Evidence map›Paper›PMID 40632203›Full record

ArticleAnnals of surgical oncology2025

Intratumoral Lipopolysaccharide Positivity Related to Tumor-Associated Macrophage Infiltration and Poor Prognosis in Esophageal Squamous Cell Carcinoma.

Shintaro Uchida, Takehiko Yokobori, Kota Yanagisawa, Bilguun Erkhem-Ochir, Gendensuren Dorjkhorloo, Haruka Okami, Chika Katayama, Yuta Shibasaki, Nobuhiro Nakazawa, Chika Komine and 9 more

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Article in Annals of surgical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
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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

19 authors.

Shintaro UchidaDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Takehiko YokoboriDivision of Gene Therapy Science, Gunma University, Initiative for Advanced Research (GIAR), Maebashi, Gunma, Japan. bori45@gunma-u.ac.jp.ORCID http://orcid.org/0000-0003-3284-4796
Kota YanagisawaLaboratory for Mucosal Ecosystem Design, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.
Bilguun Erkhem-OchirDivision of Gene Therapy Science, Gunma University, Initiative for Advanced Research (GIAR), Maebashi, Gunma, Japan.
Gendensuren DorjkhorlooDivision of Gene Therapy Science, Gunma University, Initiative for Advanced Research (GIAR), Maebashi, Gunma, Japan.
Haruka OkamiDivision of Gene Therapy Science, Gunma University, Initiative for Advanced Research (GIAR), Maebashi, Gunma, Japan.
Chika KatayamaDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Yuta ShibasakiDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Nobuhiro NakazawaDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Chika KomineDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Takuya ShiraishiDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Takuhisa OkadaDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Katsuya OsoneDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Akiharu KimuraDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Akihiko SanoDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Makoto SakaiDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Nobuo SasakiLaboratory for Mucosal Ecosystem Design, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma, Japan.
Ken ShirabeDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Hiroshi SaekiDepartment of General Surgical Science, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.

Funding

Makoto Sakai 22K08766Makoto Sohda 23K08147
6 · The paper itself

Abstract

backgroundPrognosis in esophageal squamous cell carcinoma (ESCC) is influenced by the tumor microenvironment, where CD163-positive M2-like tumor-associated macrophages promote immune suppression and tumor progression. Lipopolysaccharide (LPS), markers of intratumoral microbiota, activate nuclear factor-kappa B (NF-κB) signaling and inflammation. Inflammation-based prognostic scores, such as the lymphocyte-to-monocyte ratio (LMR), are poor prognostic factors in various types of cancers. This study evaluated the impact of intratumoral LPS on systemic inflammation and the tumor microenvironment in ESCC.

methodsSurgical specimens from 134 patients with ESCC were analyzed. Immunohistochemical staining was performed to evaluate intratumoral LPS positivity and its associations with clinicopathological factors, prognosis, inflammation-based prognostic scores, including LMR, CD163-positive TAM infiltration, and nuclear NF-κB expression, and tumoral vimentin expression as an epithelial-mesenchymal transition/mesenchymal marker in patients with ESCC.

resultsLPS was identified in ESCC cell nuclei and cytoplasm. High intratumoral LPS positivity was associated with N factor progression, high NF-κB nuclear positivity, low LMR, and high stromal CD163-positive TAM infiltration, and it served as an independent poor prognostic factor. Lipopolysaccharide positivity was significantly related to poor prognosis in CD163-positive TAM cases, compared with LPS negativity.

conclusionsDetection of LPS in resected ESCC tissues could be a reliable biomarker for identifying high-risk patients with aggressive tumor characteristics, systemic inflammation, and impaired tumor immunity.

Indexed as

Biomarkers, TumorCarcinoma, Squamous CellEsophageal NeoplasmsLipopolysaccharidesTumor-Associated MacrophagesTumor MicroenvironmentAgedAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenEpithelial-Mesenchymal TransitionEsophageal Squamous Cell CarcinomaFemaleFollow-Up StudiesHumansMaleAntigens, CDAntigens, Differentiation, MyelomonocyticBiomarkers, TumorCD163 AntigenLipopolysaccharidesNF-kappa BReceptors, Cell SurfaceEsophageal squamous cell carcinomaIntratumoral microbiotaLipopolysaccharideTumor-associated macrophageTumor microenvironment

Identifiers

PMID40632203

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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.