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    Jiang, Yi-Zhou; Ma, Ding; Suo, Chen; Shi, Jinxiu; Xue, Mengzhu; Hu, Xin; Xiao, Yi; Yu, Ke-Da; Liu, Yi-Rong; Yu, Ying; Zheng, Yuanting; Li, Xiangnan; Zhang, Chenhui; Hu, Pengchen; Zhang, Jing; Hua, Qi; Zhang, Jiyang; Hou, Wanwan; Ren, Luyao; Bao, Ding; Li, Bingying; Yang, Jingcheng; Yao, Ling; Zuo, Wen-Jia; Zhao, Shen; Gong, Yue; Ren, Yi-Xing; Zhao, Ya-Xin; Yang, Yun-Song; Niu, Zhenmin; Cao, Zhi-Gang; Stover, Daniel G.; Verschraegen, Claire; Kaklamani, Virginia; Daemen, Anneleen; Benson, John R.; Takabe, Kazuaki; Bai, Fan; Li, Da-Qiang; Wang, Peng; Shi, Leming; Huang, Wei; Shao, Zhi-Ming

    Cancer cell, 03/2019, Volume: 35, Issue: 3
    Journal Article

    We comprehensively analyzed clinical, genomic, and transcriptomic data of a cohort of 465 primary triple-negative breast cancer (TNBC). PIK3CA mutations and copy-number gains of chromosome 22q11 were more frequent in our Chinese cohort than in The Cancer Genome Atlas. We classified TNBCs into four transcriptome-based subtypes: (1) luminal androgen receptor (LAR), (2) immunomodulatory, (3) basal-like immune-suppressed, and (4) mesenchymal-like. Putative therapeutic targets or biomarkers were identified among each subtype. Importantly, the LAR subtype showed more ERBB2 somatic mutations, infrequent mutational signature 3 and frequent CDKN2A loss. The comprehensive profile of TNBCs provided here will serve as a reference to further advance the understanding and precision treatment of TNBC. Display omitted •We build the genomic and transcriptomic landscape of 465 primary TNBCs•Chinese TNBC cases demonstrate more PIK3CA mutations and LAR subtype•Transcriptomic data classify TNBCs into four subtypes•Multi-omics profiling identifies potential targets within specific TNBC subtypes Jiang et al. characterize primary Chinese triple-negative breast cancer (TNBC) and classify it into four subtypes. They find that these TNBCs have more frequent PIK3CA mutations and chromosome 22q11 copy-number gains than non-Asian TNBCs and that the LAR subtype has more ERBB2 somatic mutations and CDKN2A loss.