Evidence map›Paper›PMID 35797269›Full record

ArticlePloS one2022

Interaction of immune checkpoint PD-1 and chemokine receptor 4 (CXCR4) promotes a malignant phenotype in pancreatic cancer cells.

Megan M Harper, Miranda Lin, Michael J Cavnar, Prakash K Pandalai, Reema A Patel, Mei Gao, Joseph Kim

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Megan M HarperDivision of Surgical Oncology, University of Kentucky, Lexington, Kentucky, United States of America.ORCID 0000-0002-2935-6292
Miranda LinDivision of Surgical Oncology, University of Kentucky, Lexington, Kentucky, United States of America.
Michael J CavnarDivision of Surgical Oncology, University of Kentucky, Lexington, Kentucky, United States of America.
Prakash K PandalaiDivision of Surgical Oncology, University of Kentucky, Lexington, Kentucky, United States of America.ORCID 0000-0002-2729-0058
Reema A PatelDivision of Medical Oncology, University of Kentucky, Lexington, Kentucky, United States of America.ORCID 0000-0001-8650-6122
Mei GaoDivision of Surgical Oncology, University of Kentucky, Lexington, Kentucky, United States of America.
Joseph KimDivision of Surgical Oncology, University of Kentucky, Lexington, Kentucky, United States of America.
University of Kentucky · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
Oncology Research Training for Surgeon-ScientistsT32CA160003 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers, Pamela Carmen Hull · 2011 to 2026
$3.2M
NCI NIH HHS P30 CA177558NCI NIH HHS T32 CA160003
6 · The paper itself

Abstract

Despite recent therapeutic advances, pancreatic ductal adenocarcinoma (PDAC) remains a devastating disease with limited therapeutic options. Immune checkpoint inhibitors (ICIs) have demonstrated promising results in many cancers, but thus far have yielded little clinical benefit in PDAC. Based on recent combined targeting of programmed cell death protein-1 (PD-1) and C-X-C chemokine receptor 4 (CXCR4) in patient-derived xenografts (PDXs) and a pilot clinical trial, we sought to elucidate potential interactions between PD-1 and CXCR4. We observed concomitant expression and direct interaction of PD-1 and CXCR4 in PDAC cells. This interaction was disrupted upon CXCR4 antagonism with AMD3100 and led to increased cell surface expression of PD-1. Importantly, CXCR4-mediated PDAC cell migration was also blocked by PD-1 inhibition. Our work provides a possible mechanism by which prior studies have demonstrated that combined CXCR4 and PD-1 inhibition leads to decreased tumor growth. This is the first report investigating PD-1 and CXCR4 interactions in PDAC cells and our results can serve as the basis for further investigation of combined therapeutic targeting of CXCR4 and PD-1.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsHumansPhenotypeProgrammed Cell Death 1 ReceptorReceptors, CXCR4Tumor MicroenvironmentCXCR4 protein, humanProgrammed Cell Death 1 ReceptorReceptors, CXCR4

Identifiers

PMID35797269
PMCPMC9262213
OpenAlexW4284710655

What OpenQuestion holds

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Registered trials

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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.