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DOI . ORG {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Doi.org Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. Social Networks
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We began analyzing https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-025-06422-5, but it redirected us to https://translational-medicine.biomedcentral.com/articles/10.1186/s12967-025-06422-5. The analysis below is for the second page.

Title[redir]:
Epithelial-mesenchymal transition orchestrates tumor microenvironment: current perceptions and challenges | Journal of Translational Medicine | Full Text
Description:
The epithelial-mesenchymal transition (EMT) is a critical process in cancer progression, facilitating tumor cells to develop invasive traits and augmenting their migratory capabilities. EMT is primed by tumor microenvironment (TME)-derived signals, whereupon cancer cells undergoing EMT in turn remodel the TME, thereby modulating tumor progression and therapeutic response. This review discusses the mechanisms by which EMT coordinates TME dynamics, including secretion of soluble factors, direct cell contact, release of exosomes and enzymes, as well as metabolic reprogramming. Recent evidence also indicates that cells undergoing EMT may differentiate into cancer-associated fibroblasts, thereby establishing themselves as functional constituents of the TME. Elucidating the relationship between EMT and the TME offers novel perspectives for therapeutic strategies to enhance cancer treatment efficacy. Although EMT-directed therapies present significant therapeutic potential, the current lack of effective targeting approaches—attributable to EMT complexity and its microenvironmental context dependency—underscores the necessity for mechanistic investigations and translational clinical validation.

Matching Content Categories {šŸ“š}

  • Science
  • Education
  • Health & Fitness

Content Management System {šŸ“}

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 {šŸ“ˆ}

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

šŸ™ļø Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 75,529,999 visitors per month in the current month.

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How Does Doi.org Make Money? {šŸ’ø}

We can't tell how the site generates income.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Doi.org might be earning cash quietly, but we haven't detected the monetization method.

Keywords {šŸ”}

pubmed, cancer, article, cells, google, scholar, emt, cell, cas, central, tumor, immune, expression, pdl, transition, breast, zeb, tme, mesenchymal, epithelialmesenchymal, signaling, ecm, extracellular, wang, nat, metastasis, collagen, carcinoma, snail, metabolic, progression, promotes, immunol, epithelial, ecadherin, liu, target, function, process, targeting, vimentin, receptor, res, chen, activation, matrix, tgfβ, inhibition, therapeutic, immunosuppressive,

Topics {āœ’ļø}

fgd5-as1/mir-454-3p/zeb1-vegf axis apkc-ι/snail-induced cca cells ccl18-zeb1-m-csf feedback loop mir-30-5p/snail/dpp4 axis ccr5-dependent t-cell retention grhl2/zeb1/pd-l1 axis tgf-β-mediated myofibroblastic differentiation tgf-β1-induced emt resulted double-negative feedback loop pro-angiogenic cd14+/kdr+ population virus counteracts mir-200c regulating pd-1/pd-l1 checkpoint pd-l1-mediated emt induction anti-erbb2 monoclonal antibody microrna-200/zeb1 axis control tumor-specific tumor-infiltrating lymphocytes pd-l1 prominently activates mirna-rich exosome delivery tumor necrosis factor-α lox/hypoxia axis reverses downstream phospho-cascades triggers mir-199a-5p loss piezo1-yap signalling axis loxl2-mediated metastatic cascade emt-driven pd-l1 upregulation cell-cell contacts mediated additional information publisher' pd-l1 induces epithelial single-cell rna sequencing positive feedback loop enhanced gm-csf production hypoxia-induced lysyl oxidase pd-1/pd-l1 signaling [52] promotes anti-tumor immunity binary epithelial/mesenchymal paradigm transforming growth factor-β emt-selective inhibitors exist single emt-tf recapitulate inhibitory c-type lectin delivering mir-21-abundant exosomes potentiating anti-tumor immunity lactate-induced ph reduction her2/erbb2 antibody therapy pd-l1-mediated immunosuppression her2-positive breast cancer enhance t-cell function pd-1/pd-l1 checkpoint induces cd4+foxp3+ regulatory increased pd-l1 expression jnk/c-jun activation

Questions {ā“}

  • T cell adhesion and cytolysis of pancreatic cancer cells: A role for E-cadherin in immunotherapy?
  • While EMT-TFs are indeed crucial initiators of the process, can the upregulation of a single EMT-TF recapitulate the pathophysiological EMT spectrum in vivo?

Schema {šŸ—ŗļø}

WebPage:
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         headline:Epithelial-mesenchymal transition orchestrates tumor microenvironment: current perceptions and challenges
         description:The epithelial-mesenchymal transition (EMT) is a critical process in cancer progression, facilitating tumor cells to develop invasive traits and augmenting their migratory capabilities. EMT is primed by tumor microenvironment (TME)-derived signals, whereupon cancer cells undergoing EMT in turn remodel the TME, thereby modulating tumor progression and therapeutic response. This review discusses the mechanisms by which EMT coordinates TME dynamics, including secretion of soluble factors, direct cell contact, release of exosomes and enzymes, as well as metabolic reprogramming. Recent evidence also indicates that cells undergoing EMT may differentiate into cancer-associated fibroblasts, thereby establishing themselves as functional constituents of the TME. Elucidating the relationship between EMT and the TME offers novel perspectives for therapeutic strategies to enhance cancer treatment efficacy. Although EMT-directed therapies present significant therapeutic potential, the current lack of effective targeting approaches—attributable to EMT complexity and its microenvironmental context dependency—underscores the necessity for mechanistic investigations and translational clinical validation.
         datePublished:2025-04-02T00:00:00Z
         dateModified:2025-04-02T00:00:00Z
         pageStart:1
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      headline:Epithelial-mesenchymal transition orchestrates tumor microenvironment: current perceptions and challenges
      description:The epithelial-mesenchymal transition (EMT) is a critical process in cancer progression, facilitating tumor cells to develop invasive traits and augmenting their migratory capabilities. EMT is primed by tumor microenvironment (TME)-derived signals, whereupon cancer cells undergoing EMT in turn remodel the TME, thereby modulating tumor progression and therapeutic response. This review discusses the mechanisms by which EMT coordinates TME dynamics, including secretion of soluble factors, direct cell contact, release of exosomes and enzymes, as well as metabolic reprogramming. Recent evidence also indicates that cells undergoing EMT may differentiate into cancer-associated fibroblasts, thereby establishing themselves as functional constituents of the TME. Elucidating the relationship between EMT and the TME offers novel perspectives for therapeutic strategies to enhance cancer treatment efficacy. Although EMT-directed therapies present significant therapeutic potential, the current lack of effective targeting approaches—attributable to EMT complexity and its microenvironmental context dependency—underscores the necessity for mechanistic investigations and translational clinical validation.
      datePublished:2025-04-02T00:00:00Z
      dateModified:2025-04-02T00:00:00Z
      pageStart:1
      pageEnd:18
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         Epithelial-mesenchymal transition (EMT)
         Tumor microenvironment (TME)
         Tumor progression
         Plasticity
         Biomedicine
         general
         Medicine/Public Health
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            affiliation:
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                     type:PostalAddress
                  type:Organization
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                  address:
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         name:Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China
         type:PostalAddress
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      address:
         name:Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China
         type:PostalAddress
      name:Zhongshan Hospital, Fudan University
      address:
         name:Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China
         type:PostalAddress
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      address:
         name:Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China
         type:PostalAddress
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            name:Zhongshan Hospital, Fudan University
            address:
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               type:PostalAddress
            type:Organization
            name:Zhongshan Hospital, Fudan University
            address:
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               type:PostalAddress
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      affiliation:
            name:Zhongshan Hospital, Fudan University
            address:
               name:Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:Zhongshan Hospital, Fudan University
            address:
               name:Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China
               type:PostalAddress
            type:Organization
      name:Liang Liu
      affiliation:
            name:Zhongshan Hospital, Fudan University
            address:
               name:Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:Zhongshan Hospital, Fudan University
            address:
               name:Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China
      name:Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China
      name:Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China
      name:Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China
      name:Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China
      name:Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China
      name:Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China
      name:Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, People’s Republic of China
      name:Cancer Center, Zhongshan Hospital, Fudan University, Shanghai, China

External Links {šŸ”—}(966)

Analytics and Tracking {šŸ“Š}

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Libraries {šŸ“š}

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Mail Servers:

  • mx.zoho.eu
  • mx2.zoho.eu
  • mx3.zoho.eu

Name Servers:

  • josh.ns.cloudflare.com
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CDN Services {šŸ“¦}

  • Crossref

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