Evidence map›Paper›PMID 29455671›Full record

ReviewMolecular cancer2018

Oncogenic fusion proteins adopt the insulin-like growth factor signaling pathway.

Haim Werner, Shilhav Meisel-Sharon, Ilan Bruchim

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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 29 citations in OpenAlex.

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  13. Functional characterization of two rare BCR-FGFR1Cold Spring Harbor molecular case studies · 2020
    Article
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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

3 authors at 2 institutions in 1 country.

Haim WernerDepartment of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, 69978, Tel Aviv, Israel. hwerner@post.tau.ac.il.
Shilhav Meisel-SharonDepartment of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv University, 69978, Tel Aviv, Israel.
Ilan BruchimDepartment of Obstetrics and Gynecology, Hillel Yaffe Medical Center, Hadera 38100, affiliated with the Technion Institute of Technology, Haifa, Israel.
Tel Aviv University · ILHillel Yaffe Medical Center · IL

Funding

Israel Science Foundation 885/09
6 · The paper itself

Abstract

The insulin-like growth factor-1 receptor (IGF1R) has been identified as a potent anti-apoptotic, pro-survival tyrosine kinase-containing receptor. Overexpression of the IGF1R gene constitutes a typical feature of most human cancers. Consistent with these biological roles, cells expressing high levels of IGF1R are expected not to die, a quintessential feature of cancer cells. Tumor specific chromosomal translocations that disrupt the architecture of transcription factors are a common theme in carcinogenesis. Increasing evidence gathered over the past fifteen years demonstrate that this type of genomic rearrangements is common not only among pediatric and hematological malignancies, as classically thought, but may also provide a molecular and cytogenetic foundation for an ever-increasing portion of adult epithelial tumors. In this review article we provide evidence that the mechanism of action of oncogenic fusion proteins associated with both pediatric and adult malignancies involves transactivation of the IGF1R gene, with ensuing increases in IGF1R levels and ligand-mediated receptor phosphorylation. Disrupted transcription factors adopt the IGF1R signaling pathway and elicit their oncogenic activities via activation of this critical regulatory network. Combined targeting of oncogenic fusion proteins along with the IGF1R may constitute a promising therapeutic approach.

Indexed as

AnimalsHumansNeoplasmsOncogene Proteins, FusionReceptor, IGF Type 1Receptors, SomatomedinSignal TransductionOncogene Proteins, FusionReceptor, IGF Type 1Receptors, SomatomedinChimeric fusion proteinsDisrupted transcription factorsIGF1 receptor (IGF1R)Insulin-like growth factor-1 (IGF1)Transcription

Identifiers

PMID29455671
PMCPMC5817802
OpenAlexW2795564906

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.