Evidence map›Paper›PMID 39967410›Full record

ArticleCancer medicine2025

Prognostic Impact of Stimulator of Interferon Genes Expression in Triple Negative Breast Cancer.

Tetsuyo Maeda, Makiko Ono, Tomo Osako, Tomohiro Chiba, Satoko Baba, Asumi Iesato, Yukinori Ozaki, Yuka Inoue, Natsue Uehiro, Yoko Takahashi and 6 more

Abstract read
In one paragraph

Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Tetsuyo MaedaBreast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Makiko OnoDepartment of Medical Oncology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Tomo OsakoDepartment of Pathology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Tomohiro ChibaDepartment of Pathology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Satoko BabaDepartment of Pathology, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Asumi IesatoBreast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Yukinori OzakiBreast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Yuka InoueBreast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Natsue UehiroBreast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Yoko TakahashiBreast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Takayuki KobayashiBreast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Takahiro KogawaDepartment of Advanced Medical Development, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Tomohiko OhtaDivision of Breast and Endocrine Surgery, St Marianna University School of Medicine, Kawasaki, Japan.
Shigehisa KitanoDepartment of Advanced Medical Development, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.
Takayuki UenoBreast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.ORCID https://orcid.org/0000-0002-9080-9377
Shinji OhnoBreast Oncology Center, Cancer Institute Hospital, Japanese Foundation for Cancer Research, Tokyo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPatients with triple negative breast cancer (TNBC) who have a poor response to neoadjuvant chemotherapy (NAC) have worse survival and new treatment strategies need to be developed. TNBC is considered a subtype in which the cyclic GMP-AMP synthase (cGAS) is linked to the stimulator of interferon genes (STING) pathway, an innate immune response that recognizes cytosolic nucleic acid components, is activated when DNA damage occurs, and is attracting attention as a new therapeutic target.

methodsPatients with TNBC who underwent surgery following NAC and for whom pre- and post-treatment tissue specimens were available were enrolled in this study. To examine the association of STING expression with immune profiles and prognosis, STING, cGAS, CD8, and programmed cell death ligand 1 (PD-L1) expressions in tumor cells (TCs) and immune cells (ICs), and tumor infiltrating lymphocytes (TILs) were assessed using immunohistochemistry of specimens obtained at pre-treatment and at surgery.

resultsNinety-one cases were eligible, of which 68 cases were evaluable and included in the analysis. The high STING expression at baseline was marginally correlated with TILs, but not with CD8

conclusionTNBCs with sustained high STING expression following NAC demonstrated a poor prognosis and will be a target for new treatment strategies.

Indexed as

Biomarkers, TumorMembrane ProteinsTriple Negative Breast NeoplasmsAdultAgedB7-H1 AntigenCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseFemaleHumansLymphocytes, Tumor-InfiltratingMiddle AgedNeoadjuvant TherapyNucleotidyltransferasesPrognosisSTING ProteinB7-H1 AntigenBiomarkers, TumorCD274 protein, humancGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING Proteinchanges in STING expressionNACprognosisSTINGTNBC

Identifiers

PMID39967410
PMCPMC11836529

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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.