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Search Results to Heide L Ford

This is a "connection" page, showing the details of why an item matched the keywords from your search.


One or more keywords matched the following items that are connected to Ford, Heide

Item TypeName
Academic Article Transcriptional control of the cell cycle in mammary gland development and tumorigenesis.
Academic Article The Six1 homeoprotein stimulates tumorigenesis by reactivation of cyclin A1.
Academic Article Gene amplification is a mechanism of Six1 overexpression in breast cancer.
Academic Article The Six1 homeoprotein induces human mammary carcinoma cells to undergo epithelial-mesenchymal transition and metastasis in mice through increasing TGF-beta signaling.
Academic Article Homeoprotein Six1 increases TGF-beta type I receptor and converts TGF-beta signaling from suppressive to supportive for tumor growth.
Academic Article Characterization of the Six1 homeobox gene in normal mammary gland morphogenesis.
Academic Article Six1 overexpression in mammary cells induces genomic instability and is sufficient for malignant transformation.
Academic Article Epithelial-mesenchymal transition in cancer: parallels between normal development and tumor progression.
Academic Article Mammary gland studies as important contributors to the cause of epithelial mesenchymal plasticity in malignancy.
Academic Article Six1 expands the mouse mammary epithelial stem/progenitor cell pool and induces mammary tumors that undergo epithelial-mesenchymal transition.
Academic Article SIX1 induces lymphangiogenesis and metastasis via upregulation of VEGF-C in mouse models of breast cancer.
Academic Article Breast cancer epithelial-to-mesenchymal transition: examining the functional consequences of plasticity.
Concept Breast Neoplasms
Academic Article Expression of Six1 in luminal breast cancers predicts poor prognosis and promotes increases in tumor initiating cells by activation of extracellular signal-regulated kinase and transforming growth factor-beta signaling pathways.
Academic Article Homeoprotein Six2 promotes breast cancer metastasis via transcriptional and epigenetic control of E-cadherin expression.
Academic Article Vascular endothelial growth factor C promotes breast cancer progression via a novel antioxidant mechanism that involves regulation of superoxide dismutase 3.
Academic Article The SIX1-EYA transcriptional complex as a therapeutic target in cancer.
Academic Article TWIST1-Induced miR-424 Reversibly Drives Mesenchymal Programming while Inhibiting Tumor Initiation.
Grant Developing cancer therapies through targeting the Six1/Eya transcriptional complex
Grant Role of Six1 and the miR106b 25 cluster in EMT and Tumor Progression
Grant The anti-tumorigenic and anti-metastatic potential of Eya phosphatase inhibitors
Grant TRAIL Receptor Signaling in Human Tumors
Grant The Six1/Eya Transcriptional complex as a mediator of lymphangiogenesis and lymph
Grant Identify inhibitors of the Eya phosphatase activity using high throughput screeni
Academic Article EMT cells increase breast cancer metastasis via paracrine GLI activation in neighbouring tumour cells.
Grant 2017 Mammary Gland Biology Gordon Research Conference & Gordon Research Seminar
Grant Role of Eya3 in regulating the immune microenvironment to promote breast tumor progression
Academic Article Eya3 promotes breast tumor-associated immune suppression via threonine phosphatase-mediated PD-L1 upregulation.
Academic Article Publisher Correction: EMT cells increase breast cancer metastasis via paracrine GLI activation in neighbouring tumour cells.
Academic Article SIX2 Mediates Late-Stage Metastasis via Direct Regulation of SOX2 and Induction of a Cancer Stem Cell Program.
Concept Triple Negative Breast Neoplasms
Academic Article Identification of a Small-Molecule Inhibitor That Disrupts the SIX1/EYA2 Complex, EMT, and Metastasis.
Academic Article Cellular Plasticity in Breast Cancer Progression and Therapy.
Academic Article VEGF-C mediates tumor growth and metastasis through promoting EMT-epithelial breast cancer cell crosstalk.
Academic Article Interferon-Induced Bone Marrow Stromal Antigen 2 (BST2) Is A Functional Tumor-Initiating Cell Marker In Triple-Negative Breast Cancer.

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  • Breast Neoplasms

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