ArticleNature communications2020
NOTCH1 activation compensates BRCA1 deficiency and promotes triple-negative breast cancer formation.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
What it found
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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.
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Who cites it
76 citing papers in PubMed, 118 citations in OpenAlex.
- Trial
- Notch receptors in breast cancer: context-dependent roles and therapeutic targeting.Cell communication and signaling : CCS · 2026Review
- Integrated Liquid Biopsy and Tumor Tissue Genomic Profiling of Appendiceal Cancer: cfDNA Burden, Mutation Landscapes, and Clinical Outcomes.Annals of surgical oncology · 2026Article
- MAML1 drives Notch and Hedgehog oncogenic pathways by inhibiting Itch activity in triple-negative breast cancer.Cell death and differentiation · 2026Article
- Multiple Regulatory Mechanisms of Post-Translational Modifications and Therapeutic Potential of Mitotic Catastrophe.International journal of molecular sciences · 2026Review
- DUSP22 dephosphorylates LGALS1 to enhance T cell-driven antitumor immunity.Journal for immunotherapy of cancer · 2026Article
- Recent advances in targeted therapies and immunotherapies for triple-negative breast cancer.Frontiers in oncology · 2026Review
- Subtype-Independent Dysregulation of the Notch Signaling Pathway and Its miRNA Regulators in Breast Cancer.Biomedicines · 2025Article
- RAD51B-EZH2 axis as a potential therapeutic target for TNBC through cell fate conversion.Cell death & disease · 2025Article
- Application of Gene Editing Technology Based on Targeted Delivery Materials in TNBC.ACS omega · 2025Review
- Cross-level Cross-Scale Inference and Imputation of Single-cell Spatial Proteomics.Research square · 2025Article
- Enhanced prediction of breast cancer patient response to chemotherapy by integrating deconvolved expression patterns of immune, stromal and tumor cells.bioRxiv : the preprint server for biology · 2025Article
- NOTCH1 combined with chemotherapy synergistically inhibits triple-negative breast cancer.World journal of clinical oncology · 2025Article
- Co-inhibition of Notch1 and ChK1 triggers genomic instability and melanoma cell death increasing the lifespan of mice bearing melanoma brain metastasis.Journal of experimental & clinical cancer research : CR · 2025Article
- Oncogenic activation of SMYD3-SHCBP1 promotes breast cancer development and is coupled with resistance to immune therapy.Cell death & disease · 2025Article
- Triple-Negative Breast Cancer Progression and Drug Resistance in the Context of Epithelial-Mesenchymal Transition.Cancers · 2025Review
- Multi-omics reveals that NOTCH1 promotes cervical cancer progression and reduces radiosensitivity.Frontiers in immunology · 2025Article
- The role of notch signaling pathway and non-coding RNAs in cancer and inflammation: progress, therapeutic insights, and future directions.Frontiers in immunology · 2025Review
- Article
- Advances in predicting breast cancer driver mutations: Tools for precision oncology (Review).International journal of molecular medicine · 2025Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BRCA1 mutation carriers have a higher risk of developing triple-negative breast cancer (TNBC), which is a refractory disease due to its non-responsiveness to current clinical targeted therapies. Using the Sleeping Beauty transposon system in Brca1-deficient mice, we identified 169 putative cancer drivers, among which Notch1 is a top candidate for accelerating TNBC by promoting the epithelial-mesenchymal transition (EMT) and regulating the cell cycle. Activation of NOTCH1 suppresses mitotic catastrophe caused by BRCA1 deficiency by restoring S/G2 and G2/M cell cycle checkpoints, which may through activation of ATR-CHK1 signalling pathway. Consistently, analysis of human breast cancer tissue demonstrates NOTCH1 is highly expressed in TNBCs, and the activated form of NOTCH1 correlates positively with increased phosphorylation of ATR. Additionally, we demonstrate that inhibition of the NOTCH1-ATR-CHK1 cascade together with cisplatin synergistically kills TNBC by targeting the cell cycle checkpoint, DNA damage and EMT, providing a potent clinical option for this fatal disease.
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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.