Evidence map›Paper›PMID 24421843›Full record

ArticleKorean journal of pathology2013

Endogenous gastric-resident mesenchymal stem cells contribute to formation of cancer stroma and progression of gastric cancer.

Eun-Kyung Kim, Hye-Jung Kim, Young-Il Yang, Jong Tae Kim, Min-Young Choi, Chang Soo Choi, Kwang-Hee Kim, Jeong-Han Lee, Won-Hee Jang, Soon-Ho Cheong

Abstract read
In one paragraph

Article in Korean journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
–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

18 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

10 authors.

Eun-Kyung KimDepartment of Pathology, Inje University School of Medicine, Busan, Korea.
Hye-Jung KimDepartment of Pathology, Inje University School of Medicine, Busan, Korea.
Young-Il YangDepartment of Pathology, Inje University School of Medicine, Busan, Korea. ; Paik Institute for Clinical Research, Inje University School of Medicine, Busan, Korea.
Jong Tae KimPaik Institute for Clinical Research, Inje University School of Medicine, Busan, Korea.
Min-Young ChoiPaik Institute for Clinical Research, Inje University School of Medicine, Busan, Korea.
Chang Soo ChoiDepartment of Surgery, Inje University School of Medicine, Busan, Korea.
Kwang-Hee KimDepartment of Surgery, Inje University School of Medicine, Busan, Korea.
Jeong-Han LeePaik Institute for Clinical Research, Inje University School of Medicine, Busan, Korea. ; Department of Anesthesiology, Inje University School of Medicine, Busan, Korea.
Won-Hee JangPaik Institute for Clinical Research, Inje University School of Medicine, Busan, Korea.
Soon-Ho CheongPaik Institute for Clinical Research, Inje University School of Medicine, Busan, Korea. ; Department of Anesthesiology, Inje University School of Medicine, Busan, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCarcinoma-associated fibroblasts (CAFs) contribute to carcinogenesis and cancer progression, although their origin and role remain unclear. We recently identified and investigated the in situ identity and implications of gastric submucosa-resident mesenchymal stem cells (GS-MSCs) in the progression of gastric carcinogenesis.

methodsWe isolated GS-MSCs from gastric submucosa using hydrogel-supported organ culture and defined their identity. Isolated cells were assessed in vitro by immunophenotype and mesengenic multipotency. Reciprocal interactions between GS-MSCs and gastric cancer cells were evaluated. To determine the role of GS-MSCs, xenografts were constructed of gastric cancer cells admixed with or without GS-MSCs.

resultsIsolated cells fulfilled MSCs requirements in regard to plastic adherence, stromal cell immunophenotype, and multipotency. We demonstrated a paracrine loop that gastric cancer cells enhanced the migration, proliferation, and differentiation of GS-MSCs; additionally, GS-MSCs promoted the proliferation of gastric cancer cell in vitro. Xenograft experiments showed that GS-MSCs significantly promoted cancer growth and angiogenesis. GS-MSCs that integrated into gastric cancer became not only CAFs but also rarely endothelial cells which contributed to the formation of cellular and vascular cancer stroma.

conclusionsEndogenous GS-MSCs play an important role in gastric cancer progression.

Indexed as

Cancer stromaCarcinoma-associated fibroblastGastric-resident mesenchymal stem cellStomach neoplasms

Identifiers

PMID24421843
PMCPMC3887152

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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.