ArticleiScience2024
Increased prevalence of hybrid epithelial/mesenchymal state and enhanced phenotypic heterogeneity in basal breast cancer.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Clusters, fingers, and singles: A mechanical landscape of tumor invasion.PLoS computational biology · 2026Article
- Intrinsic cellular heterogeneity directs divergent epithelial-to-mesenchymal transition outcomes.The FEBS journal · 2026Article
- Varying susceptibility of subpopulations along the epithelial-mesenchymal spectrum to undergo EMT.The FEBS journal · 2026Article
- Systems-level analysis identifies IRF6 as an inhibitor of epithelial-mesenchymal transition.Journal of biological engineering · 2026Article
- CD4+ T Cells Sensitize Quasimesenchymal Breast Tumors Lacking CD73 to Anti-CTLA4 Immune Checkpoint Blockade Therapy.Cancer research communications · 2026Article
- SOX9 and SEMA7A regulate cell plasticity in the postpartum mammary gland with implications for breast cancer.bioRxiv : the preprint server for biology · 2026Article
- Endocrine therapy-specific lineage and partial epithelial-mesenchymal reprogramming defines divergent resistant cell-states in ER+ breast cancer.bioRxiv : the preprint server for biology · 2026Article
- Bidirectional coupling among EMT, AXL-RB1 signaling and lineage switch drives resistance to osimertinib and worse clinical outcomes in NSCLC.bioRxiv : the preprint server for biology · 2026Article
- Contribution of Mesenchymal-like and Epithelial Cellular Subsets to Chemotherapy Resistance in Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
- Gene regulatory network transitions reveal the central transcription factors in lung adenocarcinoma progression.NPJ systems biology and applications · 2026Article
- MMP9 shapes cell mechanics to enable collective invasion in cancer.NPJ systems biology and applications · 2025Article
- Shared and Context-Specific Mechanisms of EMT and Cellular Plasticity in Cancer and Fibrotic Diseases.International journal of molecular sciences · 2025Review
- Spatial Transcriptomics Decodes Breast Cancer Microenvironment Heterogeneity: From Multidimensional Dynamic Profiling to Precision Therapy Blueprint Construction.Biomolecules · 2025Review
- Recurring cycles of deprivation of serum and migration in confined spaces augments ganglioside SSEA-4 expression, boosting clonogenicity and cisplatin resistance in TNBC cell line.Scientific reports · 2025Article
- The Clinical Relevance of Epithelial-to-Mesenchymal Transition Hallmarks: A Cut-Off-Based Approach in Healthy and Cancerous Cell Lines.International journal of molecular sciences · 2025Article
- Role of EMT in drug resistance of breast cancer: molecular mechanisms and therapeutic strategies.Frontiers in oncology · 2025Review
- GABA Type A receptors expressed in triple negative breast cancer cells mediate chloride ion flux.Frontiers in pharmacology · 2024Article
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15 authors.
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Abstract
Intra-tumoral phenotypic heterogeneity promotes tumor relapse and therapeutic resistance and remains an unsolved clinical challenge. Decoding the interconnections among different biological axes of plasticity is crucial to understand the molecular origins of phenotypic heterogeneity. Here, we use multi-modal transcriptomic data-bulk, single-cell, and spatial transcriptomics-from breast cancer cell lines and primary tumor samples, to identify associations between epithelial-mesenchymal transition (EMT) and luminal-basal plasticity-two key processes that enable heterogeneity. We show that luminal breast cancer strongly associates with an epithelial cell state, but basal breast cancer is associated with hybrid epithelial/mesenchymal phenotype(s) and higher phenotypic heterogeneity. Mathematical modeling of core underlying gene regulatory networks representative of the crosstalk between the luminal-basal and epithelial-mesenchymal axes elucidate mechanistic underpinnings of the observed associations from transcriptomic data. Our systems-based approach integrating multi-modal data analysis with mechanism-based modeling offers a predictive framework to characterize intra-tumor heterogeneity and identify interventions to restrict it.
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