Evidence map›Paper›PMID 40963562›Full record

ArticleFrontiers in medicine2025

Malignant epithelia cells-derived spermine induces APOE+ macrophages to suppress tumor immunity in adenocarcinoma of the esophagogastric junction.

Yan Zhang, Zhaoyang Liu, Huihui Sun, Zhenxiang Wang, Ye Chen, Zhiqian Hu, Xinxing Li, Kai Xu, Ying Chen, Yanping Xu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in medicine, 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. Article
  2. Review
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

12 authors.

Yan Zhang *Department of Gastroenterology, Tongji Institute of Digestive Disease, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Zhaoyang Liu *Key Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Department of Orthopedics, Tongji Hospital, School of Life Science and Technology, Tongji University, Shanghai, China.
Huihui Sun *Department of Gastroenterology, Tongji Institute of Digestive Disease, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Zhenxiang WangDepartment of Gastroenterology, Tongji Institute of Digestive Disease, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Ye ChenDepartment of Gastroenterology, Tongji Institute of Digestive Disease, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Zhiqian HuDepartment of General Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Xinxing LiDepartment of General Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Kai XuDepartment of General Surgery, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Ying ChenDepartment of Gastroenterology, Tongji Institute of Digestive Disease, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Yanping XuTongji Hospital, Shanghai Key Laboratory of Signaling and Disease Research, Frontier Science Center for Stem Cell Research, School of Life Sciences and Technology, Tongji University, Shanghai, China.
Chenfei WangKey Laboratory of Spine and Spinal Cord Injury Repair and Regeneration of Ministry of Education, Department of Orthopedics, Tongji Hospital, School of Life Science and Technology, Tongji University, Shanghai, China.
Shuchang XuDepartment of Gastroenterology, Tongji Institute of Digestive Disease, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Adenocarcinoma of the esophagogastric junction (AEG) is increasingly recognized as a distinct gastrointestinal tumor type with a poor prognosis. However, the mechanisms driving AEG progression, particularly the interplay between metabolic reprogramming and the immune microenvironment, remain poorly understood. Methods: We integrated multi-omics to profile the tumor microenvironment and metabolic reprogramming of AEG. Tumor tissues and paired normal adjacent tissues from AEG patients were subjected to single-cell RNA sequencing ( Results: Our analysis revealed an AEG-specific malignant subtype originating from the esophagogastric junction, characterized by heightened proliferation and poor differentiation. These malignant cells exhibited metabolic reprogramming marked by hyperactivation of the glutamine-arginine-spermine axis with concomitant spermine accumulation. Spermine was found to drive the polarization of tumor-associated macrophages into an APOE Conclusion: This study identified AEG-like malignant cells as a high-risk subtype, revealed the metabolic-immune crosstalk driven by the spermine-STAT3-APOE axis in AEG progression, and provided potential targets for AEG metabolic intervention and immunotherapy.

Indexed as

adenocarcinoma of the esophagogastric junctioncancer metabolismsingle-cell RNA sequencingspatial transcriptomicstumor microenvironment

Identifiers

PMID40963562
PMCPMC12436273

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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.