Evidence map›Paper›PMID 22610072›Full record

ArticleCarcinogenesis2012

Release of TGFβig-h3 by gastric myofibroblasts slows tumor growth and is decreased with cancer progression.

Chris Holmberg, Michael Quante, Islay Steele, Jothi Dinesh Kumar, Silviya Balabanova, Cedric Duval, Matyas Czepan, Zoltan Rakonczay, Laszlo Tiszlavicz, Istvan Nemeth and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 38 citations in OpenAlex.

  1. Cancer-associated fibroblasts influence Wnt/PCP signaling in gastric cancer cells by cytoneme-based dissemination of ROR2.Proceedings of the National Academy of Sciences of the United States of America · 2023
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  17. Distinct miRNA profiles in normal and gastric cancer myofibroblasts and significance in Wnt signaling.American journal of physiology. Gastrointestinal and liver physiology · 2016
    Article
  18. Cancer-associated fibroblasts promote angiogenesis in gastric cancer through galectin-1 expression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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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

17 authors at 5 institutions in 4 countries.

Chris HolmbergDepartment of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, Liverpool, UK.
Michael Quante
Islay Steele
Jothi Dinesh Kumar
Silviya Balabanova
Cedric Duval
Matyas Czepan
Zoltan Rakonczay
Laszlo Tiszlavicz
Istvan Nemeth
Gyorgy Lazar
Zsolt Simonka
Rosalind Jenkins
Peter Hegyi
Timothy C Wang
Graham J Dockray
Andrea Varro
University of Liverpool · GBHealth First · USUniversity of Szeged · HUColumbia University · USKlinikum rechts der Isar · DE

Funding

The Role of Inflammation and Stroma in Digestive CancerU54CA126513 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TYCKO, BENJAMIN · 2006 to 2010
$5.1M
NCI NIH HHS 5 U54 CA126513-04/1NCI NIH HHS U54 CA126513
6 · The paper itself

Abstract

Tumor progression has been linked to changes in the stromal environment. Myofibroblasts are stromal cells that are often increased in tumors but their contribution to cancer progression is not well understood. Here, we show that the secretomes of myofibroblasts derived from gastric cancers [cancer-associated myofibroblasts (CAMs)] differ in a functionally significant manner from those derived from adjacent tissue [adjacent tissue myofibroblasts (ATMs)]. CAMs showed increased rates of migration and proliferation compared with ATMs or normal tissue myofibroblasts (NTMs). Moreover, conditioned medium (CM) from CAMs significantly stimulated migration, invasion and proliferation of gastric cancer cells compared with CM from ATMs or NTMs. Proteomic analysis of myofibroblast secretomes revealed decreased abundance of the extracellular matrix (ECM) adaptor protein like transforming growth factor-β-induced gene-h3 (TGFβig-h3) in CAMs, which was correlated with lymph node involvement and shorter survival. TGFβig-h3 inhibited IGF-II-stimulated migration and proliferation of both cancer cells and myofibroblasts, and suppressed IGF-II activation of p42/44 MAPkinase; TGFβig-h3 knockdown increased IGF-II- and CM-stimulated migration. Furthermore, administration of TGFβig-h3 inhibited myofibroblast-stimulated growth of gastric cancer xenografts. We conclude that stromal cells exert inhibitory as well as stimulatory effects on tumor cells; TGFβig-h3 is a stromal inhibitory factor that is decreased with progression of gastric cancers.

Indexed as

Disease ProgressionGastric MucosaHumansImmunohistochemistryMyofibroblastsStomachTransforming Growth FactorsTransforming Growth Factors

Identifiers

PMID22610072
PMCPMC3499060
OpenAlexW2076478342

What OpenQuestion holds

Textmetadata
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.