Evidence map›Paper›PMID 24717244›Full record

ArticleThe Journal of investigative dermatology2014

Cellular intrinsic factors involved in the resistance of squamous cell carcinoma to photodynamic therapy.

Yolanda Gilaberte, Laura Milla, Nerea Salazar, Jesús Vera-Alvarez, Omar Kourani, Alejandra Damian, Viviana Rivarola, Maria José Roca, Jesús Espada, Salvador González and 1 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.8field-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

25 citing papers in PubMed, 51 citations in OpenAlex.

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  13. Observational
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  15. An In Vitro Approach to Photodynamic Therapy.Journal of visualized experiments : JoVE · 2018
    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 3 countries.

Yolanda GilaberteUnidad de Dermatología, Hospital de San Jorge de Huesca, and Institute of Health Science of Aragón, Zaragoza, Spain.
Laura MillaDepartamento de Biología Molecular, Facultad de Ciencias Exactas, Físico-Químicas y Naturales, Universidad Nacional de Río Cuarto, Córdoba, Argentina.
Nerea SalazarDepartamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Madrid, Spain.
Jesús Vera-AlvarezDepartamento de Patología, Hospital de San Jorge de Huesca, Huesca, Spain.
Omar KouraniDepartamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Madrid, Spain.
Alejandra DamianDepartamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Madrid, Spain.
Viviana RivarolaDepartamento de Biología Molecular, Facultad de Ciencias Exactas, Físico-Químicas y Naturales, Universidad Nacional de Río Cuarto, Córdoba, Argentina.
Maria José RocaDepartamento de Patología, Hospital de San Jorge de Huesca, Huesca, Spain.
Jesús EspadaDepartamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Madrid, Spain.
Salvador GonzálezDermatology Service, Memorial Sloan-Kettering Cancer Center, New York, New York, USA.
Angeles JuarranzDepartamento de Biología, Facultad de Ciencias, Universidad Autónoma de Madrid, Madrid, Spain. Electronic address: angeles.juarranz@uam.es.
Universidad Autónoma de Madrid · ESHospital General San Jorge · ESNational University of Río Cuarto · ARMemorial Sloan Kettering Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Photodynamic therapy (PDT) is widely used to treat non-melanoma skin cancer. However, some patients affected with squamous cell carcinoma (SCC) do not respond adequately to PDT with methyl-δ-aminolevulinic acid (MAL-PDT) and the tumors acquire an infiltrative phenotype and became histologically more aggressive, less differentiated, and more fibroblastic. To search for potential factors implicated in SCC resistance to PDT, we have used the SCC-13 cell line (parental) and resistant SCC-13 cells obtained by repeated MAL-PDT treatments (5th and 10th PDT-resistant generations). Xenografts assays in immunodeficient mice showed that the tumors generated by resistant cells were bigger than those induced by parental cells. Comparative genomic hybridization array (aCGH) showed that the three cell types presented amplicons in 3p12.1 CADM2, 7p11.2 EFGR, and 11q13.3 CCND1 genes. The 5th and 10th PDT-resistant cells showed an amplicon in 5q11.2 MAP3K1, which was not present in parental cells. The changes detected by aCGH on CCND1, EFGR, and MAP3K1 were confirmed in extracts of SCC-13 cells by reverse-transcriptase PCR and by western blot, and by immunohistochemistry in human biopsies from persistent tumors after MAL-PDT. Our data suggest that genomic imbalances related to CCND1, EFGR, and particularly MAP3K1 seem to be involved in the development of the resistance of SCC to PDT.

Indexed as

Aged, 80 and overAminolevulinic AcidAnimalsBiopsyCell Line, TumorComparative Genomic HybridizationCyclin D1Drug Resistance, NeoplasmErbB ReceptorsFemaleHumansMaleMAP Kinase Kinase Kinase 1Mice, NudeNeoplasm InvasivenessNeoplasms, Squamous CellAminolevulinic AcidCCND1 protein, humanCyclin D1ErbB ReceptorsMAP3K1 protein, humanMAP Kinase Kinase Kinase 1Photosensitizing Agents

Identifiers

PMID24717244
OpenAlexW2050538949

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.