Evidence mapPaperPMID 30453495Full record

ReviewInternational journal of molecular sciences2018

Insulin Receptor Isoforms in Cancer.

Veronica Vella, Agostino Milluzzo, Nunzio Massimo Scalisi, Paolo Vigneri, Laura Sciacca

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

71 citing papers in PubMed, 114 citations in OpenAlex.

  1. Article
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  7. Aptamers in Drug Delivery Development.Materials today (Kidlington, England) · 2025
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  19. Article
  20. Changes in Cells Associated with Insulin Resistance.International journal of molecular sciences · 2024
    Review

11 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

5 authors at 2 institutions in 1 country.

Veronica VellaDepartment of Clinical and Experimental Medicine, Endocrinology Section, University of Catania Medical School, Garibaldi-Nesima Hospital, via Palermo 636, 95122 Catania, Italy. vellave@hotmail.com.
Agostino MilluzzoDepartment of Clinical and Experimental Medicine, Endocrinology Section, University of Catania Medical School, Garibaldi-Nesima Hospital, via Palermo 636, 95122 Catania, Italy. agomil@alice.it.ORCID 0000-0003-1536-5697
Nunzio Massimo ScalisiDepartment of Clinical and Experimental Medicine, Endocrinology Section, University of Catania Medical School, Garibaldi-Nesima Hospital, via Palermo 636, 95122 Catania, Italy. m.scalisi@hotmail.it.ORCID 0000-0002-6459-1378
Paolo VigneriDepartment of Clinical and Experimental Medicine, University of Catania Medical School, Center of Experimental Oncology and Hematology, A.O.U. Policlinico Vittorio Emanuele, via Santa Sofia, 78, 95123 Catania, Italy. vigneri.p@unict.it.
Laura SciaccaDepartment of Clinical and Experimental Medicine, Endocrinology Section, University of Catania Medical School, Garibaldi-Nesima Hospital, via Palermo 636, 95122 Catania, Italy. lsciacca@unict.it.ORCID 0000-0002-3258-7200
University of Catania · ITUniversità degli Studi di Enna Kore · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The insulin receptor (IR) mediates both metabolic and mitogenic effects especially when overexpressed or in clinical conditions with compensatory hyperinsulinemia, due to the metabolic pathway resistance, as obesity diabetes. In many cancers, IR is overexpressed preferentially as IR-A isoform, derived by alternative splicing of exon 11. The IR-A overexpression, and the increased IR-A:IR-B ratio, are mechanisms that promote the mitogenic response of cancer cells to insulin and IGF-2, which is produced locally by both epithelial and stromal cancer cells. In cancer IR-A, isoform predominance may occur for dysregulation at both mRNA transcription and post-transcription levels, including splicing factors, non-coding RNAs and protein degradation. The mechanisms that regulate IR isoform expression are complex and not fully understood. The IR isoform overexpression may play a role in cancer cell stemness, in tumor progression and in resistance to target therapies. From a clinical point of view, the IR-A overexpression in cancer may be a determinant factor for the resistance to IGF-1R target therapies for this issue. IR isoform expression in cancers may have the meaning of a predictive biomarker and co-targeting IGF-1R and IR-A may represent a new more efficacious treatment strategy.

Indexed as

AnimalsGene Expression Regulation, NeoplasticHumansModels, BiologicalNeoplasmsProtein IsoformsReceptor, InsulinProtein IsoformsReceptor, Insulincancerhybrid receptorsIGF-1RIGF-2insulininsulin receptorinsulin receptor isoformssplicing factors

Identifiers

PMID30453495
PMCPMC6274710
OpenAlexW2901863400

What Socratic 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 Socratic graph.