Fibroblast-secreted hepatocyte growth factor mediates epidermal growth factor receptor tyrosine kinase inhibitor resistance in triple-negative breast cancers through paracrine activation of Met - Wikidata - awgldk - TriplyDB

Fibroblast-secreted hepatocyte growth factor mediates epidermal growth factor receptor tyrosine kinase inhibitor resistance in triple-negative breast cancers through paracrine activation of Met

Fibroblast-secreted hepatocyte growth factor mediates epidermal growth factor receptor tyrosine kinase inhibitor resistance in triple-negative breast cancers through paracrine activation of Met

http://www.wikidata.org/entity/Q36924414

about

Breast Cancer-Associated Fibroblasts: Where We Are and Where We Need to Go TGF-β Negatively Regulates CXCL1 Chemokine Expression in Mammary Fibroblasts through Enhancement of Smad2/3 and Suppression of HGF/c-Met Signaling Mechanisms Four individually druggable MET hotspots mediate HGF-driven tumor progression.Microenvironmental regulation of therapeutic response in cancer Weight Loss Reversed Obesity-Induced HGF/c-Met Pathway and Basal-Like Breast Cancer Progression Is the future of personalized therapy in triple-negative breast cancer based on molecular subtype?Inhibition of breast cancer growth and metastasis by a biomimetic peptide.Redundant kinase activation and resistance of EGFR-tyrosine kinase inhibitors.The role of HGF/MET and FGF/FGFR in fibroblast-derived growth stimulation and lapatinib-resistance of esophageal squamous cell carcinoma.Translational horizons in the tumor microenvironment: harnessing breakthroughs and targeting cures.Stromal cells in tumor microenvironment and breast cancer Dual inhibition of EGFR and MET induces synthetic lethality in triple-negative breast cancer cells through downregulation of ribosomal protein S6 Steroid Receptor Coactivator-3 (SRC-3/AIB1) as a Novel Therapeutic Target in Triple Negative Breast Cancer and Its Inhibition with a Phospho-Bufalin Prodrug.PTP1B-dependent regulation of receptor tyrosine kinase signaling by the actin-binding protein Mena.Mechanisms of resistance to EGFR tyrosine kinase inhibitors.Clinical implications of molecular heterogeneity in triple negative breast cancer.Humanized anti-hepatocyte growth factor (HGF) antibody suppresses innate irinotecan (CPT-11) resistance induced by fibroblast-derived HGF.Targeting matriptase in breast cancer abrogates tumour progression via impairment of stromal-epithelial growth factor signalling.LRIG1 opposes epithelial-to-mesenchymal transition and inhibits invasion of basal-like breast cancer cells.Impact of tumor microenvironment and epithelial phenotypes on metabolism in breast cancer Inhibition of the PI3K/AKT pathway potentiates cytotoxicity of EGFR kinase inhibitors in triple-negative breast cancer cells.cMET in triple-negative breast cancer: is it a therapeutic target for this subset of breast cancer patients?Breast cancer-associated fibroblasts: their roles in tumor initiation, progression and clinical applications.Knockdown of c-MET induced apoptosis in ABCB1-overexpressed multidrug-resistance cancer cell lines.Cancer-associated fibroblasts induce trastuzumab resistance in HER2 positive breast cancer cells.Differential expression of cancer-associated fibroblast-related proteins according to molecular subtype and stromal histology in breast cancer.Opioid growth factor - opioid growth factor receptor axis inhibits proliferation of triple negative breast cancer.The Therapeutic Potential of Targeting Tumor Microenvironment in Breast Cancer: Rational Strategies and Recent Progress.Changes in the Secretory Profile of NSCLC-Associated Fibroblasts after Ablative Radiotherapy: Potential Impact on Angiogenesis and Tumor Growth.Interleukin-6 receptor in spindle-shaped stromal cells, a prognostic determinant of early breast cancer.The HGF/c-MET Pathway Is a Driver and Biomarker of VEGFR-inhibitor Resistance and Vascular Remodeling in Non-Small Cell Lung Cancer.Targeting tumour microenvironment by tyrosine kinase inhibitor.Targeting the tumour stroma to improve cancer therapy.M2-polarized macrophages contribute to the decreased sensitivity of EGFR-TKIs treatment in patients with advanced lung adenocarcinoma.

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Fibroblast-secreted hepatocyte growth factor mediates epidermal growth factor receptor tyrosine kinase inhibitor resistance in triple-negative breast cancers through paracrine activation of Met

http://www.wikidata.org/entity/Q36924414

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2012 nî lūn-bûn

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2012年论文

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2012年论文

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name

Fibroblast-secreted hepatocyte ...... gh paracrine activation of Met

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Breast Cancer Research

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Fibroblast-secreted hepatocyte ...... gh paracrine activation of Met

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Charlotte Kuperwasser

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Gina L Zoratti

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Julie L Boerner

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Julie M Madden

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Karin List

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Kelly L Mueller

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P2860

Identification of the hepatocyte growth factor receptor as the c-met proto-oncogene product

EGFR/Met association regulates EGFR TKI resistance in breast cancer

Extracellular proteolytic cleavage by urokinase is required for activation of hepatocyte growth factor/scatter factor

EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.

MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.

Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib

Regulation of c-Met-dependent gene expression by PTEN

A third-generation lentivirus vector with a conditional packaging system

Met and c-Src cooperate to compensate for loss of epidermal growth factor receptor kinase activity in breast cancer cells

Lipid raft localization of EGFR alters the response of cancer cells to the EGFR tyrosine kinase inhibitor gefitinib

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10.1186/BCR3224

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4

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14

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3680928

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