1. Genomic and Transcriptomic Landscape of Triple-Negative Breast Cancers: Subtypes and Treatment Strategies.
- Author
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Jiang YZ, Ma D, Suo C, Shi J, Xue M, Hu X, Xiao Y, Yu KD, Liu YR, Yu Y, Zheng Y, Li X, Zhang C, Hu P, Zhang J, Hua Q, Zhang J, Hou W, Ren L, Bao D, Li B, Yang J, Yao L, Zuo WJ, Zhao S, Gong Y, Ren YX, Zhao YX, Yang YS, Niu Z, Cao ZG, Stover DG, Verschraegen C, Kaklamani V, Daemen A, Benson JR, Takabe K, Bai F, Li DQ, Wang P, Shi L, Huang W, and Shao ZM
- Subjects
- Asian People genetics, Biomarkers, Tumor genetics, Chromosomes, Human, Pair 22 genetics, DNA Copy Number Variations, Female, Gene Deletion, Gene Expression Regulation, Neoplastic, Humans, Mutation, Neoplasm Metastasis, Prognosis, Triple Negative Breast Neoplasms genetics, Class I Phosphatidylinositol 3-Kinases genetics, Cyclin-Dependent Kinase Inhibitor p16 genetics, Gene Expression Profiling methods, Genomics methods, Receptor, ErbB-2 genetics, Triple Negative Breast Neoplasms classification
- 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., (Copyright © 2019 Elsevier Inc. All rights reserved.)
- Published
- 2019
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