ArticleNeoplasia (New York, N.Y.)2012
Novel model for basaloid triple-negative breast cancer: behavior in vivo and response to therapy.
Article in Neoplasia (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Live-Cell Optical Redox Imaging Reveals Metabolic Heterogeneity and Context-Dependent Responses to Metabolic Perturbation in TNBC Cells.Metabolites · 2026Article
- Synergistic lethality of combination treatment with Trop2-directed antibody-drug conjugate sacituzumab govitecan and TRAIL agonists in triple negative breast cancer.Breast cancer research : BCR · 2026Article
- Arginine methylation of human DNA topoisomerase I by PRMT5 facilitates DNA relaxation.Nucleic acids research · 2026Article
- Exploring the 89Zr/177Lu Theranostic Pairing with an Extracellular Matrix-Targeted Radiopharmaceutical against Triple-Negative Breast Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Article
- The involvement of exosomes in the tumorigenicity of breast cancer cell lines through the crosstalk between STAT3, Notch, and Wnt signaling pathways.Discover oncology · 2025Article
- Utilizing human cerebral organoids to model breast cancer brain metastasis in culture.Breast cancer research : BCR · 2024Article
- Influence of copper(I) nicotinate complex on the Notch1 signaling pathway in triple negative breast cancer cell lines.Scientific reports · 2024Article
- EZH2-H3K27me3 mediated KRT14 upregulation promotes TNBC peritoneal metastasis.Nature communications · 2022Article
- Article
- Optical Redox Imaging of Treatment Responses to Nampt Inhibition and Combination Therapy in Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2021Article
- Quantitative systems pharmacology model predictions for efficacy of atezolizumab and nab-paclitaxel in triple-negative breast cancer.Journal for immunotherapy of cancer · 2021Article
- BRD4 modulates vulnerability of triple-negative breast cancer to targeting of integrin-dependent signaling pathways.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- Oncogenic TRIM37 Links Chemoresistance and Metastatic Fate in Triple-Negative Breast Cancer.Cancer research · 2020Article
- Combined targeting EGFR and SRC as a potential novel therapeutic approach for the treatment of triple negative breast cancer.Therapeutic advances in medical oncology · 2020Article
- Scalable nanolaminated SERS multiwell cell culture assay.Microsystems & nanoengineering · 2020Article
- Synergistic Action of Stilbenes in Muscadine Grape Berry Extract Shows Better Cytotoxic Potential Against Cancer Cells Than Resveratrol Alone.Biomedicines · 2019Article
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- ΔNp63-driven recruitment of myeloid-derived suppressor cells promotes metastasis in triple-negative breast cancer.The Journal of clinical investigation · 2018Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
introductionThe basaloid triple-negative breast cancer (B-TNBC) is one of the most aggressive, therapy-resistant, and metastatic tumors. Current models do not recapitulate the basaloid phenotype of TNBC, thus limiting the understanding of its biology and designing new treatments. We identified HCC1806 as a line expressing typical B-TNBC markers, engineered a subline with traceable reporters, and determined growth, drug sensitivity, recurrence, and vascular and metastatic patterns of orthotopic xenografts in immunodeficient mice.
methodsmRNA and protein analyses showed that HCC1806 expresses basal but not luminal or mesenchymal markers. HCC1806-RR subline stably expressing red fluorescent protein and Renilla luciferase was generated and characterized for sensitivity to chemodrugs, orthotopic growth, vascular properties, recurrence, metastasis, and responsiveness in vivo.
resultsThe HCC1806 cells were highly sensitive to paclitaxel, but cytotoxicity was accompanied by pro-survival vascular endothelial growth factor-A loop. In vivo, HCC1806-RR tumors display linear growth, induce peritumoral lymphatics, and spontaneously metastasize to lymph nodes (LNs) and lungs. Similarly to human B-TNBC, HCC1806-RR tumors were initially sensitive to taxane therapy but subsequently recur. Bevacizumab significantly suppressed recurrence by 50% and reduced the incidence of LN and pulmonary metastases by, respectively, 50% and 87%.
conclusionsThe HCC1806-RR is a new model that expresses bona fide markers of B-TNBC and traceable markers for quantifying metastases. Combination of bevacizumab with nab-paclitaxel significantly improved the outcome, suggesting that this approach can apply to human patients with B-TNBC. This model can be used for defining the metastatic mechanisms of B-TNBC and testing new therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.