Evidence map›Paper›PMID 34208581›Full record

ArticleCancers2021

Upper Aerodigestive Tract Squamous Cell Carcinomas Show Distinct Overall DNA Methylation Profiles and Different Molecular Mechanisms behind WNT Signaling Disruption.

Sheila Coelho Soares-Lima, Hisham Mehanna, Diego Camuzi, Paulo Thiago de Souza-Santos, Tatiana de Almeida Simão, Pedro Nicolau-Neto, Monique de Souza Almeida Lopes, Cyrille Cuenin, Fazlur Rahman Talukdar, Nikolaos Batis and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

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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

16 authors at 5 institutions in 3 countries.

Sheila Coelho Soares-LimaMolecular Carcinogenesis Program, Brazilian National Cancer Institute, Rua André Cavalcanti, 37-6° Andar, Bairro de Fátima, Rio de Janeiro 20231-050, Brazil.
Hisham MehannaInstitute of Head and Neck Studies and Education (InHANSE), Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham B15 2TT, UK.
Diego CamuziMolecular Carcinogenesis Program, Brazilian National Cancer Institute, Rua André Cavalcanti, 37-6° Andar, Bairro de Fátima, Rio de Janeiro 20231-050, Brazil.ORCID 0000-0002-3807-3796
Paulo Thiago de Souza-SantosLaboratório de Hanseníase, Instituto Oswaldo Cruz, Fiocruz, Av. Brasil, 4365, Rio de Janeiro 21040-360, Brazil.ORCID 0000-0002-0493-6661
Tatiana de Almeida SimãoDepartamento de Bioquímica, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, Av. 28 de Setembro 87 fundos, Vila Isabel, Rio de Janeiro 20551-013, Brazil.
Pedro Nicolau-NetoMolecular Carcinogenesis Program, Brazilian National Cancer Institute, Rua André Cavalcanti, 37-6° Andar, Bairro de Fátima, Rio de Janeiro 20231-050, Brazil.ORCID 0000-0003-3322-2120
Monique de Souza Almeida LopesMolecular Carcinogenesis Program, Brazilian National Cancer Institute, Rua André Cavalcanti, 37-6° Andar, Bairro de Fátima, Rio de Janeiro 20231-050, Brazil.
Cyrille CueninEpigenetics Group, International Agency for Research on Cancer, 150 Cours Albert Thomas, CEDEX 08, 69372 Lyon, France.
Fazlur Rahman TalukdarEpigenetics Group, International Agency for Research on Cancer, 150 Cours Albert Thomas, CEDEX 08, 69372 Lyon, France.ORCID 0000-0002-6558-5543
Nikolaos BatisInstitute of Head and Neck Studies and Education (InHANSE), Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham B15 2TT, UK.ORCID 0000-0002-2305-7427
Izabella CostaSeção de Cirurgia de Cabeça e Pescoço, Instituto Nacional de Câncer-INCA, Praça da Cruz Vermelha, Rio de Janeiro 20230-130, Brazil.
Fernando DiasSeção de Cirurgia de Cabeça e Pescoço, Instituto Nacional de Câncer-INCA, Praça da Cruz Vermelha, Rio de Janeiro 20230-130, Brazil.
Davide Degli EspostiEpigenetics Group, International Agency for Research on Cancer, 150 Cours Albert Thomas, CEDEX 08, 69372 Lyon, France.
Mariana BoroniBioinformatics and Computational Biology Lab, Brazilian National Cancer Institute, Rua André Cavalcanti, 37-1° Andar, Bairro de Fátima, Rio de Janeiro 20231-050, Brazil.ORCID 0000-0003-3495-9917
Zdenko HercegEpigenetics Group, International Agency for Research on Cancer, 150 Cours Albert Thomas, CEDEX 08, 69372 Lyon, France.
Luis Felipe Ribeiro PintoMolecular Carcinogenesis Program, Brazilian National Cancer Institute, Rua André Cavalcanti, 37-6° Andar, Bairro de Fátima, Rio de Janeiro 20231-050, Brazil.
Instituto Nacional de Câncer - INCA · BRCentre international de recherche sur le cancer · FRUniversidade do Estado do Rio de Janeiro · BRUniversity of Birmingham · GBFundação Oswaldo Cruz · BR

Funding

World Health Organization 001
6 · The paper itself

Abstract

Upper aerodigestive tract (UADT) tumors present different biological behavior and prognosis, suggesting specific molecular mechanisms underlying their development. However, they are rarely considered as single entities (particularly head and neck subsites) and share the most common genetic alterations. Therefore, there is a need for a better understanding of the global DNA methylation differences among UADT tumors. We performed a genome-wide DNA methylation analysis of esophageal (ESCC), laryngeal (LSCC), oral (OSCC) and oropharyngeal (OPSCC) squamous cell carcinomas, and their non-tumor counterparts. The unsupervised analysis showed that non-tumor tissues present markedly distinct DNA methylation profiles, while tumors are highly heterogeneous. Hypomethylation was more frequent in LSCC and OPSCC, while ESCC and OSCC presented mostly hypermethylation, with the latter showing a CpG island overrepresentation. Differentially methylated regions affected genes in 127 signaling pathways, with only 3.1% of these being common among different tumor subsites, but with different genes affected. The WNT signaling pathway, known to be dysregulated in different epithelial tumors, is a frequent hit for DNA methylation and gene expression alterations in ESCC and OPSCC, but mostly for genetic alterations in LSCC and OSCC. UADT tumor subsites present differences in genome-wide methylation regarding their profile, intensity, genomic regions and signaling pathways affected.

Indexed as

DNA methylationesophageal squamous cell carcinomahead and neck cancerWNT signaling pathway

Identifiers

PMID34208581
PMCPMC8234055
OpenAlexW3166326451

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.