We are analyzing https://link.springer.com/article/10.1007/s10911-010-9178-9.

Title:
Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor Progression | Journal of Mammary Gland Biology and Neoplasia
Description:
From the earliest stages of embryonic development, cells of epithelial and mesenchymal origin contribute to the structure and function of developing organs. However, these phenotypes are not always permanent, and instead, under the appropriate conditions, epithelial and mesenchymal cells convert between these two phenotypes. These processes, termed Epithelial-Mesenchymal Transition (EMT), or the reverse Mesenchymal-Epithelial Transition (MET), are required for complex body patterning and morphogenesis. In addition, epithelial plasticity and the acquisition of invasive properties without the full commitment to a mesenchymal phenotype are critical in development, particularly during branching morphogenesis in the mammary gland. Recent work in cancer has identified an analogous plasticity of cellular phenotypes whereby epithelial cancer cells acquire mesenchymal features that permit escape from the primary tumor. Because local invasion is thought to be a necessary first step in metastatic dissemination, EMT and epithelial plasticity are hypothesized to contribute to tumor progression. Similarities between developmental and oncogenic EMT have led to the identification of common contributing pathways, suggesting that the reactivation of developmental pathways in breast and other cancers contributes to tumor progression. For example, developmental EMT regulators including Snail/Slug, Twist, Six1, and Cripto, along with developmental signaling pathways including TGF-β and Wnt/β-catenin, are misexpressed in breast cancer and correlate with poor clinical outcomes. This review focuses on the parallels between epithelial plasticity/EMT in the mammary gland and other organs during development, and on a selection of developmental EMT regulators that are misexpressed specifically during breast cancer.
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Keywords {🔍}

emt, cells, cancer, cell, pubmed, google, scholar, cas, epithelial, development, tumor, mammary, breast, mesenchymal, expression, developmental, gland, transition, plasticity, migration, signaling, branching, including, phenotype, progression, snail, cripto, tgfβ, biol, epithelialmesenchymal, morphogenesis, growth, metastasis, induces, factor, dev, twist, undergo, carcinoma, regulators, transcription, spread, metastatic, numerous, formation, induction, ecadherin, invasive, invasion, pathways,

Topics {✒️}

epidermal growth factor-cripto/frl-1/cryptic smad2-smad4-lef1 transcription complex beta-catenin/lef-1 signaling pathway hypoxia-dependent epithelial-mesenchymal transition increasing tgf-beta signaling including nuclear β-catenin zinc-finger protein slug basal/claudin-low subtypes variable beta-catenin expression termed epithelial-mesenchymal transition epithelial-mesenchymal transition induced mmtv-cripto-1 transgenic mice beta-catenin regulates cripto wnt/β-catenin pathway multi-layered epithelial structure epithelial-mesenchymal cell transformation defining epithelial-mesenchymal transition long-range cell communication spindle-shaped mesenchymal cell extensive cell-cell interactions fibroblast growth factor reverse mesenchymal-epithelial transition premature epithelial-mesenchymal transition article download pdf ii tgf-β receptors undergo epithelial-mesenchymal transition genome-wide transcript analysis activated tgf-β signaling spindle-cell carcinoma tumors tgf-β family ligand epithelial-mesenchymal transition biomarkers squamous cell carcinoma tgf-β signaling plays e-cadherin gene expression e-cadherin repressor proteins tumor-initiating cell phenotype hypoxia inducible factor-1 six1 transcription factor related subjects transcription factor snail snail transcription factor human breast cancer-observations cell fate determination myc transgenic mice privacy choices/manage cookies e-cadherin repressors snail cell fate specification postnatal mammary gland mouse mammary gland emt/tumor-initiating cells

Schema {🗺️}

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         headline:Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor Progression
         description:From the earliest stages of embryonic development, cells of epithelial and mesenchymal origin contribute to the structure and function of developing organs. However, these phenotypes are not always permanent, and instead, under the appropriate conditions, epithelial and mesenchymal cells convert between these two phenotypes. These processes, termed Epithelial-Mesenchymal Transition (EMT), or the reverse Mesenchymal-Epithelial Transition (MET), are required for complex body patterning and morphogenesis. In addition, epithelial plasticity and the acquisition of invasive properties without the full commitment to a mesenchymal phenotype are critical in development, particularly during branching morphogenesis in the mammary gland. Recent work in cancer has identified an analogous plasticity of cellular phenotypes whereby epithelial cancer cells acquire mesenchymal features that permit escape from the primary tumor. Because local invasion is thought to be a necessary first step in metastatic dissemination, EMT and epithelial plasticity are hypothesized to contribute to tumor progression. Similarities between developmental and oncogenic EMT have led to the identification of common contributing pathways, suggesting that the reactivation of developmental pathways in breast and other cancers contributes to tumor progression. For example, developmental EMT regulators including Snail/Slug, Twist, Six1, and Cripto, along with developmental signaling pathways including TGF-β and Wnt/β-catenin, are misexpressed in breast cancer and correlate with poor clinical outcomes. This review focuses on the parallels between epithelial plasticity/EMT in the mammary gland and other organs during development, and on a selection of developmental EMT regulators that are misexpressed specifically during breast cancer.
         datePublished:2010-05-19T00:00:00Z
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            Breast cancer metastasis
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            Cancer Research
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      headline:Epithelial-Mesenchymal Transition in Cancer: Parallels Between Normal Development and Tumor Progression
      description:From the earliest stages of embryonic development, cells of epithelial and mesenchymal origin contribute to the structure and function of developing organs. However, these phenotypes are not always permanent, and instead, under the appropriate conditions, epithelial and mesenchymal cells convert between these two phenotypes. These processes, termed Epithelial-Mesenchymal Transition (EMT), or the reverse Mesenchymal-Epithelial Transition (MET), are required for complex body patterning and morphogenesis. In addition, epithelial plasticity and the acquisition of invasive properties without the full commitment to a mesenchymal phenotype are critical in development, particularly during branching morphogenesis in the mammary gland. Recent work in cancer has identified an analogous plasticity of cellular phenotypes whereby epithelial cancer cells acquire mesenchymal features that permit escape from the primary tumor. Because local invasion is thought to be a necessary first step in metastatic dissemination, EMT and epithelial plasticity are hypothesized to contribute to tumor progression. Similarities between developmental and oncogenic EMT have led to the identification of common contributing pathways, suggesting that the reactivation of developmental pathways in breast and other cancers contributes to tumor progression. For example, developmental EMT regulators including Snail/Slug, Twist, Six1, and Cripto, along with developmental signaling pathways including TGF-β and Wnt/β-catenin, are misexpressed in breast cancer and correlate with poor clinical outcomes. This review focuses on the parallels between epithelial plasticity/EMT in the mammary gland and other organs during development, and on a selection of developmental EMT regulators that are misexpressed specifically during breast cancer.
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         Epithelial-Mesenchymal transition
         Epithelial plasticity
         Breast cancer metastasis
         Branching morphogenesis
         Oncology
         Cancer Research
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