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/PMC3367003/, but it redirected us to https://pmc.ncbi.nlm.nih.gov/articles/PMC3367003/. The analysis below is for the second page.

Title[redir]:
CLONAL EVOLUTION IN CANCER - PMC
Description:
Cancers evolve by a reiterative process of clonal expansion, genetic diversification and clonal selection within the adaptive landscapes of tissue ecosystems. The dynamics are complex with highly variable patterns of genetic diversity and resultant ...

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 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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

We don’t know how the website earns money.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Ncbi.nlm.nih.gov might have a hidden revenue stream, but it's not something we can detect.

Keywords {🔍}

doi, cancer, google, scholar, pubmed, cells, cell, clonal, pmc, article, free, genetic, mutations, nature, stem, evolution, evolutionary, selection, progression, selective, therapy, cancers, single, tissue, mutation, subclones, therapeutic, clones, time, clone, cscs, diversity, subclonal, mutational, lesions, expansion, common, driver, data, sequencing, tumor, biology, information, dynamics, human, tumour, inhibitors, nat, pnas, pii,

Topics {✒️}

trp53-/-p16ink4a-/-p19arf-/-multipotent progenitors dna damage-mediated induction pmc beta search bone-marrow endosteal region acute lymphoblastic leukemia long-term haematopoietic reconstitution error-prone repair processes include environmentally-derived genotoxicity pre-existing genetic variants supplementary materials included philadelphia-positive stem cells evolutionary dead-ends generated pre-clinical models suggest detect tmprss2/erg fusion bcr-abl1 fusion abl1 kinase-directed therapy functionally relevant ‘drivers micro-environmental constraints limit chronic myeloid leukaemia cell-population genetic analysis testicular germ-cell tumours selectively advantageous alterations [google scholar] 7 [google scholar] 59 pre-malignant clonal lesions patient-specific genomic profiles chronic myeloid leukemia restraining cancer progression suggest alternative strategies selectively advantageous mutations concordant acute leukaemia55 tissue micro-environments full-blown malignancies granulocyte-macrophage progenitors egfr kinase inhibitors92 evolutionarily neutral alterations carcinogen-specific induction ultra-deep sequencing ecosystem paradigm suggests large scale punctuated clonal evolution posits publisher site pdf testable predictions follow license information pmcid require deep sequencing40 mammary stem cells leukemic stem cells selectively neutral mutations candidate gene sequencing cellular processes relevant

Questions {❓}

  • Cancer escape: need for a Darwinian bypass?
  • Cancer stem cells: back to Darwin?
  • Do malignant clones, with their dramatically altered genomes, evolve gradually through a sequence of many genetic alterations and clonal expansions, or are there few, large scale punctuated changes, possibly prompted by acute insult, a single, catastrophic mitosis that generates multiple lesions across the genome or on a single chromosome (chromothripsis)39, or through the accumulation of many lesions over time in a rare, undetected subclone?
  • The problem of intrinsically resistant (and quiescent?
  • We should be asking what phenotypes can we select for that would make neoplasm less deadly and more clinically manageable?
  • What is a way out of this impasse?
  • Why don’t we get more cancer?

Social Networks {👍}(6)

External Links {🔗}(210)

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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