Identification of human triple-negative breast cancer subtypes and preclinical models for selection of targeted therapies
Open accessAbstract
Triple-negative breast cancer (TNBC) is a highly diverse group of cancers, and subtyping is necessary to better identify molecular-based therapies. In this study, we analyzed gene expression (GE) profiles from 21 breast cancer data sets and identified 587 TNBC cases. Cluster analysis identified 6 TNBC subtypes displaying unique GE and ontologies, including 2 basal-like (BL1 and BL2), an immunomodulatory (IM), a mesenchymal (M), a mesenchymal stem-like (MSL), and a luminal androgen receptor (LAR) subtype. Further, GE analysis allowed us to identify TNBC cell line models representative of these subtypes. Predicted "driver" signaling pathways were pharmacologically targeted in these cell line models as proof of concept that analysis of distinct GE signatures can inform therapy selection. BL1 and BL2 subtypes had higher expression of cell cycle and DNA damage response genes, and representative cell lines preferentially responded to cisplatin. M and MSL subtypes were enriched in GE for epithelial-mesenchymal transition, and growth factor pathways and cell models responded to NVP-BEZ235 (a PI3K/mTOR inhibitor) and dasatinib (an abl/src inhibitor). The LAR subtype includes patients with decreased relapse-free survival and was characterized by androgen receptor (AR) signaling. LAR cell lines were uniquely sensitive to bicalutamide (an AR antagonist). These data may be useful in biomarker selection, drug discovery, and clinical trial design that will enable alignment of TNBC patients to appropriate targeted therapies.
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Expression-based profiling and Integrative Clusters cannot adequately discriminate HRDetect groups, suggesting HRDetect provides a novel independent angle to TNBC stratification.
“expression-based profiling (e.g., PAM50) and Integrative Clusters13,15 are not adequately able to discriminate HRDetect groups, suggesting that HRDetect provides a novel, independent angle to TNBC stratification.”
From Whole-genome sequencing of triple-negative breast cancers in a population-based clinical study (2019) · cites this paper as [13]
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- Authors
- Lehmann, B. D., Bauer, J. A., Chen, X., Sanders, M. E., Chakravarthy, A. B., Shyr, Y., & Pietenpol, J. A.
- Affiliations
- Vanderbilt University (US)
- Corresponding author
- Pietenpol, Jennifer A.
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2011-07-01
- Volume
- 121
- Issue
- 7
- Pages
- 2750-2767
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3127435
- OpenAlex
- W2134539328
- Cited by
- 5,592
- References
- 78
- Citations by year
- 2026: 301 · 2025: 367 · 2024: 370 · 2023: 492 · 2022: 506 · 2021: 596 · 2020: 485 · 2019: 409 · 2018: 429 · 2017: 377 · 2016: 379 · 2015: 342 · 2014: 259 · 2013: 185 · 2012: 69
- FWCI
- 58.09
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Vanderbilt University (CA68485)
- Vanderbilt-Ingram Cancer Center (CA68485)
- National Institutes of Health (CA68485, CA95131)
- National Cancer Institute (CA 009385, CA 105436, R01CA105436, R01CA070856, CA95131, CA68485, CA-070856, RC2CA148375, T32CA009385, P30CA068485, CA148375)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Health Sciences › Medicine › Pathology and Forensic Medicine › Breast Lesions and Carcinomas
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- triple-negative breast cancer, tumor subtypes, gene expression profiling, basal-like breast cancer, immunomodulatory subtype, mesenchymal subtype, mesenchymal stem-like subtype, luminal androgen receptor subtype, epithelial-mesenchymal transition, androgen receptor signaling, targeted therapy selection, cisplatin sensitivity, PI3K/mTOR inhibition, dasatinib, bicalutamide, DNA damage response, relapse-free survival
- MeSH terms
- Animals, Antineoplastic Agents, Breast Neoplasms, Female, Humans, Mice, Nude, Phenotype, Transplantation, Heterologous, Signal Transduction, Gene Expression Regulation, Neoplastic, Gene Expression Profiling, Cell Line, Tumor, Mice, Kaplan-Meier Estimate
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