| Literature DB >> 30853353 |
Yi-Zhou Jiang1, Ding Ma1, Chen Suo2, Jinxiu Shi3, Mengzhu Xue4, Xin Hu1, Yi Xiao1, Ke-Da Yu1, Yi-Rong Liu1, Ying Yu5, Yuanting Zheng5, Xiangnan Li5, Chenhui Zhang3, Pengchen Hu3, Jing Zhang3, Qi Hua3, Jiyang Zhang5, Wanwan Hou5, Luyao Ren5, Ding Bao5, Bingying Li5, Jingcheng Yang5, Ling Yao1, Wen-Jia Zuo1, Shen Zhao1, Yue Gong1, Yi-Xing Ren1, Ya-Xin Zhao1, Yun-Song Yang1, Zhenmin Niu3, Zhi-Gang Cao1, Daniel G Stover6, Claire Verschraegen6, Virginia Kaklamani7, Anneleen Daemen8, John R Benson9, Kazuaki Takabe10, Fan Bai11, Da-Qiang Li1, Peng Wang12, Leming Shi13, Wei Huang14, Zhi-Ming Shao15.
Abstract
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.Entities:
Keywords: genomic; molecular subtype; precision therapies; target; transcriptomic; triple-negative breast cancer
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Year: 2019 PMID： 30853353 DOI： 10.1016/j.ccell.2019.02.001
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743