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Search Results to Heide L Ford

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Ford, Heide

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

Item Type	Name
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	The miR-106b-25 cluster targets Smad7, activates TGF-? signaling, and induces EMT and tumor initiating cell characteristics downstream of Six1 in human breast cancer.
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.
Academic Article	Eya2 is required to mediate the pro-metastatic functions of Six1 via the induction of TGF-ß signaling, epithelial-mesenchymal transition, and cancer stem cell properties.
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	The miR-106b-25 cluster mediates breast tumor initiation through activation of NOTCH1 via direct repression of NEDD4L.
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	The interferon/STAT1 signaling axis is a common feature of tumor-initiating cells in breast cancer.
Grant	Deciphering the role of EYA3/PP2A in triple negative breast cancer metastasis
Academic Article	Remembering Hypoxia: Uncovering the Long-Term Effects of Transient Oxygen Deprivation on IFN Signaling and Progression of Breast Cancer.
Academic Article	Lineage Tracing and Single-Cell RNA Sequencing Reveal a Common Transcriptional State in Breast Cancer Tumor-Initiating Cells Characterized by IFN/STAT1 Activity.
Academic Article	EYA3 regulation of NF-?B and CCL2 suppresses cytotoxic NK cells in the premetastatic niche to promote TNBC metastasis.
Academic Article	MIRO2 promotes cancer invasion and metastasis via MYO9B suppression of RhoA activity.
Academic Article	An EYA3/NF-?B/CCL2 signaling axis suppresses cytotoxic NK cells in the pre-metastatic niche to promote triple negative breast cancer metastasis.
Academic Article	Two Sides of the Same Coin: The Role of Developmental pathways and pluripotency factors in normal mammary stem cells and breast cancer metastasis.

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Breast Neoplasms