Evidence map›Paper›PMID 34064969›Full record

ArticleInternational journal of molecular sciences2021

Initiation of Pancreatic Cancer: The Interplay of Hyperglycemia and Macrophages Promotes the Acquisition of Malignancy-Associated Properties in Pancreatic Ductal Epithelial Cells.

Lilli Otto, Sascha Rahn, Tina Daunke, Frederik Walter, Elsa Winter, Julia Luisa Möller, Stefan Rose-John, Daniela Wesch, Heiner Schäfer, Susanne Sebens

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

14 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

10 authors.

Lilli OttoInstitute for Experimental Cancer Research, Kiel University (CAU) and University Medical Center Schleswig-Holstein (UKSH), Campus Kiel, 24105 Kiel, Germany.
Sascha RahnInstitute of Biochemistry, Kiel University, 24118 Kiel, Germany.
Tina DaunkeInstitute for Experimental Cancer Research, Kiel University (CAU) and University Medical Center Schleswig-Holstein (UKSH), Campus Kiel, 24105 Kiel, Germany.ORCID 0000-0002-1062-1076
Frederik WalterInstitute for Experimental Cancer Research, Kiel University (CAU) and University Medical Center Schleswig-Holstein (UKSH), Campus Kiel, 24105 Kiel, Germany.
Elsa WinterInstitute for Experimental Cancer Research, Kiel University (CAU) and University Medical Center Schleswig-Holstein (UKSH), Campus Kiel, 24105 Kiel, Germany.
Julia Luisa MöllerDepartment of Hematology and Oncology, University Medical Center Schleswig-Holstein (UKSH) Campus Kiel, 24105 Kiel, Germany.
Stefan Rose-JohnInstitute of Biochemistry, Kiel University, 24118 Kiel, Germany.ORCID 0000-0002-7519-3279
Daniela WeschInstitute of Immunology, Kiel University and University Medical Center Schleswig-Holstein (UKSH) Campus Kiel, 24105 Kiel, Germany.
Heiner SchäferInstitute for Experimental Cancer Research, Kiel University (CAU) and University Medical Center Schleswig-Holstein (UKSH), Campus Kiel, 24105 Kiel, Germany.ORCID 0000-0001-6936-9090
Susanne SebensInstitute for Experimental Cancer Research, Kiel University (CAU) and University Medical Center Schleswig-Holstein (UKSH), Campus Kiel, 24105 Kiel, Germany.

Funding

Medical Faculty of Kiel University does not existUKSH Förderstiftung does not exist
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is still one of the most aggressive solid malignancies with a poor prognosis. Obesity and type 2 diabetes mellitus (T2DM) are two major risk factors linked to the development and progression of PDAC, both often characterized by high blood glucose levels. Macrophages represent the main immune cell population in PDAC contributing to PDAC development. It has already been shown that pancreatic ductal epithelial cells (PDEC) undergo epithelial-mesenchymal transition (EMT) when exposed to hyperglycemia or macrophages. Thus, this study aimed to investigate whether concomitant exposure to hyperglycemia and macrophages aggravates EMT-associated alterations in PDEC. Exposure to macrophages and elevated glucose levels (25 mM glucose) impacted gene expression of EMT inducers such as IL-6 and TNF-α as well as EMT transcription factors in benign (H6c7-

Indexed as

Epithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticCarcinoma, Pancreatic DuctalCell MovementCell ProliferationCoculture TechniquesDiabetes Mellitus, Type 2Epithelial CellsHumansHyperglycemiaMacrophagesPancreatic NeoplasmsSignal Transductioncell migrationEMThyperglycemiamacrophagespancreatic cancertumor microenvironmenttype 2 diabetes

Identifiers

PMID34064969
PMCPMC8151031

What OpenQuestion holds

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LicenceCC BY
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.