Evidence map›Paper›PMID 29259015›Full record

ArticleCancer research2018

Inactivation of Cancer-Associated-Fibroblasts Disrupts Oncogenic Signaling in Pancreatic Cancer Cells and Promotes Its Regression.

Patricia Dauer, Xianda Zhao, Vineet K Gupta, Nikita Sharma, Kousik Kesh, Prisca Gnamlin, Vikas Dudeja, Selwyn M Vickers, Sulagna Banerjee, Ashok Saluja

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 113 citations in OpenAlex.

  1. Trial
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  9. Nuclear Galectin-1 promotesProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  15. TAK1 Promotes an Immunosuppressive Tumor Microenvironment through Cancer-Associated Fibroblast Phenotypic Conversion in Pancreatic Ductal Adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  16. Review
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7 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Patricia DauerDepartment of Surgery, University of Miami, Miami, Florida.
Xianda ZhaoDepartment of Surgery, University of Minnesota, Minneapolis, Minnesota.
Vineet K GuptaDepartment of Surgery, University of Miami, Miami, Florida.
Nikita SharmaDepartment of Surgery, University of Miami, Miami, Florida.
Kousik KeshDepartment of Surgery, University of Miami, Miami, Florida.
Prisca GnamlinDepartment of Surgery, University of Miami, Miami, Florida.
Vikas DudejaDepartment of Surgery, University of Miami, Miami, Florida.
Selwyn M VickersDepartment of Surgery, University of Minnesota, Minneapolis, Minnesota.
Sulagna BanerjeeDepartment of Surgery, University of Miami, Miami, Florida. asaluja@miami.edu Sulagna.banerjee@med.miami.edu.
Ashok SalujaDepartment of Surgery, University of Miami, Miami, Florida. asaluja@miami.edu Sulagna.banerjee@med.miami.edu.
University of Miami · USUniversity of Minnesota · US

Funding

The Inhibition of HSP70 Induces Apoptosis in Pancreatic Cancer CellsR01CA124723 · NCI · UNIVERSITY OF MINNESOTA · PI GILBOA, ELI, RAMAKRISHNAN, SUNDARAM · 2007 to 2022
$4.5M
Triptolide Augments Death Receptor Mediated Apoptosis in Pancreatic CancerR01CA170946 · NCI · UNIVERSITY OF MINNESOTA · PI SALUJA, ASHOK K · 2012 to 2016
$2.4M
Functional Significance of CD133 in Pancreatic CancerR01CA184274 · NCI · UNIVERSITY OF MINNESOTA · PI BANERJEE, SULAGNA · 2014 to 2018
$1.6M
NCI NIH HHS R01 CA124723NCI NIH HHS R01 CA170946NCI NIH HHS R01 CA184274
6 · The paper itself

Abstract

Resident fibroblasts that contact tumor epithelial cells (TEC) can become irreversibly activated as cancer-associated-fibroblasts (CAF) that stimulate oncogenic signaling in TEC. In this study, we evaluated the cross-talk between CAF and TEC isolated from tumors generated in a mouse model of KRAS/mut p53-induced pancreatic cancer (KPC mice). Transcriptomic profiling conducted after treatment with the anticancer compound Minnelide revealed deregulation of the TGFβ signaling pathway in CAF, resulting in an apparent reversal of their activated state to a quiescent, nonproliferative state. TEC exposed to media conditioned by drug-treated CAFs exhibited a decrease in oncogenic signaling, as manifested by downregulation of the transcription factor Sp1. This inhibition was rescued by treating TEC with TGFβ. Given promising early clinical studies with Minnelide, our findings suggest that approaches to inactivate CAF and prevent tumor-stroma cross-talk may offer a viable strategy to treat pancreatic cancer.

Indexed as

CarcinogenesisDisease Models, AnimalAnimalsApoptosisCancer-Associated FibroblastsCarcinoma, Pancreatic DuctalCell ProliferationDiterpenesEpithelial CellsEpoxy CompoundsGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMiceMice, Inbred C57BLMutation14-O-phosphonooxymethyltriptolide disodium saltDiterpenesEpoxy CompoundsHras protein, mouseOrganophosphatesPhenanthrenesProto-Oncogene Proteins p21(ras)Transforming Growth Factor betaTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID29259015
PMCPMC5935584
OpenAlexW2777823129

What OpenQuestion 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 OpenQuestion graph.