ArticleOncotarget2015
Cell type of origin as well as genetic alterations contribute to breast cancer phenotypes.
Article in Oncotarget, 2015. 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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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.
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Who cites it
17 citing papers in PubMed, 23 citations in OpenAlex.
- Endogenous promoter G-quadruplexes scaffold apurinic/apyrimidinic endonuclease (APE1) to drive gene expression.Nucleic acids research · 2026Article
- Cytokeratin expression in breast cancer: from mechanisms, progression, diagnosis, and prognosis to therapeutic implications.Molecular & cellular oncology · 2025Review
- A triple hormone receptor ER, AR, and VDR signature is a robust prognosis predictor in breast cancer.Breast cancer research : BCR · 2024Article
- Article
- ZNF92, an unexplored transcription factor with remarkably distinct breast cancer over-expression associated with prognosis and cell-of-origin.NPJ breast cancer · 2022Article
- Know thy cells: commonly used triple-negative human breast cancer cell lines carry mutations in RAS and effectors.Breast cancer research : BCR · 2022Article
- Myoepithelial progenitors as founder cells of hyperplastic human breast lesions upon PIK3CA transformation.Communications biology · 2022Article
- Keratin 19 maintains E-cadherin localization at the cell surface and stabilizes cell-cell adhesion of MCF7 cells.Cell adhesion & migration · 2021Article
- The Mammalian Ecdysoneless Protein Interacts with RNA Helicase DDX39A To Regulate Nuclear mRNA Export.Molecular and cellular biology · 2021Article
- Screening and Identification of Novel Potential Biomarkers for Breast Cancer Brain Metastases.Frontiers in oncology · 2021Article
- Keratin 19 regulates cell cycle pathway and sensitivity of breast cancer cells to CDK inhibitors.Scientific reports · 2019Article
- Review
- PI3K Signaling in Tissue Hyper-Proliferation: From Overgrowth Syndromes to Kidney Cysts.Cancers · 2017Review
- Establishment of a normal-derived estrogen receptor-positive cell line comparable to the prevailing human breast cancer subtype.Oncotarget · 2017Article
- Mutant PIK3CA Induces EMT in a Cell Type Specific Manner.PloS one · 2016Article
- Cancer stem cell-driven efficacy of trastuzumab (Herceptin): towards a reclassification of clinically HER2-positive breast carcinomas.Oncotarget · 2015Article
- Mammary stem cells: angels or demons in mammary gland?Signal transduction and targeted therapyReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Breast cancer is classified into different subtypes that are associated with different patient survival outcomes, underscoring the importance of understanding the role of precursor cell and genetic alterations in determining tumor subtypes. In this study, we evaluated the oncogenic phenotype of two distinct mammary stem/progenitor cell types designated as K5+/K19- or K5+/K19+ upon introduction of identical combinations of oncogenes-mutant H-Ras (mRas) and mutant p53 (mp53), together with either wild-type ErbB2(wtErbB2) or wild-type EGFR (wtEGFR). We examined their tumor forming and metastasis potential, using both in-vitro and in-vivo assays. Both the combinations efficiently transformed K5+/K19- or K5+/K19+ cells. Xenograft tumors formed by these cells were histologically heterogeneous, with variable proportions of luminal, basal-like and claudin-low type components depending on the cell types and oncogene combinations. Notably, K5+/K19- cells transformed with mRas/mp53/wtEGFR combination had a significantly longer latency for primary tumor development than other cell lines but more lung metastasis incidence than same cells expressing mRas/mp53/wtErbB2. K5+/K19+ cells exhibit shorter overall tumor latency, and high metastatic potential than K5+/K19- cells, suggesting that these K19+ progenitors are more susceptible to oncogenesis and metastasis. Our results suggest that both genetic alterations and cell type of origin contribute to oncogenic phenotype of breast tumors.
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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.