Evidence map›Paper›PMID 35383278›Full record

ReviewBritish journal of cancer2022

The STING pathway: Therapeutic vulnerabilities in ovarian cancer.

Noor Shakfa, Deyang Li, Sarah Nersesian, Juliette Wilson-Sanchez, Madhuri Koti

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in British journal of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  16. Review
  17. Review
  18. Heterogeneity and treatment landscape of ovarian carcinoma.Nature reviews. Clinical oncology · 2023
    Review
  19. Chromosomal instability and inflammation: a catch-22 for cancer cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023
    Review
  20. Article
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

5 authors at 2 institutions in 1 country.

Noor ShakfaDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada.
Deyang LiDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada.
Sarah NersesianDepartment of Microbiology and Immunology, Dalhousie University, Halifax, NS, Canada.
Juliette Wilson-SanchezDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada.
Madhuri KotiDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada. kotim@queensu.ca.ORCID http://orcid.org/0000-0003-1490-2577
Queen's University · CADalhousie University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer is the leading cause of mortality due to gynecologic malignancy. The majority of women diagnosed with the most common subtype, high-grade serous ovarian carcinoma (HGSC), develop resistance to conventional therapies despite initial response to treatment. HGSC tumors displaying DNA damage repair (DDR) gene deficiency and high chromosomal instability mainly associate with higher cytotoxic immune cell infiltration and expression of genes associated with these immune pathways. Despite the high level of immune infiltration observed, the majority of patients with HGSC have not benefited from immunomodulatory treatments as the mechanistic basis of this infiltration is unclear. This lack of response can be primarily attributed to heterogeneity at the levels of both cancer cell genetic alterations and the tumour immune microenvironment. Strategies to enhance anti-tumour immunity have been investigated in ovarian cancer, of which interferon activating therapies present as an attractive option. Of the several type I interferon (IFN-1) stimulating therapies, exogenously activating the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway is emerging as a promising avenue. Herein, we highlight our current understanding of how constitutive and induced cGAS-STING pathway activation influences the ovarian tumour microenvironment. We further elaborate on the links between the genomic alterations prevalent in ovarian tumours and how the resultant immune phenotypes can make them more susceptible to exogenous STING pathway activation and potentiate immune-mediated killing of cancer cells. The therapeutic potential of cGAS-STING pathway activation in ovarian cancer and factors implicating treatment outcomes are discussed, providing a rationale for future combinatorial treatment approaches on the backbone of chemotherapy.

Indexed as

Interferon Type IOvarian NeoplasmsCarcinoma, Ovarian EpithelialFemaleHumansMembrane ProteinsNucleotidyltransferasesSignal TransductionSTING ProteinTumor MicroenvironmentInterferon Type IMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING Protein

Identifiers

PMID35383278
PMCPMC9381712
OpenAlexW4226025919

What OpenQuestion holds

Textmetadata
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.