Evidence map›Paper›PMID 38829570›Full record

ArticlePancreas

Increased Gremlin1 Expression in Pancreatic Ductal Adenocarcinoma Promotes a Fibrogenic Stromal Microenvironment.

Rachel R Tindall, Erika Y Faraoni, Jiajing Li, Yinjie Zhang, Shun-Ming Ting, Beanna Okeugo, Xiurong Zhao, Yuying Liu, Mamoun Younes, Qiang Shen and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pancreas. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. CTHRC1Scientific reports · 2024
    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

13 authors.

Rachel R TindallFrom the Department of Surgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX.
Erika Y FaraoniDepartment of Anesthesiology, Critical Care and Pain Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX.
Jiajing LiFrom the Department of Surgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX.
Yinjie ZhangFrom the Department of Surgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX.
Shun-Ming TingDepartment of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX.
Beanna OkeugoDivision of Gastroenterology, Department of Pediatrics, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX.
Xiurong ZhaoDepartment of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX.
Yuying LiuDivision of Gastroenterology, Department of Pediatrics, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX.
Mamoun YounesDepartment of Pathology, George Washington University, Washington, DC.
Qiang ShenDepartment of Interdisciplinary Oncology, Louisiana State University Health Sciences Center, New Orleans, LA.
Jennifer M Bailey-LundbergDepartment of Anesthesiology, Critical Care and Pain Medicine, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX.
Yanna CaoFrom the Department of Surgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX.
Tien C KoFrom the Department of Surgery, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX.

Funding

Protective Signaling Pathway in Alcohol-Induced PancreatitisR21AA027014 · NIAAA · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KO, TIEN C · 2019 to 2020
$406k
NIAAA NIH HHS R21 AA027014
6 · The paper itself

Abstract

objectivePancreatic ductal adenocarcinoma (PDAC) microenvironment is primarily composed of cancer-associated fibroblasts and immune cells. Gremlin1 (Grem1) is a profibrogenic factor that promotes tumorigenesis in several cancers. However, the role of Grem1 in the PDAC microenvironment is not defined. MATERIALS AND

methodsWe correlated Grem1 levels with activated stroma and immune cells in human PDAC using The Cancer Genome Atlas RNA-sequencing data and characterized expression of Grem1 transcripts and isoforms in pancreatic cell lines and PDAC tissues. We assessed the role of Grem1 in the microenvironment by in vitro studies.

resultsGrem1 expression is associated with an activated stroma and increased M1 and M2 macrophages. Only full length Grem1 variant 1 and isoform 1 were detectable in human pancreatic cells, and remarkably high levels of Grem1 were observed in pancreatic fibroblasts. Immunohistochemistry detected Grem1 protein in PDAC tumor and stromal cells, which correlated with infiltrating macrophages in PDAC tumors. Grem1 knockdown in cancer-associated fibroblasts suppressed transforming growth factor β-induced extracellular matrix proteins. Grem1 recombinant protein treatment in vitro increased M1 and M2 macrophages.

conclusionsGrem1 acts as a profibrogenic factor in the PDAC microenvironment via modulation of fibroblasts and macrophages. Grem1 may have the potential to be developed as a therapeutic target for PDAC.

Indexed as

Carcinoma, Pancreatic DuctalIntercellular Signaling Peptides and ProteinsMacrophagesPancreatic NeoplasmsStromal CellsTumor MicroenvironmentCancer-Associated FibroblastsCell Line, TumorFibrosisGene Expression Regulation, NeoplasticHumansGREM1 protein, humanIntercellular Signaling Peptides and Proteins

Identifiers

PMID38829570
PMCPMC11615151

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.