Evidence map›Paper›PMID 20023704›Full record

ArticleOncogene2010

IGFBP-3 hypermethylation-derived deficiency mediates cisplatin resistance in non-small-cell lung cancer.

I Ibanez de Caceres, M Cortes-Sempere, C Moratilla, R Machado-Pinilla, V Rodriguez-Fanjul, C Manguán-García, P Cejas, F López-Ríos, L Paz-Ares, J de CastroCarpeño and 3 more

Abstract read
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In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
2.7field-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

87 citing papers in PubMed, 135 citations in OpenAlex.

  1. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
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  13. [Research Progress of DNA Methylation in Cisplatin Resistance in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023
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27 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

13 authors at 3 institutions in 1 country.

I Ibanez de CaceresOncology Research Laboratory, Research Unit, FIB-La Paz University Hospital, Madrid, Spain. inma.ibanezca@salud.madrid.org
M Cortes-Sempere
C Moratilla
R Machado-Pinilla
V Rodriguez-Fanjul
C Manguán-García
P Cejas
F López-Ríos
L Paz-Ares
J de CastroCarpeño
M Nistal
C Belda-Iniesta
R Perona
Universidad Autónoma de Madrid · ESHospital Universitario La Paz · ESResearch Institute Hospital 12 de Octubre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin-based chemotherapy is the paradigm of non-small-cell lung cancer (NSCLC) treatment; however, it also induces de novo DNA-hypermethylation, a process that may be involved in the development of drug-resistant phenotypes by inactivating genes required for drug-cytotoxicity. By using an expression microarray analysis, we aimed to identify those genes reactivated in a set of two cisplatin (CDDP) resistant and sensitive NSCLC cell lines after epigenetic treatment. Gene expression, promoter methylation and CDDP-chemoresponse were further analyzed in three matched sets of sensitive/resistant cell lines, 23 human cancer cell lines and 36 NSCLC specimens. Results revealed specific silencing by promoter hypermethylation of IGFBP-3 in CDDP resistant cells, whereas IGFBP-3 siRNA interference, induced resistance to CDDP in sensitive cells (P<0.001). In addition, we found a strong correlation between methylation status and CDDP response in tumor specimens (P<0.001). Thus, stage I patients, whose tumors harbor an unmethylated promoter, had a trend towards increased disease-free survival (DFS). We report that a loss of IGFBP-3 expression, mediated by promoter-hypermethylation, results in a reduction of tumor cell sensitivity to cisplatin in NSCLC. Basal methylation status of IGFBP-3 before treatment may be a clinical biomarker and a predictor of the chemotherapy outcome, helping to identify patients who are most likely to benefit from CDDP therapy alone or in combination with epigenetic treatment.

Indexed as

Antineoplastic AgentsAzacitidineBase SequenceCarcinoma, Non-Small-Cell LungCell Line, TumorCell SurvivalCisplatinDNA MethylationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHeLa CellsHT29 CellsHumansHydroxamic AcidsInsulin-Like Growth Factor Binding Protein 3Kaplan-Meier EstimateAntineoplastic AgentsAzacitidineCisplatinHydroxamic AcidsInsulin-Like Growth Factor Binding Protein 3trichostatin A

Identifiers

PMID20023704
OpenAlexW2007283154

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.