Evidence map›Paper›PMID 30172240›Full record

ArticleTranslational oncology2018

Mutations, Differential Gene Expression, and Chimeric Transcripts in Esophageal Squamous Cell Carcinoma Show High Heterogeneity.

Paulo Thiago de Souza-Santos, Sheila Coelho Soares Lima, Pedro Nicolau-Neto, Mariana Boroni, Nathalia Meireles Da Costa, Lilian Brewer, Albert Nobre Menezes, Carolina Furtado, Miguel Angelo Martins Moreira, Hector N Seuanez and 2 more

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Genes · 2024
    Article
  2. Article
  3. Signaling pathways and their potential therapeutic utility in esophageal squamous cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  4. Drugging multiple same-allele driver mutations in cancer.Expert opinion on drug discovery · 2021
    Article
  5. Article
  6. Review
  7. Article
  8. 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

12 authors at 3 institutions in 2 countries.

Paulo Thiago de Souza-SantosMolecular Carcinogenesis Program, Instituto Nacional de Câncer-INCA, Rua Andre Cavalcanti, 37-6° andar, Centro, Rio de Janeiro, RJ, Brasil, 20231-050. Electronic address: pthiagoss@gmail.com.
Sheila Coelho Soares LimaMolecular Carcinogenesis Program, Instituto Nacional de Câncer-INCA, Rua Andre Cavalcanti, 37-6° andar, Centro, Rio de Janeiro, RJ, Brasil, 20231-050. Electronic address: sheilacoelho@gmail.com.
Pedro Nicolau-NetoMolecular Carcinogenesis Program, Instituto Nacional de Câncer-INCA, Rua Andre Cavalcanti, 37-6° andar, Centro, Rio de Janeiro, RJ, Brasil, 20231-050. Electronic address: pedronicolau.n@gmail.com.
Mariana BoroniBioinformatics and Computational Biology Laboratory, Instituto Nacional de Câncer-INCA, Rua Andre Cavalcanti, 37-1° andar, Centro, Rio de Janeiro, RJ, Brasil, 20231-050. Electronic address: mariana.boroni@inca.gov.br.
Nathalia Meireles Da CostaMolecular Carcinogenesis Program, Instituto Nacional de Câncer-INCA, Rua Andre Cavalcanti, 37-6° andar, Centro, Rio de Janeiro, RJ, Brasil, 20231-050. Electronic address: natmeireles@gmail.com.
Lilian BrewerBiochemistry Department, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Boulevard 28 de Setembro, 77-Maracanã, Rio de Janeiro, RJ, Brasil, 20551-030. Electronic address: lilian.brewer06@gmail.com.
Albert Nobre MenezesCollege of Medical and Dental Sciences, University of Birmingham, Vicent Drive, Edgbaston, Birmingham, B15 2TT, UK. Electronic address: albertmenezes@gmail.com.
Carolina FurtadoGenetics Program, Instituto Nacional de Câncer-INCA, Rua Andre Cavalcanti, 37-4° andar, Centro, Rio de Janeiro, RJ, Brasil, 20231-050. Electronic address: carolfts@gmail.com.
Miguel Angelo Martins MoreiraGenetics Program, Instituto Nacional de Câncer-INCA, Rua Andre Cavalcanti, 37-4° andar, Centro, Rio de Janeiro, RJ, Brasil, 20231-050. Electronic address: miguelm@inca.gov.br.
Hector N SeuanezGenetics Program, Instituto Nacional de Câncer-INCA, Rua Andre Cavalcanti, 37-4° andar, Centro, Rio de Janeiro, RJ, Brasil, 20231-050. Electronic address: hseuanez@inca.gov.br.
Tatiana de Almeida SimãoBiochemistry Department, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Boulevard 28 de Setembro, 77-Maracanã, Rio de Janeiro, RJ, Brasil, 20551-030. Electronic address: tasimao@gmail.com.
Luis Felipe Ribeiro PintoMolecular Carcinogenesis Program, Instituto Nacional de Câncer-INCA, Rua Andre Cavalcanti, 37-6° andar, Centro, Rio de Janeiro, RJ, Brasil, 20231-050; Biochemistry Department, Instituto de Biologia Roberto Alcântara Gomes, Universidade do Estado do Rio de Janeiro, Boulevard 28 de Setembro, 77-Maracanã, Rio de Janeiro, RJ, Brasil, 20551-030. Electronic address: lfrpinto@inca.gov.br.
Instituto Nacional de Câncer - INCA · BRUniversidade do Estado do Rio de Janeiro · BRUniversity of Birmingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal squamous cell carcinoma (ESCC) is a frequent and lethal neoplasia. As recent advances in targeted therapy have not improved ESCC prognosis, characterization of molecular alterations associated to this tumor is of foremost relevance. In this study, we analyze, for the first time, the complete genomic profile of ESCC by RNA-seq. TP53 was the most frequently mutated gene in the investigation and validation sets (78.6% and 67.4%, respectively). Differential expression analysis between tumor and nontumor adjacent mucosa showed 6698 differentially expressed genes, most of which were overexpressed (74%). Enrichment analysis identified overrepresentation of Wnt pathway, with overexpressed activators and underexpressed inactivators, suggesting activation of canonical and noncanonical Wnt signaling pathways. Higher WNT7B expression was associated with poor prognosis. Twenty-one gene fusions were identified in 50% of tumors, none of which involving the same genes in different patients; 71% of fusions involved syntenic genes. Comparisons with TCGA data showed co-amplification of seven gene pairs involved in fusions in the present study (~33%), suggesting that these rearrangements might have been driven by chromoanagenesis. In conclusion, genomic alterations in ESCC are highly heterogeneous, impacting negatively in target therapy development.

Identifiers

PMID30172240
PMCPMC6121831
OpenAlexW2888889994

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.