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DOI . ORG {}

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We began analyzing https://www.nature.com/articles/s41580-018-0080-4, but it redirected us to https://www.nature.com/articles/s41580-018-0080-4. The analysis below is for the second page.

Title[redir]:
New insights into the mechanisms of epithelial–mesenchymal transition and implications for cancer | Nature Reviews Molecular Cell Biology
Description:
Epithelial–mesenchymal transition (EMT) is a cellular programme that is known to be crucial for embryogenesis, wound healing and malignant progression. During EMT, cell–cell and cell–extracellular matrix interactions are remodelled, which leads to the detachment of epithelial cells from each other and the underlying basement membrane, and a new transcriptional programme is activated to promote the mesenchymal fate. In the context of neoplasias, EMT confers on cancer cells increased tumour-initiating and metastatic potential and a greater resistance to elimination by several therapeutic regimens. In this Review, we discuss recent findings on the mechanisms and roles of EMT in normal and neoplastic tissues, and the cell-intrinsic signals that sustain expression of this programme. We also highlight how EMT gives rise to a variety of intermediate cell states between the epithelial and the mesenchymal state, which could function as cancer stem cells. In addition, we describe the contributions of the tumour microenvironment in inducing EMT and the effects of EMT on the immunobiology of carcinomas. Epithelial–mesenchymal transition (EMT) is crucial for embryogenesis, wound healing and cancer development, and confers greater resistance to cancer therapies. This Review discusses the mechanisms of EMT and its roles in normal and neoplastic tissues, the contribution of cell-intrinsic signals and the microenvironment to inducing EMT, and its effects on the immunobiology of carcinomas.

Matching Content Categories {📚}

  • Education
  • Science
  • Health & Fitness

Content Management System {📝}

What CMS is doi.org built with?

Custom-built

No common CMS systems were detected on Doi.org, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of doi.org audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Doi.org Make Money? {💸}

We don’t know how the website earns money.

Earning money isn't the goal of every website; some are designed to offer support or promote social causes. People have different reasons for creating websites. This might be one such reason. Doi.org might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {🔍}

pubmed, google, scholar, cas, cancer, central, cell, transition, cells, epithelialmesenchymal, metastasis, emt, breast, biol, epithelial, nature, nat, stem, mesenchymal, tumor, res, carcinoma, development, signaling, snail, growth, factor, promotes, pathway, signalling, expression, epithelialtomesenchymal, immune, lung, progression, rev, sci, notch, weinberg, clin, mol, article, oncogene, induces, oncotarget, molecular, med, research, mechanisms, access,

Topics {✒️}

akt/gsk-3beta/beta-catenin signaling pathway nature portfolio journals permissions reprints c-met /pi3k/akt/mtor pathway nature portfolio privacy policy lncrna-hit-mediated tgfbeta-induced epithelial tgf-beta-induced epithelial–mesenchymal transition tgf-β-induced epithelial-mesenchymal transition tgf-β-mediated epithelial–mesenchymal transition advertising phospho-smad2/3-snail signaling pathway wnt/beta-catenin signaling pathway activating wnt/beta-catenin signaling twist1-induced epithelial-mesenchymal transition snail1-mediated epithelial-mesenchymal transition myeloid-derived suppressor cells transforming growth factor-beta social media triple-negative breast cancer stromal cell-derived factor-1 wnt/beta-catenin signaling tgf-beta-induced epithelial author information authors snail1-induced partial epithelial mapk/egr-1-mediated upregulation c-met drives metastasis transforming growth factor tgf-beta-induced emt membrane-bound transcription factor egf-induced e-cadherin called contact-dependent signalling antagonizing p53-mediated apoptosis author correspondence nature+ nature 525 nature 527 nature 547 nature 545 nature 543 nature cancer research epithelial–mesenchymal plasticity landscape induce epithelial–mesenchymal transition promotes cell-cell adhesion glossary high-grade malignancy zeb1 represses e-cadherin biomedical research epidermal growth factor single-cell transcriptomic analysis

Questions {❓}

  • Tackling the cancer stem cells — what challenges do they pose?

Schema {🗺️}

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         description:Epithelial–mesenchymal transition (EMT) is a cellular programme that is known to be crucial for embryogenesis, wound healing and malignant progression. During EMT, cell–cell and cell–extracellular matrix interactions are remodelled, which leads to the detachment of epithelial cells from each other and the underlying basement membrane, and a new transcriptional programme is activated to promote the mesenchymal fate. In the context of neoplasias, EMT confers on cancer cells increased tumour-initiating and metastatic potential and a greater resistance to elimination by several therapeutic regimens. In this Review, we discuss recent findings on the mechanisms and roles of EMT in normal and neoplastic tissues, and the cell-intrinsic signals that sustain expression of this programme. We also highlight how EMT gives rise to a variety of intermediate cell states between the epithelial and the mesenchymal state, which could function as cancer stem cells. In addition, we describe the contributions of the tumour microenvironment in inducing EMT and the effects of EMT on the immunobiology of carcinomas. Epithelial–mesenchymal transition (EMT) is crucial for embryogenesis, wound healing and cancer development, and confers greater resistance to cancer therapies. This Review discusses the mechanisms of EMT and its roles in normal and neoplastic tissues, the contribution of cell-intrinsic signals and the microenvironment to inducing EMT, and its effects on the immunobiology of carcinomas.
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Social Networks {👍}(2)

External Links {🔗}(825)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

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Mail Servers:

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CDN Services {📦}

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