Evidence map›Paper›PMID 32050925›Full record

ArticleBMC cancer2020

Potential biomarkers of ductal carcinoma in situ progression.

Raquel Spinassé Dettogni, Elaine Stur, Ana Carolina Laus, René Aloísio da Costa Vieira, Márcia Maria Chiquitelli Marques, Iara Viana Vidigal Santana, José Zago Pulido, Laura Fregonassi Ribeiro, Narelle de Jesus Parmanhani, Lidiane Pignaton Agostini and 8 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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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

18 authors at 4 institutions in 2 countries.

Raquel Spinassé DettogniDepartment of Biological Sciences-Human and Molecular Genetics Nucleus, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil. rasdett@yahoo.com.br.ORCID http://orcid.org/0000-0002-9869-3321
Elaine SturDepartment of Biological Sciences-Human and Molecular Genetics Nucleus, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil.
Ana Carolina LausMolecular Oncology Research Center-Barretos Cancer Hospital, Barretos, Sao Paulo, Brazil.
René Aloísio da Costa VieiraDepartment of Mastology and Breast Reconstruction-Barretos Cancer Hospital, Barretos, Sao Paulo, Brazil.
Márcia Maria Chiquitelli MarquesMolecular Oncology Research Center-Barretos Cancer Hospital, Barretos, Sao Paulo, Brazil.
Iara Viana Vidigal SantanaDepartment of Pathology-Barretos Cancer Hospital, Barretos, Sao Paulo, Brazil.
José Zago PulidoEvangelical Hospital of Cachoeiro de Itapemirim, Cachoeiro de Itapemirim, Espirito Santo, Brazil.
Laura Fregonassi RibeiroEvangelical Hospital of Cachoeiro de Itapemirim, Cachoeiro de Itapemirim, Espirito Santo, Brazil.
Narelle de Jesus ParmanhaniEvangelical Hospital of Cachoeiro de Itapemirim, Cachoeiro de Itapemirim, Espirito Santo, Brazil.
Lidiane Pignaton AgostiniDepartment of Biological Sciences-Human and Molecular Genetics Nucleus, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil.
Raquel Silva Dos ReisDepartment of Biological Sciences-Human and Molecular Genetics Nucleus, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil.
Eldamária de Vargas Wolfgramm Dos SantosDepartment of Biological Sciences-Human and Molecular Genetics Nucleus, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil.
Lyvia Neves Rebello AlvesDepartment of Biological Sciences-Human and Molecular Genetics Nucleus, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil.
Fernanda Mariano GarciaDepartment of Biological Sciences-Human and Molecular Genetics Nucleus, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil.
Jéssica Aflávio SantosDepartment of Biological Sciences-Human and Molecular Genetics Nucleus, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil.
Diego do Prado VentorimDepartment of Biological Sciences-Human and Molecular Genetics Nucleus, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil.
Rui Manuel ReisMolecular Oncology Research Center-Barretos Cancer Hospital, Barretos, Sao Paulo, Brazil.
Iúri Drumond LouroDepartment of Biological Sciences-Human and Molecular Genetics Nucleus, Federal University of Espirito Santo, Vitoria, Espirito Santo, Brazil.
Universidade Federal do Espírito Santo · BRHospital de Câncer de Barretos · BRInstituto Federal do Espírito Santo · BRCentro Universitário da Fundação Educacional de Barretos · BR

Funding

Fundação de Amparo à Pesquisa do Espirito Santo-Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (FAPES-CAPES) 0698/2015Fundação Estadual de Amparo à Pesquisa do Estado do Espírito Santo 0468/2015Fundação Estadual de Amparo à Pesquisa do Estado do Espírito Santo 66141494/2014Fundação Estadual de Amparo à Pesquisa do Estado do Espírito Santo 66271126/2014
6 · The paper itself

Abstract

backgroundDuctal carcinoma in situ is a non-obligate precursor of invasive breast carcinoma and presents a potential risk of over or undertreatment. Finding molecular biomarkers of disease progression could allow for more adequate patient treatment. We aimed to identify potential biomarkers that can predict invasiveness risk.

methodsIn this epithelial cell-based study archival formalin-fixed paraffin-embedded blocks from six patients diagnosed with invasive lesions (pure invasive ductal carcinoma), six with in-situ lesions (pure ductal carcinoma in situ), six with synchronous lesions (invasive ductal carcinoma with an in-situ component) and three non-neoplastic breast epithelium tissues were analyzed by gene expression profiling of 770 genes, using the nCounter® PanCancer Pathways panel of NanoString Technologies.

resultsThe results showed that in comparison with non-neoplastic tissue the pure ductal carcinoma in situ was one with the most altered gene expression profile. Comparing pure ductal carcinoma in situ and in-situ component six differentially expressed genes were found, three of them (FGF2, GAS1, and SFRP1), play a role in cell invasiveness. Importantly, these genes were also differentially expressed between invasive and noninvasive groups and were negatively regulated in later stages of carcinogenesis.

conclusionsWe propose these three genes (FGF2, GAS1, and SFRP1) as potential biomarkers of ductal carcinoma in situ progression, suggesting that their downregulation may be involved in the transition of stationary to migrating invasive epithelial cells.

Indexed as

Biomarkers, TumorAgedAged, 80 and overCarcinoma, Ductal, BreastCarcinoma, Intraductal, NoninfiltratingComputational BiologyDisease ProgressionDisease SusceptibilityFemaleGene Expression ProfilingHumansMiddle AgedNeoplasm GradingNeoplasm StagingProtein Interaction MappingProtein Interaction MapsBiomarkers, TumorDuctal carcinoma in situFGF2GAS1SFRP1Tumor progression

Identifiers

PMID32050925
PMCPMC7017577
OpenAlexW3008382510

What OpenQuestion holds

Textmetadata
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.