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

Author

Listed:
  • Xi-Xi Chen

    (Peking University)

  • Qian Zhong

    (Sun Yat-Sen University Cancer Center)

  • Yang Liu

    (Peking University)

  • Shu-Mei Yan

    (Sun Yat-Sen University Cancer Center
    Sun Yat-Sen University Cancer Center)

  • Zhang-Hua Chen

    (Peking University)

  • Shan-Zhao Jin

    (Peking University)

  • Tian-Liang Xia

    (Sun Yat-Sen University Cancer Center)

  • Ruo-Yan Li

    (Peking University)

  • Ai-Jun Zhou

    (Sun Yat-Sen University Cancer Center)

  • Zhe Su

    (Peking University)

  • Yu-Hua Huang

    (Sun Yat-Sen University Cancer Center
    Sun Yat-Sen University Cancer Center)

  • Qi-Tao Huang

    (Sun Yat-Sen University Cancer Center
    Sun Yat-Sen University Cancer Center)

  • Li-Yun Huang

    (Sun Yat-Sen University Cancer Center
    Sun Yat-Sen University Cancer Center)

  • Xing Zhang

    (Sun Yat-Sen University Cancer Center)

  • Yan-Na Zhao

    (Peking University)

  • Jin-Ping Yun

    (Sun Yat-Sen University Cancer Center
    Sun Yat-Sen University Cancer Center)

  • Qiu-Liang Wu

    (Sun Yat-Sen University Cancer Center
    Sun Yat-Sen University Cancer Center)

  • Dong-Xin Lin

    (Sun Yat-Sen University Cancer Center
    Chinese Academy of Medical Science and Peking Union Medical College)

  • Fan Bai

    (Peking University)

  • Mu-Sheng Zeng

    (Sun Yat-Sen University Cancer Center)

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.

Suggested Citation

  • 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 & Yu-Hua Huang & Qi-Tao Huang & Li-Yun Huang & Xing Zhang & Yan-N, 2017. "Genomic comparison of esophageal squamous cell carcinoma and its precursor lesions by multi-region whole-exome sequencing," Nature Communications, Nature, vol. 8(1), pages 1-12, December.
  • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00650-0
    DOI: 10.1038/s41467-017-00650-0
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    Cited by:

    1. Sijia Cui & Nicholas McGranahan & Jing Gao & Peng Chen & Wei Jiang & Lingrong Yang & Li Ma & Junfang Liao & Tian Xie & Congying Xie & Tariq Enver & Shixiu Wu, 2023. "Tracking the evolution of esophageal squamous cell carcinoma under dynamic immune selection by multi-omics sequencing," Nature Communications, Nature, vol. 14(1), pages 1-14, December.
    2. Xuejiao Liu & Simin Zhao & Keke Wang & Liting Zhou & Ming Jiang & Yunfeng Gao & Ran Yang & Shiwen Yan & Wen Zhang & Bingbing Lu & Feifei Liu & Ran Zhao & Wenting Liu & Zihan Zhang & Kangdong Liu & Xia, 2023. "Spatial transcriptomics analysis of esophageal squamous precancerous lesions and their progression to esophageal cancer," Nature Communications, Nature, vol. 14(1), pages 1-20, December.
    3. Kasumi Murai & Stefan Dentro & Swee Hoe Ong & Roshan Sood & David Fernandez-Antoran & Albert Herms & Vasiliki Kostiou & Irina Abnizova & Benjamin A. Hall & Moritz Gerstung & Philip H. Jones, 2022. "p53 mutation in normal esophagus promotes multiple stages of carcinogenesis but is constrained by clonal competition," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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