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NCBI . NLM . NIH . GOV {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Ncbi.nlm.nih.gov Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Social Networks
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. Hosting Providers
  14. CDN Services

We began analyzing https://pmc.ncbi.nlm.nih.gov/articles/PMC6606363/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC6606363/. The analysis below is for the second page.

Title[redir]:
Cellular Plasticity in Cancer - PMC
Description:
During cancer progression, tumor cells undergo molecular and phenotypic changes collectively referred to as cellular plasticity. Such changes result from microenvironmental cues, stochastic genetic and epigenetic alterations, and/or ...

Matching Content Categories {📚}

  • Science
  • Health & Fitness
  • Education

Content Management System {📝}

What CMS is ncbi.nlm.nih.gov built with?

Custom-built

No common CMS systems were detected on Ncbi.nlm.nih.gov, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of ncbi.nlm.nih.gov audience?

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


Based on our best estimate, this website will receive around 5,000,005 visitors per month in the current month.

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How Does Ncbi.nlm.nih.gov Make Money? {💸}

We don't see any clear sign of profit-making.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Ncbi.nlm.nih.gov might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

cells, cancer, pubmed, google, scholar, doi, plasticity, cell, pmc, article, free, tumor, emt, cellular, epithelial, metaplasia, epithelialmesenchymal, mesenchymal, state, resistance, tumors, transition, nature, therapy, carcinoma, mechanisms, squamous, pancreatic, metastasis, lung, studies, molecular, phenotype, including, stem, states, programs, lineage, esophagus, ductal, normal, arise, gastric, liver, development, factors, expression, research, resistant, egfr,

Topics {✒️}

intrinsically anti-proliferative/anti-metastatic [115] microrna-200/zeb1 axis control pmc beta search enzyme-rich pancreatic juice induce gender-specific squamous true endothelium-lined vasculature variable beta-catenin expression tgf-beta-induced epithelial emt-related gene signature kdm6a activates super-enhancers anti-pd1 treatment display large population-based study multi-lineage hematopoietic stem represent distinct end-states post-transcriptionally regulate cadherin lose cell-cell interactions altered gm-csf secretion cytokines including gm-csf repressing e-cadherin expression small-cell lung cancer small-cell lung cancer rb1-deficient prostate cancer spasmolytic polypeptide-expressing metaplasia e-cadherin gene expression e-cadherin protein levels epithelial-mesenchymal plasticity involves egf-mediated endocytosis utilize epithelial-mesenchymal plasticity tumor suppressor lkb1 therapy-induced selective pressures snail-induced emt promotes tumour-initiating cells treatment-imposed selective pressures pro-tumor inflammatory microenvironment tumor-initiating cells radiotherapy controls cd44v6 high e-cadherin expression low e-cadherin expression context-dependent differences dictate overlapping cell populations epithelial-mesenchymal plasticity plays liver-specific kras activation rendering tumor-promoting genes epithelial-mesenchymal plasticity shift tgfbeta-mediated hepatocyte transdifferentiation egfr-mutant lung cancers specific oncogenic drivers gain fat-lose metastasis high-grade cervical dysplasia mdck cells results

Questions {❓}

  • By what molecular mechanisms does epithelial-mesenchymal plasticity shift the sensitivity profile?
  • Do similar opportunities exist for carcinomas, whereby targeting tumor drivers can promote differentiation and slow malignant growth?
  • How should we define “partial EMT” versus “complete EMT”?
  • In what cellular/molecular settings does metaplasia also facilitate tumor initiation?
  • Is the epithelial-mesenchymal state of a cell itself responsible for increased drug tolerance?
  • Specifically, if EMT (and its associated loss of epithelial features) is important for invasion and metastasis, then why don’t metastatic lesions exhibit a more mesenchymal histology?
  • What determines the “equilibrium constants” governing transitions between these states, thereby giving rise to poorly-differentiated or well-differentiated tumors?
  • The expression of a drug transporter) account for resistance, making any role for EMT more indirect?

Social Networks {👍}(6)

External Links {🔗}(245)

Analytics and Tracking {📊}

  • Google Analytics
  • Google Analytics 4
  • Google Tag Manager

Libraries {📚}

  • jQuery
  • jQuery module (jquery-3.6.0)
  • Zoom.js

Emails and Hosting {✉️}

Mail Servers:

  • nihcesxway.hub.nih.gov
  • nihcesxway2.hub.nih.gov
  • nihcesxway3.hub.nih.gov
  • nihcesxway4.hub.nih.gov
  • nihcesxway5.hub.nih.gov

Name Servers:

  • dns1-ncbi.ncbi.nlm.nih.gov
  • dns2-ncbi.ncbi.nlm.nih.gov
  • lhcns1.nlm.nih.gov
  • lhcns2.nlm.nih.gov

CDN Services {📦}

  • Ncbi

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