Evidence map›Paper›PMID 23951028›Full record

ArticlePloS one2013

IL-1α expression in pancreatic ductal adenocarcinoma affects the tumor cell migration and is regulated by the p38MAPK signaling pathway.

Vegard Tjomsland, Linda Bojmar, Per Sandström, Charlotte Bratthäll, Davorka Messmer, Anna Spångeus, Marie Larsson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

25 citing papers in PubMed, 42 citations in OpenAlex.

  1. Interleukin-1α (IL-1α) in pancreatic ductal adenocarcinoma: implications for immunotherapy and molecular biomarkers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
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  4. Role of Interleukins in Pancreatic Cancer: A Literature Review.Journal of gastrointestinal cancer · 2024
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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 2 institutions in 2 countries.

Vegard TjomslandMolecular Virology, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Linda Bojmar
Per Sandström
Charlotte Bratthäll
Davorka Messmer
Anna Spångeus
Marie Larsson
Linköping University · SEUniversity of California, San Diego · US

Funding

Innate NKT Cells in HIV InfectionR37AI052731 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NIXON, DOUGLAS F · 2007 to 2016
$3.1M
Innate NKT Cells in HIV InfectionR01AI052731 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NIXON, DOUGLAS F · 2002 to 2006
$2.1M
NIAID NIH HHS R01 AI052731NIAID NIH HHS R37 AI052731
6 · The paper itself

Abstract

The interplay between the tumor cells and the surrounding stroma creates inflammation, which promotes tumor growth and spread. The inflammation is a hallmark for pancreatic adenocarcinoma (PDAC) and is to high extent driven by IL-1α. IL-1α is expressed and secreted by the tumor cells and exerting its effect on the stroma, i.e. cancer associated fibroblasts (CAF), which in turn produce massive amount of inflammatory and immune regulatory factors. IL-1 induces activation of transcription factors such as nuclear factor-κβ (NF-κβ), but also activator protein 1 (AP-1) via the small G-protein Ras. Dysregulation of Ras pathways are common in cancer as this oncogene is the most frequently mutated in many cancers. In contrast, the signaling events leading up to the expression of IL-1α by tumor cells are not well elucidated. Our aim was to examine the signaling cascade involved in the induction of IL-1α expression in PDAC. We found p38MAPK, activated by the K-Ras signaling pathway, to be involved in the expression of IL-1α by PDAC as blocking this pathway decreased both the gene and protein expression of IL-1α. Blockage of the P38MAPK signaling in PDAC also dampened the ability of the tumor cell to induce inflammation in CAFs. In addition, the IL-1α autocrine signaling regulated the migratory capacity of PDAC cells. Taken together, the blockage of signaling pathways leading to IL-1α expression and/or neutralization of IL-1α in the PDAC microenvironment should be taken into consideration as possible treatment or complement to existing treatment of this cancer.

Indexed as

MAP Kinase Signaling SystemAdenocarcinomaCarcinoma, Pancreatic DuctalCell CommunicationCell Line, TumorCell MovementExtracellular Signal-Regulated MAP KinasesFibroblastsGene Expression Regulation, NeoplasticHumansInflammationInterleukin-1alphaInterleukin 1 Receptor Antagonist Proteinp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsExtracellular Signal-Regulated MAP KinasesInterleukin-1alphaInterleukin 1 Receptor Antagonist Proteinp38 Mitogen-Activated Protein KinasesProtein Kinase Inhibitors

Identifiers

PMID23951028
PMCPMC3741369
OpenAlexW2107727497

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.