Evidence map›Paper›PMID 22543588›Full record

ArticleOncogene2013

IGFBP-3 methylation-derived deficiency mediates the resistance to cisplatin through the activation of the IGFIR/Akt pathway in non-small cell lung cancer.

M Cortés-Sempere, M P de Miguel, O Pernía, C Rodriguez, J de Castro Carpeño, M Nistal, E Conde, F López-Ríos, C Belda-Iniesta, R Perona and 1 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

47 citing papers in PubMed, 76 citations in OpenAlex.

  1. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
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  10. [Research Progress of DNA Methylation in Cisplatin Resistance in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023
    Review
  11. Diagnostic Significance of HypomethylatedAdvanced biomedical research · 2023
    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

11 authors at 4 institutions in 1 country.

M Cortés-SempereInstituto de Investigaciones Biomedicas CSIC/UAM, CIBER de Enfermedades Raras CIBERER, Madrid, Spain.
M P de Miguel
O Pernía
C Rodriguez
J de Castro Carpeño
M Nistal
E Conde
F López-Ríos
C Belda-Iniesta
R Perona
I Ibanez de Caceres
Hospital Universitario La Paz · ESHospital Universitario HM Sanchinarro · ESInstituto de Investigación de Enfermedades Raras · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although many cancers initially respond to cisplatin (CDDP)-based chemotherapy, resistance frequently develops. Insulin-like growth factor-binding protein-3 (IGFBP-3) silencing by promoter methylation is involved in the CDDP-acquired resistance process in non-small cell lung cancer (NSCLC) patients. Our purpose is to design a translational-based profile to predict resistance in NSCLC by studying the role of IGFBP-3 in the phosphatidyl inositol 3-kinase (PI3K) signaling pathway. We have first examined the relationship between IGFBP-3 expression regulated by promoter methylation and activation of the epidermal growth factor receptor (EGFR), insulin-like growth factor-I receptor (IGFIR) and PI3K/AKT pathways in 10 human cancer cell lines and 25 NSCLC patients with known IGFBP-3 methylation status and response to CDDP. Then, to provide a helpful tool that enables clinicians to identify patients with a potential response to CDDP, we have calculated the association between our diagnostic test and the true outcome of analyzed samples in terms of cisplatin IC50; the inhibitory concentration that kills 50% of the cell population. Our results suggest that loss of IGFBP-3 expression by promoter methylation in tumor cells treated with CDDP may activate the PI3K/AKT pathway through the specific derepression of IGFIR signaling, inducing resistance to CDDP. This study also provides a predictive test for clinical practice with an accuracy and precision of 0.84 and 0.9, respectively, (P=0.0062). We present a biomarker test that could provide clinicians with a robust tool with which to decide on the use of CDDP, improving patient clinical outcomes.

Indexed as

DNA MethylationAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell Line, TumorCisplatinDrug Resistance, NeoplasmErbB ReceptorsHumansInsulin-Like Growth Factor Binding Protein 3Lung NeoplasmsPhosphorylationPromoter Regions, GeneticProto-Oncogene Proteins c-aktReceptor, IGF Type 1Signal TransductionTransfectionAntineoplastic AgentsCisplatinErbB ReceptorsIGFBP3 protein, humanInsulin-Like Growth Factor Binding Protein 3Proto-Oncogene Proteins c-aktReceptor, IGF Type 1

Identifiers

PMID22543588
OpenAlexW2079909703

What OpenQuestion holds

Textmetadata
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.