Evidence map›Paper›PMID 30665410›Full record

ReviewMolecular cancer2019

Tumor-stromal crosstalk in pancreatic cancer and tissue fibrosis.

Divya Thomas, Prakash Radhakrishnan

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05775107 (Assessment of Pancreatic Fibrosis as a Prognostic Factor of Its Course), which is not on this map. Cited by 238 papers.

0numbers the graph read from it
0cells of the map it votes in
238citing papers in PubMed
21.2field-weighted citation impact, top 1% 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.

NCT05775107 unknown statusnot on this mapstarted 2022, after this paper: background citation

Assessment of Pancreatic Fibrosis as a Prognostic Factor of Its Course

TypeobservationalSponsorMoscow Clinical Scientific CenterRan2022 to 2025Enrolled150ConditionsPancreatic Fibrosis
3 · Its place in the literature

Who cites it

238 citing papers in PubMed, 385 citations in OpenAlex.

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  18. Personalizing DNA Cancer Vaccines.Journal of personalized medicine · 2025
    Review
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178 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

2 authors at 2 institutions in 1 country.

Divya ThomasEppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, 986805 Nebraska Medical Center, Omaha, NE, 68198-6805, USA.
Prakash RadhakrishnanEppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, 986805 Nebraska Medical Center, Omaha, NE, 68198-6805, USA. pradhakr@unmc.edu.ORCID 0000-0001-5314-1630
Nebraska Medical Center · USUniversity of Nebraska Medical Center · US

Funding

MUC16 in Pancreatic Cancer Progression and MetastasisR01CA208108 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI RADHAKRISHNAN, PRAKASH · 2017 to 2021
$1.7M
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease with high morbidity and mortality worldwide. To date, limited therapeutic achievements targeting cell proliferation and related mechanisms has led researchers to focus on the microenvironment where pancreatic cancers develop. The anomalous proliferation of stromal cells, such as pancreatic stellate cells, and an increased deposition of altered matrix proteins create an environment that facilitates tumor growth, metastasis and drug resistance. Here, we summarize our understanding of recent advances in research about the role of fibrosis in pancreatic cancer progression, with particular emphasize on the involvement of fibrotic machineries such as wound healing, extra cellular matrix degradation, and epithelial-to-mesenchymal transition. The precise influence of these mechanisms on the biological behaviors and growth of cancer cells has great impact on clinical therapy and therefore deserves more attention. We also discuss the role of various stromal components in conferring drug resistance to PDAC which further worsening the pessimistic disease prognosis. A more in depth understanding of cancer-stroma crosstalk within the tumor microenvironment and stroma based clinical and translational therapies may provide new therapeutic strategies for the prevention of pancreatic cancer progression.

Indexed as

AnimalsCarcinoma, Pancreatic DuctalCell CommunicationCell ProliferationFibrosisHumansPancreatic NeoplasmsPrognosisStromal CellsTumor MicroenvironmentDesmoplasiaExtracellular matrixFibrosisPancreatic CancerStellate cellsTumor microenvironment

Identifiers

PMID30665410
PMCPMC6341551
OpenAlexW2920686366

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.