ArticleCancers2021
Drug-Induced Resistance and Phenotypic Switch in Triple-Negative Breast Cancer Can Be Controlled via Resolution and Targeting of Individualized Signaling Signatures.
Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 28 citations in OpenAlex.
- Metabolic stress conditions dictate MAPKAPK2-dependent efficiency of MEK1/2 inhibition in colorectal carcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Omics-based large language models: A new engine for drug discovery innovation.Acta pharmaceutica Sinica. B · 2026Review
- Large-scale foundation model on single-cell transcriptomics.Nature methods · 2024Article
- Patient-specific signaling signatures predict optimal therapeutic combinations for triple negative breast cancer.Molecular cancer · 2024Article
- AURKAIP1 actuates tumor progression through stabilizing DDX5 in triple negative breast cancer.Cell death & disease · 2023Article
- Quantification of ligand and mutation-induced bias in EGFR phosphorylation in direct response to ligand binding.Nature communications · 2023Article
- Understanding Glioblastoma Signaling, Heterogeneity, Invasiveness, and Drug Delivery Barriers.International journal of molecular sciences · 2023Review
- PRR15 deficiency facilitates malignant progression by mediating PI3K/Akt signaling and predicts clinical prognosis in triple-negative rather than non-triple-negative breast cancer.Cell death & disease · 2023Article
- Enabling Single-Cell Drug Response Annotations from Bulk RNA-Seq Using SCAD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Review
- Research progress of cancer cell membrane coated nanoparticles for the diagnosis and therapy of breast cancer.Frontiers in oncology · 2023Review
- Computational quantification and characterization of independently evolving cellular subpopulations within tumors is critical to inhibit anti-cancer therapy resistance.Genome medicine · 2022Article
- Identification of a novel signature with prognostic value in triple-negative breast cancer through clinico-transcriptomic analysis.Annals of translational medicine · 2022Article
- Overcoming resistance to EGFR monotherapy in HNSCC by identification and inhibition of individualized cancer processes.Theranostics · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Triple-negative breast cancer (TNBC) is an aggressive subgroup of breast cancers which is treated mainly with chemotherapy and radiotherapy. Epidermal growth factor receptor (EGFR) was considered to be frequently expressed in TNBC, and therefore was suggested as a therapeutic target. However, clinical trials of EGFR inhibitors have failed. In this study, we examine the relationship between the patient-specific TNBC network structures and possible mechanisms of resistance to anti-EGFR therapy. Using an information-theoretical analysis of 747 breast tumors from the TCGA dataset, we resolved individualized protein network structures, namely patient-specific signaling signatures (PaSSS) for each tumor. Each PaSSS was characterized by a set of 1-4 altered protein-protein subnetworks. Thirty-one percent of TNBC PaSSSs were found to harbor EGFR as a part of the network and were predicted to benefit from anti-EGFR therapy as long as it is combined with anti-estrogen receptor (ER) therapy. Using a series of single-cell experiments, followed by in vivo support, we show that drug combinations which are not tailored accurately to each PaSSS may generate evolutionary pressure in malignancies leading to an expansion of the previously undetected or untargeted subpopulations, such as ER+ populations. This corresponds to the PaSSS-based predictions suggesting to incorporate anti-ER drugs in certain anti-TNBC treatments. These findings highlight the need to tailor anti-TNBC targeted therapy to each PaSSS to prevent diverse evolutions of TNBC tumors and drug resistance development.
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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.