ArticleBMC cancer2019
Cisplatin-resistant triple-negative breast cancer subtypes: multiple mechanisms of resistance.
Article in BMC cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 126 citations in OpenAlex.
- NRF2/SLC7A11/GPX4 Antioxidant Axis Suppression by Camel Milk Whey Protein Sensitizes MCF-7 Breast Cancer Cells to Cisplatin.International journal of molecular sciences · 2026Article
- Red blood cell-derived extracellular vesicles enable cisplatin and cetuximab combined therapy against triple-negative breast cancer.Journal of nanobiotechnology · 2026Article
- Eugenoplatin (a phyto-chemo drug conjugate) targets cancer stem cells through inhibition of the β-catenin signaling in triple-negative breast cancer cells.Journal of translational medicine · 2026Article
- circSCAP-encoded SCAP-129aa mediates platinum resistance in triple-negative breast cancer via the PI3K/AKT pathway.Science China. Life sciences · 2026Article
- An Investigation to Identify the Anti-Cancer Properties of Novel Rhenium Compounds in Prostate and Lung Cancer Cell Lines.Journal of biotechnology and biomedicine · 2026Article
- Diphenyl Disulfide Induces Nonapoptotic Paraptosis in Breast Cancer Cells via ROS-Mediated ER Stress.International journal of medical sciences · 2026Article
- Modular Design of Mesoporous Silica Nanoparticles Enables Bioimaging, Dual Chemotherapy, and Combinatorial Gene Silencing in Triple-Negative Breast Cancer.ACS applied materials & interfaces · 2025Article
- Metabolomics as a tool for understanding and treating triple-negative breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- HDAC2-Mediated METTL3 Delactylation Promotes DNA Damage Repair and Chemotherapy Resistance in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Synthesis, Structure, and Stability of Copper(II) Complexes Containing Imidazoline-Phthalazine Ligands with Potential Anticancer Activity.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Classifications of triple-negative breast cancer: insights and current therapeutic approaches.Cell & bioscience · 2025Review
- Synergistic Effects of Mistletoe Lectin and Cisplatin on Triple-Negative Breast Cancer Cells: Insights from 2D and 3D In Vitro Models.International journal of molecular sciences · 2025Article
- Response of MDA-MB231 cells to cisplatin and paclitaxel - viability, migration and gene expression estimation in mono- and co-culture with macrophages.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 2025Article
- FOXA2 Activates RND1 to Regulate Arachidonic Acid Metabolism Pathway and Suppress Cisplatin Resistance in Lung Squamous Cell Carcinoma.The clinical respiratory journal · 2024Article
- The therapeutic efficacy of 5-ALA based photodynamic therapy and chemotherapy combination in triple negative breast cancer cells.Lasers in medical science · 2024Article
- Systemic oncological therapy in breast cancer patients on dialysis.World journal of clinical oncology · 2024Review
- BUB1 Inhibition Sensitizes TNBC Cell Lines to Chemotherapy and Radiotherapy.Biomolecules · 2024Article
- Oncogenic miR-106b-5p promotes cisplatin resistance in triple-negative breast cancer by targeting GDF11.Histology and histopathology · 2024Article
- Enhancement of targeted therapy in combination with metformin on human breast cancer cell lines.Cell communication and signaling : CCS · 2024Article
- Downregulation of TAB182 promotes cancer stem-like cell properties and therapeutic resistance in triple-negative breast cancer cells.BMC cancer · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundUnderstanding mechanisms underlying specific chemotherapeutic responses in subtypes of cancer may improve identification of treatment strategies most likely to benefit particular patients. For example, triple-negative breast cancer (TNBC) patients have variable response to the chemotherapeutic agent cisplatin. Understanding the basis of treatment response in cancer subtypes will lead to more informed decisions about selection of treatment strategies.
methodsIn this study we used an integrative functional genomics approach to investigate the molecular mechanisms underlying known cisplatin-response differences among subtypes of TNBC. To identify changes in gene expression that could explain mechanisms of resistance, we examined 102 evolutionarily conserved cisplatin-associated genes, evaluating their differential expression in the cisplatin-sensitive, basal-like 1 (BL1) and basal-like 2 (BL2) subtypes, and the two cisplatin-resistant, luminal androgen receptor (LAR) and mesenchymal (M) subtypes of TNBC.
resultsWe found 20 genes that were differentially expressed in at least one subtype. Fifteen of the 20 genes are associated with cell death and are distributed among all TNBC subtypes. The less cisplatin-responsive LAR and M TNBC subtypes show different regulation of 13 genes compared to the more sensitive BL1 and BL2 subtypes. These 13 genes identify a variety of cisplatin-resistance mechanisms including increased transport and detoxification of cisplatin, and mis-regulation of the epithelial to mesenchymal transition.
conclusionsWe identified gene signatures in resistant TNBC subtypes indicative of mechanisms of cisplatin. Our results indicate that response to cisplatin in TNBC has a complex foundation based on impact of treatment on distinct cellular pathways. We find that examination of expression data in the context of heterogeneous data such as drug-gene interactions leads to a better understanding of mechanisms at work in cancer therapy response.
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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.