Evidence map›Paper›PMID 35688943›Full record

ArticleOncogene2022

IGF1R acts as a cancer-promoting factor in the tumor microenvironment facilitating lung metastasis implantation and progression.

Elvira Alfaro-Arnedo, Icíar P López, Sergio Piñeiro-Hermida, Marta Canalejo, Carolina Gotera, Jesús Javier Sola, Alejandra Roncero, Germán Peces-Barba, Carlos Ruíz-Martínez, José G Pichel

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
11.4field-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

59 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
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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 at 4 institutions in 2 countries.

Elvira Alfaro-ArnedoLung Cancer and Respiratory Diseases Unit, Center for Biomedical Research of La Rioja (CIBIR), Fundación Rioja Salud, Logroño, Spain.
Icíar P López *Lung Cancer and Respiratory Diseases Unit, Center for Biomedical Research of La Rioja (CIBIR), Fundación Rioja Salud, Logroño, Spain.
Sergio Piñeiro-Hermida *Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Centre (CNIO), Madrid, Spain.
Marta CanalejoLung Cancer and Respiratory Diseases Unit, Center for Biomedical Research of La Rioja (CIBIR), Fundación Rioja Salud, Logroño, Spain.
Carolina GoteraIIS Fundación Jiménez Díaz, Madrid, Spain.
Jesús Javier SolaPathological Anatomy Service, Hospital Universitario San Pedro, Rioja Salud, Logroño, Spain.
Alejandra RonceroPneumology Service, Hospital Universitario San Pedro, Rioja Salud, Logroño, Spain.
Germán Peces-BarbaIIS Fundación Jiménez Díaz, Madrid, Spain.
Carlos Ruíz-MartínezPneumology Service, Hospital Universitario San Pedro, Rioja Salud, Logroño, Spain.
José G PichelLung Cancer and Respiratory Diseases Unit, Center for Biomedical Research of La Rioja (CIBIR), Fundación Rioja Salud, Logroño, Spain. jgpichel@riojasalud.es.ORCID 0000-0001-8580-0952
Center for Biomedical Research of La Rioja · ESCentro de Investigación Biomédica en Red · ESHospital San Pedro · ESSpanish National Cancer Research Centre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Given the long-term ineffectiveness of current therapies and late-stage diagnoses, lung cancer is a leading cause of malignant diseases. Tumor progression is influenced by cancer cell interactions with the tumor microenvironment (TME). Insulin-like growth factor 1 receptor (IGF1R) was reported to affect the TME; however, the role of IGF1R in lung TME has not been investigated. First, we assessed IGF1R genomic alterations and expression in NSCLC patient tissue samples, as well as IGF1R serum levels. Next, we performed tumor heterotopic transplantation and pulmonary metastases in IGF1R-deficient mice using melanoma and Lewis lung carcinoma (LLC) cells. Herein we report increased amplification and mRNA expression, as well as increased protein expression (IGF1R/p-IGF1R) and IGF1R levels in tumor samples and serum from NSCLC patients, respectively. Moreover, IGF1R deficiency in mice reduced tumor growth, proliferation, inflammation and vascularization, and increased apoptosis after tumor heterotopic transplantation. Following induction of lung metastasis, IGF1R-deficient lungs also demonstrated a reduced tumor burden, and decreased expression of tumor progression markers, p-IGF1R and p-ERK1/2. Additionally, IGF1R-deficient lungs showed increased apoptosis and diminished proliferation, vascularization, EMT and fibrosis, along with attenuated inflammation and immunosuppression. Accordingly, IGF1R deficiency decreased expression of p-IGF1R in blood vessels, fibroblasts, tumor-associated macrophages and FOXP3

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsReceptor, IGF Type 1AnimalsBiomarkers, TumorCell Line, TumorCell ProliferationHumansInflammationMiceTumor MicroenvironmentBiomarkers, TumorIGF1R protein, humanIgf1r protein, mouseReceptor, IGF Type 1

Identifiers

PMID35688943
PMCPMC9184253
OpenAlexW4281887537

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.