Evidence map›Paper›PMID 25920609›Full record

ArticleMedical oncology (Northwood, London, England)2015

Cancer-associated fibroblast-derived CXCL12 causes tumor progression in adenocarcinoma of the esophagogastric junction.

Hidetaka Sugihara, Takatsugu Ishimoto, Tadahito Yasuda, Daisuke Izumi, Kojiro Eto, Hiroshi Sawayama, Keisuke Miyake, Junji Kurashige, Yu Imamura, Yukiharu Hiyoshi and 9 more

Abstract read
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In one paragraph

Article in Medical oncology (Northwood, London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  6. Article
  7. Review
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  15. Article
  16. Hypoxia and the phenomenon of immune exclusion.Journal of translational medicine · 2021
    Review
  17. Article
  18. Frontiers in immunology · 2021
    Review
  19. Chemokines and their receptors as biomarkers in esophageal cancer.Esophagus : official journal of the Japan Esophageal Society · 2020
    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

19 authors at 3 institutions in 2 countries.

Hidetaka SugiharaDepartment of Gastroenterological Surgery, Graduate School of Medical Science, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto, 860-8556, Japan.
Takatsugu Ishimoto
Tadahito Yasuda
Daisuke Izumi
Kojiro Eto
Hiroshi Sawayama
Keisuke Miyake
Junji Kurashige
Yu Imamura
Yukiharu Hiyoshi
Masaaki Iwatsuki
Shiro Iwagami
Yoshifumi Baba
Yasuo Sakamoto
Yuji Miyamoto
Naoya Yoshida
Masayuki Watanabe
Hiroshi Takamori
Hideo Baba
Kumamoto University · JPSaiseikai Kumamoto Hospital · JPDuke-NUS Medical School · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although cancer-associated fibroblasts (CAFs) mainly produce CXCL12 and stimulate CXCL12/CXCR4 signaling in cancer cells, the significance of this interaction in adenocarcinoma of the esophagogastric junction (AEG) was unclear. This study investigated the functional characteristics of CAF-derived CXCL12 in AEG. Immunohistochemical staining for CXCL12 was performed on sections from 123 AEG patients and analyzed against clinicopathological data. Newly isolated CAFs and normal fibroblasts were examined for phenotype. An invasion assay was performed with AEG cells co-cultured with CAFs isolated from AEG. CXCL12 expression was significantly associated with age, depth of invasion, lymphatic invasion, and lymph node metastases. High CXCL12 expression significantly correlated with poor prognosis. Isolated CAFs had abundant α-smooth muscle actin expression and showed various CXCL12 expression patterns. Notably, AEG cells co-cultured with CXCL(high)-expressing CAFs invaded more than when co-cultured with CXCL(low)-expressing CAFs; these invasive properties were impeded by CXCR4 antagonist AMD3100. We demonstrated that AEG cells co-cultured with CXCL12(high) CAFs were significantly more invasive than those co-cultured with CXCL12(low) CAFs and that high CXCL12 expression correlates with poor prognosis in AEG patients. CXCL12 derived from CAFs in tumor microenvironment stimulates CXCL12/CXCR4 signaling in AEG cells and promotes their invasive ability, resulting in tumor progression.

Indexed as

AdenocarcinomaAgedBiomarkers, TumorCell Line, TumorCell MovementChemokine CXCL12Disease ProgressionEsophagogastric JunctionFemaleFibroblastsHumansLymphatic MetastasisMaleNeoplasm InvasivenessPrognosisReceptors, CXCR4Biomarkers, TumorChemokine CXCL12CXCL12 protein, humanReceptors, CXCR4

Identifiers

PMID25920609
OpenAlexW2007208173

What OpenQuestion holds

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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.