Evidence map›Paper›PMID 26664298›Full record

ArticleCancer cell international2015

Clinical relevance of thyroid cell models in redox research.

Francesca Cammarota, Francesco Fiscardi, Tiziana Esposito, Gabriella de Vita, Marco Salvatore, Mikko O Laukkanen

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Redox Homeostasis in Thyroid Cancer: Implications in NaInternational journal of molecular sciences · 2022
    Review
  7. Review
  8. Article
  9. Review
  10. Extracellular superoxide dismutase and its role in cancer.Free radical biology & medicine · 2017
    Review
  11. Article
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

6 authors at 3 institutions in 1 country.

Francesca CammarotaIRCCS SDN, Via E. Gianturco 113, 80143 Naples, Italy.
Francesco FiscardiIRCCS SDN, Via E. Gianturco 113, 80143 Naples, Italy.
Tiziana EspositoIRCCS SDN, Via E. Gianturco 113, 80143 Naples, Italy.
Gabriella de VitaDepartment of Molecular Medicine and Medical Biotechnologies, University of Naples Federico II, 80014 Naples, Italy.
Marco SalvatoreIRCCS SDN, Via E. Gianturco 113, 80143 Naples, Italy.
Mikko O LaukkanenIRCCS SDN, Via E. Gianturco 113, 80143 Naples, Italy.
SDN Istituto di Ricerca Diagnostica e Nucleare · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThyroid-derived cell models are commonly used to investigate the characteristics of thyroid cancers. It is noteworthy that each in vitro single cell model system imitates only a few characteristics of thyroid cancer depending on e.g. source of cells or oncogene used to transform the cells.

methodsIn the current work we utilized rat thyroid cancer cell models to determine their clinical relevance in redox gene studies by comparing in vitro expression data to thyroid Oncomine microarray database. To survey the cell lines we analyzed mRNA expression of genes that produce superoxide anion (nox family), genes that catalyze destruction of superoxide anion to hydrogen peroxide (sod family), and genes that remove hydrogen peroxide from cellular environment (catalase, gpx family and prdx family).

resultsBased on the current results, rat thyroid PC Cl3, PC PTC1, PC E1A, or FRLT5 cell models can be used to study NOX2, NOX4, SOD2, SOD3, CATALASE, GPX1, GPX2, GPX5, PRDX2, and PRDX3 gene expression and function.

conclusionsRedox gene expression in rat originated single cell model systems used to study human thyroid carcinogenesis corresponds only partly with human redox gene expression, which may be caused by differences in redox gene activation stimulus. The data suggest careful estimation of the data observed in rat thyroid in vitro models.

Indexed as

Cell lineCell modelExtracellular superoxide dismutaseFRTL5PC Cl3RatRedox gene expressionSOD3Thyroid cancer

Identifiers

PMID26664298
PMCPMC4673788
OpenAlexW2196438755

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Registered trials

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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.