib showed the hallmarks of ICD including surface calreticulin expression and release of high mobility group box 1 (HMGB1) and ATP. Mice treated with both anti-PD1 and dinaciclib showed increased T cell infiltration and DC activation within the tumor, indicating that this combination improves the overall quality of the immune response generated. These findings identify a potential mechanism for the observed benefit of combining dinaciclib and anti-PD1, in which dinaciclib induces ICD, thereby converting the tumor cell into an endogenous vaccine and boosting the effects of anti-PD1.
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