Evidence map›Paper›PMID 34638472›Full record

ArticleCancers2021

Insulin Receptor in Pancreatic Cancer-Crown Witness in Cross Examination.

Steffen M Heckl, Lukas Kercher, Samir Abdullazade, Carolin Schneider, Sandra Krüger, Hans-Michael Behrens, Susanne Sebens, Heiner Schäfer, Stefan Schreiber, Christoph Röcken

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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 at 2 institutions in 1 country.

Steffen M HecklDepartment of Internal Medicine I, University Hospital Schleswig-Holstein, 24105 Kiel, Germany.
Lukas KercherDepartment of Pathology, Christian-Albrechts-University Kiel, 24105 Kiel, Germany.
Samir AbdullazadeDepartment of Pathology, Christian-Albrechts-University Kiel, 24105 Kiel, Germany.ORCID 0000-0002-9119-8301
Carolin SchneiderDepartment of Pathology, Christian-Albrechts-University Kiel, 24105 Kiel, Germany.
Sandra KrügerDepartment of Pathology, Christian-Albrechts-University Kiel, 24105 Kiel, Germany.
Hans-Michael BehrensDepartment of Pathology, Christian-Albrechts-University Kiel, 24105 Kiel, Germany.
Susanne SebensInstitute for Experimental Cancer Research, Christian-Albrechts-University Kiel, 24105 Kiel, Germany.
Heiner SchäferDepartment of Internal Medicine I, University Hospital Schleswig-Holstein, 24105 Kiel, Germany.ORCID 0000-0001-6936-9090
Stefan SchreiberDepartment of Internal Medicine I, University Hospital Schleswig-Holstein, 24105 Kiel, Germany.
Christoph RöckenDepartment of Pathology, Christian-Albrechts-University Kiel, 24105 Kiel, Germany.ORCID 0000-0002-6989-8002
Christian-Albrechts-Universität zu Kiel · DEUniversity Hospital Schleswig-Holstein · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe proximity of pancreatic cancer (PDAC) to the physiological source of the growth promoting hormone insulin might be exploited by this highly malignant cancer entity. We investigated if (I) PDACs express the insulin receptor (IR) in cancer cells and cancer vasculature, (II) if IR correlates with clinicopathological patient characteristics, including survival, and hence is involved in PDAC biology, (III) if IR is already expressed in precursor lesions, if (IV) the IGF1 receptor (IGF1R) is associated with clinicopathological patient characteristics and survival and (V) is linked to IR expression.

methods160 PDAC samples were examined for IR and IGF1R expression by immunohistochemistry. A modified HistoScore was correlated with clinicopathological characteristics and survival.

resultsIR overexpression was already observed in pancreatic intraepithelial neoplasia. Furthermore, it was more frequently observed in advanced disease and associated with distant metastasis, UICC stage, lymphatic invasion and an increased lymph node ratio, but without impacting survival in the end. IGF1R expression was not associated with clinicopathological parameters or survival, in contrast to former paradigms.

conclusionsWe hypothesize that the close proximity to the pancreatic islets might be advantageous for cancer growth at first, but it experiences self-limitation due to surgical removal or local destruction following accelerated cancer growth.

Indexed as

IGF1 receptorinsulininsulin receptorpancreatic cancerprognosis

Identifiers

PMID34638472
PMCPMC8508431
OpenAlexW3207377820

What OpenQuestion holds

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LicenceCC BY
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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.