Evidence map›Paper›PMID 28900112›Full record

ArticleNature communications2017

Genomic comparison of esophageal squamous cell carcinoma and its precursor lesions by multi-region whole-exome sequencing.

Xi-Xi Chen, Qian Zhong, Yang Liu, Shu-Mei Yan, Zhang-Hua Chen, Shan-Zhao Jin, Tian-Liang Xia, Ruo-Yan Li, Ai-Jun Zhou, Zhe Su and 10 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 1 pooled it
10.2field-weighted citation impact, top 1% 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

92 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

  1. Pooled it
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  7. Review
  8. Review
  9. Deciphering precursor cell dynamics in esophageal preneoplasia via genetic barcoding and single-cell transcriptomics.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Carcinoma of Esophagus.Journal of gastroenterology and hepatology · 2025
    Review
  18. Article
  19. Review
  20. Review

32 more citing papers are in PubMed but not listed here.

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

20 authors at 2 institutions in 1 country.

Xi-Xi ChenBiodynamic Optical Imaging Center (BIOPIC), School of Life Sciences, Peking University, Beijing, 100871, China.ORCID http://orcid.org/0000-0001-8914-7620
Qian ZhongState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Yang LiuBiodynamic Optical Imaging Center (BIOPIC), School of Life Sciences, Peking University, Beijing, 100871, China.
Shu-Mei YanState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Zhang-Hua ChenBiodynamic Optical Imaging Center (BIOPIC), School of Life Sciences, Peking University, Beijing, 100871, China.
Shan-Zhao JinBiodynamic Optical Imaging Center (BIOPIC), School of Life Sciences, Peking University, Beijing, 100871, China.
Tian-Liang XiaState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Ruo-Yan LiBiodynamic Optical Imaging Center (BIOPIC), School of Life Sciences, Peking University, Beijing, 100871, China.
Ai-Jun ZhouState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Zhe SuBiodynamic Optical Imaging Center (BIOPIC), School of Life Sciences, Peking University, Beijing, 100871, China.
Yu-Hua HuangState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Qi-Tao HuangState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Li-Yun HuangState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Xing ZhangState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Yan-Na ZhaoBiodynamic Optical Imaging Center (BIOPIC), School of Life Sciences, Peking University, Beijing, 100871, China.
Jin-Ping YunState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Qiu-Liang WuState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Dong-Xin LinState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Fan BaiBiodynamic Optical Imaging Center (BIOPIC), School of Life Sciences, Peking University, Beijing, 100871, China. fbai@pku.edu.cn.
Mu-Sheng ZengState Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China. zengmsh@mail.sysu.edu.cn.
Sun Yat-sen University · CNPeking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal squamous dysplasia is believed to be the precursor lesion of esophageal squamous cell carcinoma (ESCC); however, the genetic evolution from dysplasia to ESCC remains poorly understood. Here, we applied multi-region whole-exome sequencing to samples from two cohorts, 45 ESCC patients with matched dysplasia and carcinoma samples, and 13 tumor-free patients with only dysplasia samples. Our analysis reveals that dysplasia is heavily mutated and harbors most of the driver events reported in ESCC. Moreover, dysplasia is polyclonal, and remarkable heterogeneity is often observed between tumors and their neighboring dysplasia samples. Notably, copy number alterations are prevalent in dysplasia and persist during the ESCC progression, which is distinct from the development of esophageal adenocarcinoma. The sharp contrast in the prevalence of the 'two-hit' event on TP53 between the two cohorts suggests that the complete inactivation of TP53 is essential in promoting the development of ESCC.The pathogenesis of oesophageal squamous cell carcinoma is a multi-step process but the genetic determinants behind this progression are unknown. Here the authors use multi-region exome sequencing to comprehensively investigate the genetic evolution of precursor dysplastic lesions and untransformed oesophagus.

Indexed as

ExomeMutationCarcinoma, Squamous CellDNA Copy Number VariationsEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaHumansLoss of HeterozygosityPrecancerous ConditionsSequence Analysis, DNATumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID28900112
PMCPMC5595870
OpenAlexW2753395054

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.