Here's how NCBI.NLM.NIH.GOV makes money* and how much!

*Please read our disclaimer before using our estimates.
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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/PMC4264927/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC4264927/. The analysis below is for the second page.

Title[redir]:
The extracellular matrix modulates the hallmarks of cancer - PMC
Description:
The extracellular matrix regulates tissue development and homeostasis, and its dysregulation contributes to neoplastic progression. The extracellular matrix serves not only as the scaffold upon which tissues are organized but provides critical ...

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Telecommunications

Content Management System {πŸ“}

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 {πŸ“ˆ}

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 6,398,976 visitors per month in the current month.

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How Does Ncbi.nlm.nih.gov Make Money? {πŸ’Έ}

We're unsure how the site profits.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Ncbi.nlm.nih.gov could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {πŸ”}

doi, cell, pubmed, google, scholar, tumor, ecm, cancer, pmc, article, free, cells, growth, progression, matrix, signaling, extracellular, tissue, biol, adhesion, survival, proliferation, cycle, collagen, activity, development, expression, response, breast, promotes, metastasis, activation, hallmarks, receptor, protein, cellular, factor, kinase, nature, migration, mechanical, tumors, increased, angiogenesis, patients, fak, endothelial, integrin, sci, immune,

Topics {βœ’οΈ}

phosphatidylinositol 3-kinase function proto-oncogene mechanotransduction lysyl oxidase inhibitor oncogene-directed tumor–ecm interactions growth factor-dependent signaling focal adhesion kinase focal-adhesion kinase dominant rho-family gtpase enhanced post-translational modifications cyclin-dependent kinases enhancing pi3k/akt activity rat aorta model rho gtpase signaling beta4 integrin-dependent formation p75ngfr/bcl2/integrin beta4 t-cell-mediated cell death pmc beta search pro-apoptotic protein bim tgf-beta blockade improves pi3k-dependent breast tumorigenesis p27 remain high fak-p130cas complex smad phosphorylation anchorage-dependent cells detaching raf 121 adhesion-dependent cell survival cyclin d1 induction laminin-binding receptor permits nf-ΞΊb activation tgf-beta1-induced apoptosis tgf-Ξ² induces proteins anti-apoptotic molecules including inducing p130cas enabling replicative immortality p53 protein interactions epithelial-mesenchymal transition growth factor receptors tgf-Ξ² secreted ecm adhesion-induced signals require integrin-mediated adhesion suppress p53-induced apoptosis bleomycin-induced pulmonary fibrosis collagen receptor ddr1 ferm-enhanced p53 degradation bleomycin-induced lung fibrosis activating invasion stimulates erk signaling modulate vascular development hypoxia-induced lysyl oxidase cyclin d1 7

Questions {❓}

  • Are the enhanced biomechanical properties of the ECM observed in tumors a causative or correlative factor to tumor development?
  • At which point in a tumor cells' response to the altered ECM biochemical and biophysical properties it is most efficacious to therapeutically intervene?
  • Is the influence of the ECM on tumor progression consistent through various cancer origins and subtypes?
  • Mechanotransduction - a field pulling together?
  • The inflammation-fibrosis link?
  • What are the cellular sources inducing an altered ECM deposition and remodeling during cancer progression?

External Links {πŸ”—}(279)

Analytics and Tracking {πŸ“Š}

  • Google Analytics
  • Google Analytics 4
  • Google Tag Manager

Libraries {πŸ“š}

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

Emails and Hosting {βœ‰οΈ}

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 {πŸ“¦}

  • Ncbi

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