Evidence map›Paper›PMID 33081170›Full record

ReviewJournal of clinical medicine2020

Challenges and Opportunities in the Clinical Development of STING Agonists for Cancer Immunotherapy.

Leila Motedayen Aval, James E Pease, Rohini Sharma, David J Pinato

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed
10.1field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

132 citing papers in PubMed, 228 citations in OpenAlex.

  1. Review
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  12. Albumin-Bound STING Agonist Reprograms HSPCs to Antitumor Neutrophils Enhancing CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  13. Review
  14. Article
  15. Article
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  19. Controlled delivery of STING agonist and manganese ion in injectable PLGA implants for enhanced cancer immunotherapy.Journal of controlled release : official journal of the Controlled Release Society · 2026
    Article
  20. Article

72 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Leila Motedayen AvalDepartment of Surgery & Cancer, Imperial College London, Hammersmith Hospital, Du Cane Road, London W120HS, UK.
James E PeaseInflammation, Repair & Development, National Heart & Lung Institute, Imperial College London, London SW7 2AZ, UK.
Rohini SharmaDepartment of Surgery & Cancer, Imperial College London, Hammersmith Hospital, Du Cane Road, London W120HS, UK.
David J PinatoDepartment of Surgery & Cancer, Imperial College London, Hammersmith Hospital, Du Cane Road, London W120HS, UK.
Hammersmith Hospital · GBImperial College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune checkpoint inhibitors (ICI) have revolutionised cancer therapy. However, they have been effective in only a small subset of patients and a principal mechanism underlying immune-refractoriness is a 'cold' tumour microenvironment, that is, lack of a T-cell-rich, spontaneously inflamed phenotype. As such, there is a demand to develop strategies to transform the tumour milieu of non-responsive patients to one supporting T-cell-based inflammation. The cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon genes (cGAS-STING) pathway is a fundamental regulator of innate immune sensing of cancer, with potential to enhance tumour rejection through the induction of a pro-inflammatory response dominated by Type I interferons. Recognition of these positive immune-modulatory properties has rapidly elevated the STING pathway as a putative target for immunotherapy, leading to a myriad of preclinical and clinical studies assessing natural and synthetic cyclic dinucleotides and non-nucleotidyl STING agonists. Despite pre-clinical evidence of efficacy, clinical translation has resulted into disappointingly modest efficacy. Poor pharmacokinetic and physiochemical properties of cyclic dinucleotides are key barriers to the development of STING agonists, most of which require intra-tumoral dosing. Development of systemically administered non-nucleotidyl STING agonists, or conjugation with liposomes, polymers and hydrogels may overcome pharmacokinetic limitations and improve drug delivery. In this review, we summarise the body of evidence supporting a synergistic role of STING agonists with currently approved ICI therapies and discuss whether, despite the numerous obstacles encountered to date, the clinical development of STING agonist as novel anti-cancer therapeutics may still hold the promise of broadening the reach of cancer immunotherapy.

Indexed as

cGAScyclic dinucleotides (CDNs)drug delivery systems (DDS)immune checkpoint inhibitors (ICI)immune therapysmall molecule agonistSTINGSTING agonists

Identifiers

PMID33081170
PMCPMC7602874
OpenAlexW3093056664

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.