Evidence map›Paper›PMID 30355311›Full record

ArticleBMC genomics2018

Distinct esophageal adenocarcinoma molecular subtype has subtype-specific gene expression and mutation patterns.

Xiangqian Guo, Yitai Tang, Wan Zhu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC genomics, 2018. 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
0.6field-weighted citation impact, top 28% 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, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. 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

3 authors at 2 institutions in 2 countries.

Xiangqian GuoDepartment of Preventive Medicine, Joint National Laboratory for Antibody Drug Engineering, Institute of Biomedical Informatics ,School of Basic Medical Sciences, Henan University, Kaifeng, 475004, China. xqguo@henu.edu.cn.ORCID http://orcid.org/0000-0001-6645-5786
Yitai TangDepartment of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Wan ZhuDepartment of Anesthesia, Stanford University, 300 Pasteur Drive, Stanford, CA, 94305, USA.
Stanford University · USHenan University · CN

Funding

National Natural Science Foundation of China 81602362program for Innovative Talents of Science and Technology in Henan Province 18HASTIT048program for Science and Technology Development in Henan Province 162102310391program for Young Key Teacher of Henan Province 2016GGJS-214supporting grants of Henan University 2015YBZR048supporting grants of Henan University B2015151supporting grants of Henan University yqpy20170039Yellow River Scholar Program H2016012
6 · The paper itself

Abstract

backgroundEsophageal carcinoma (EC), consists of two histological types, esophageal squamous carcinoma (ESCC) and esophageal adenocarcinoma (EAC). EAC accounted for 10% of EC for centuries; however, the prevalence of EAC has alarmingly risen 6 times and increased to about 50% of EC in recent 30 years in the western countries, while treatment options for EAC patients are still limited. Stratification of molecular subtypes by gene expression profiling methods had offered opportunities for targeted therapies. However, the molecular subtype in EAC has not been defined. Hence, Identification of EAC molecular subtypes is needed and will provide important insights for future new therapies.

resultsWe performed meta-analysis of gene expression profiling data on three independent EAC cohorts and showed that there are two common molecular subtypes in EAC. Each of the two EAC molecular subtypes has subtype specific expression patterns and mutation signatures. Genes which were over-expressed in subtype I EACs rather than subtype II EAC cases, were enriched in biological processes including epithelial cell differentiation, keratinocyte differentiation, and KEGG pathways including basal cell carcinoma. TP53 and CDKN2A are significantly mutated in both EAC subtypes. 24 genes including SMAD4 were found to be only significantly mutated in subtype I EAC cases, while 30 genes including ARID1A are only significantly mutated in subtype II EACs.

conclusionTwo EAC molecular subtypes were defined and validated. This finding may offer new opportunities for targeted therapies.

Indexed as

Biomarkers, TumorGene Expression Regulation, NeoplasticMutationAdenocarcinomaComputational BiologyEsophageal NeoplasmsGene Expression ProfilingHumansTranscriptomeBiomarkers, TumorEsophageal adenocarcinomaGene expressionMolecular subtypeMutationTherapy

Identifiers

PMID30355311
PMCPMC6201634
OpenAlexW2898434194

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.