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