Evidence map›Paper›PMID 29475434›Full record

ReviewMolecular cancer2018

Insulin/IGF-driven cancer cell-stroma crosstalk as a novel therapeutic target in pancreatic cancer.

Ayse Ceren Mutgan, H Erdinc Besikcioglu, Shenghan Wang, Helmut Friess, Güralp O Ceyhan, Ihsan Ekin Demir

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 3 pooled it
9.6field-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

70 citing papers in PubMed, 3 syntheses or guidelines pooled it, 115 citations in OpenAlex.

  1. Pooled it
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  4. Review
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  8. Review
  9. PPY-Induced iCAFs Cultivate an Immunosuppressive Microenvironment in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  10. Review
  11. Article
  12. Observational
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  16. Article
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  20. Levels of retinol and retinoic acid in pancreatic cancer, type-2 diabetes and chronic pancreatitis.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2024
    Article

10 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

6 authors at 1 institution in 2 countries.

Ayse Ceren MutganDepartment of Surgery, Klinikum rechts der Isar, Technical University Munich, München, Germany.
H Erdinc BesikciogluDepartment of Surgery, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Shenghan WangDepartment of Surgery, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Helmut FriessDepartment of Surgery, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Güralp O CeyhanDepartment of Surgery, Klinikum rechts der Isar, Technical University Munich, München, Germany.
Ihsan Ekin DemirDepartment of Surgery, Klinikum rechts der Isar, Technical University Munich, München, Germany. ekin.demir@tum.de.
Klinikum rechts der Isar · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is unrivalled the deadliest gastrointestinal cancer in the western world. There is substantial evidence implying that insulin and insulin-like growth factor (IGF) signaling axis prompt PDAC into an advanced stage by enhancing tumor growth, metastasis and by driving therapy resistance. Numerous efforts have been made to block Insulin/IGF signaling pathway in cancer therapy. However, therapies that target the IGF1 receptor (IGF-1R) and IGF subtypes (IGF-1 and IGF-2) have been repeatedly unsuccessful. This failure may not only be due to the complexity and homology that is shared by Insulin and IGF receptors, but also due to the complex stroma-cancer interactions in the pancreas. Shedding light on the interactions between the endocrine/exocrine pancreas and the stroma in PDAC is likely to steer us toward the development of novel treatments. In this review, we highlight the stroma-derived IGF signaling and IGF-binding proteins as potential novel therapeutic targets in PDAC.

Indexed as

Cell CommunicationAnimalsAntineoplastic AgentsCancer-Associated FibroblastsHumansInsulinPancreatic NeoplasmsSignal TransductionSomatomedinsStromal CellsAntineoplastic AgentsInsulinSomatomedinsIGF-1InsulinPancreatic cancerStroma

Identifiers

PMID29475434
PMCPMC5824531
OpenAlexW2807210051

What OpenQuestion holds

Textmetadata
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.