Evidence map›Paper›PMID 28549596›Full record

ReviewPharmacology & therapeutics2017

Emerging roles of the CXCL12/CXCR4 axis in pancreatic cancer progression and therapy.

Richard L Sleightholm, Beth K Neilsen, Jing Li, Maria M Steele, Rakesh K Singh, Michael A Hollingsworth, David Oupicky

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Pharmacology & therapeutics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
8.8field-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.

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

96 citing papers in PubMed, 173 citations in OpenAlex.

  1. Article
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  3. Progress in the application ofAnnals of nuclear medicine · 2026
    Review
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  11. Nur77 knock-down suppresses glioma by regulating CXCR4.Archives of medical science : AMS · 2025
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36 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

7 authors at 2 institutions in 1 country.

Richard L SleightholmDepartment of Pharmaceutical Sciences, University of Nebraska Medical Center, 985830 Nebraska Medical Center, Omaha, NE, USA.
Beth K NeilsenEppley Institute, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE, USA.
Jing LiDepartment of Pharmaceutical Sciences, University of Nebraska Medical Center, 985830 Nebraska Medical Center, Omaha, NE, USA.
Maria M SteeleEppley Institute, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE, USA.
Rakesh K SinghDepartment of Pathology and Microbiology, University of Nebraska Medical Center, 985870 Nebraska Medical Center, Omaha, NE, USA.
Michael A HollingsworthEppley Institute, University of Nebraska Medical Center, 985950 Nebraska Medical Center, Omaha, NE, USA; Department of Pathology and Microbiology, University of Nebraska Medical Center, 985870 Nebraska Medical Center, Omaha, NE, USA; Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, 985870 Nebraska Medical Center, Omaha, NE, USA.
David OupickyDepartment of Pharmaceutical Sciences, University of Nebraska Medical Center, 985830 Nebraska Medical Center, Omaha, NE, USA. Electronic address: david.oupicky@unmc.edu.
Nebraska Medical Center · USUniversity of Nebraska Medical Center · US

Funding

Role of N-Cadherin in Pancreatic Tumor MicroenvironmentU54CA163120 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI HOLLINGSWORTH, MICHAEL A. · 2011 to 2015
$4.2M
NCI NIH HHS U54 CA163120
6 · The paper itself

Abstract

Chemokine networks regulate a variety of cellular, physiological, and immune processes. These normal functions can become appropriated by cancer cells to facilitate a more hospitable niche for aberrant cells by enhancing growth, proliferation, and metastasis. This is especially true in pancreatic cancer, where chemokine signaling is a vital component in the development of the supportive tumor microenvironment and the signaling between the cancer cells and surrounding stromal cells. Although expression patterns vary among cancer types, the chemokine receptor CXCR4 has been implicated in nearly every major malignancy and plays a prominent role in pancreatic cancer development and progression. This receptor, in conjunction with its primary chemokine ligand CXCL12, promotes pancreatic cancer development, invasion, and metastasis through the management of the tumor microenvironment via complex crosstalk with other pathways. Thus, CXCR4 likely contributes to the poor prognoses observed in patients afflicted with this malignancy. Recent exploration of combination therapies with CXCR4 antagonists have demonstrated improved outcomes, and abolishing the contribution of this pathway may prove crucial to effectively treat pancreatic cancer at both the primary tumor and metastases.

Indexed as

AnimalsChemokine CXCL12Disease ProgressionDrug Resistance, NeoplasmHumansPancreatic NeoplasmsReceptors, CXCR4Chemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanReceptors, CXCR4Cancer therapyCXCR4Molecular mechanismPancreatic cancerTumor microenvironment

Identifiers

PMID28549596
PMCPMC13170075
OpenAlexW2617814074

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.