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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
  11. External Links
  12. Analytics And Tracking
  13. Libraries
  14. Hosting Providers

We began analyzing https://biomarkerres.biomedcentral.com/articles/10.1186/s40364-021-00339-z, but it redirected us to https://biomarkerres.biomedcentral.com/articles/10.1186/s40364-021-00339-z. The analysis below is for the second page.

Title[redir]:
The telomere complex and the origin of the cancer stem cell | Biomarker Research | Full Text
Description:
Exquisite regulation of telomere length is essential for the preservation of the lifetime function and self-renewal of stem cells. However, multiple oncogenic pathways converge on induction of telomere attrition or telomerase overexpression and these events can by themselves trigger malignant transformation. Activation of NFκB, the outcome of telomere complex damage, is present in leukemia stem cells but absent in normal stem cells and can activate DOT1L which has been linked to MLL-fusion leukemias. Tumors that arise from cells of early and late developmental stages appear to follow two different oncogenic routes in which the role of telomere and telomerase signaling might be differentially involved. In contrast, direct malignant transformation of stem cells appears to be extremely rare. This suggests an inherent resistance of stem cells to cancer transformation which could be linked to a stem cell’specific mechanism of telomere maintenance. However, tumor protection of normal stem cells could also be conferred by cell extrinsic mechanisms.

Matching Content Categories {📚}

  • Science
  • Education
  • Telecommunications

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?

🏙️ Massive Traffic: 50M - 100M visitors per month


Based on our best estimate, this website will receive around 91,115,781 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We're unsure how the site profits.

The purpose of some websites isn't monetary gain; they're meant to inform, educate, or foster collaboration. Everyone has unique reasons for building websites. This could be an example. Doi.org might be earning cash quietly, but we haven't detected the monetization method.

Keywords {🔍}

cells, cell, stem, pubmed, article, google, scholar, telomere, cas, leukemia, expression, differentiation, cancer, myeloid, development, mice, stage, telomerase, transformation, hscs, hematopoietic, hsc, central, normal, early, progenitors, leukemias, tumor, proliferation, phenotype, signaling, lineage, loss, acute, tumors, genes, cmyc, shown, human, pathway, block, origin, activity, induced, gata, bmi, developmental, junb, selfrenewal, oncogenic,

Topics {✒️}

mrp8-cre-ires/gfp transgenic mouse mscv-ires-gfp-myr-akt construct granulocyte-macrophage-colony-stimulating factor granulocyte-colony stimulating factor article torres-montaner regulates vα-jα recombination tgf-β targets smad7 helix-loop-helix family transforming growth factor-β cell-specific pten-deficient mice notch1/c-myc induced leukemia pre-thymic t-cell progenitors tumor-promoter exogenous c-fos id-1-expressing retrovirus remained factor-dependent cell lines transcription factor networks ikaros dna-binding domain murine h-2 kb class acute t-lymphoblastic leukemia tumor necrosis factor-α aml-eto fusion protein fusion protein mll-gas7 sca-1− mac-1hi c-kitlo/− anti-cd38 conjugated cells pml-rara fusion protein mscv-ires-gfp yao-ming ns icn1-induced rag null icn1-induced cd44 + cd25+ pre-existing telomere deficit t-acute lymphoblastic lymphoma cobblestone area-forming cells nf-κb activation correlates c-fos transgenic mice lymphoid-primed multipotent progenitors e2a-pbx1 induces leukemia mll-enl transduced clones late-born cell types torres-montaner contributions small-cell lung carcinomas downregulate c-myc resulted t-lineage developmental programme early-born cell types post-stem cell endowed bcr/abl-gfp found blocks β-catenin degradation altered n-terminal region post-stem cell population telomere-shortened epithelial field etv-runx1 fusion protein

Questions {❓}

  • Do some early cancers arise directly from stem cells?
  • In addition, this answer raises another question: Does tumor development require exit from the stem cell pool and, then, why developmental arrest predisposes to tumor formation?
  • Since all these changes (myeloid maturation, Foxo nuclear exclusion and inactivation are a consequence of Akt activation, the reappearance of the stem cell pattern of Akt activity during tumorigenesis can only be explained by the occurrence of a process similar to reprogramming (partial reprogramming?
  • Telomere shortening occurs early during breast tumorigenesis: a cause of vhromosome destabilization underlying malignant transformation?
  • Why deregulated expression of transcription factors that are expressed in HSCs is associated with leukemias/lymphomas that display neoplastic phenotypes corresponding to committed cells but not the HSC stage phenotype?

Schema {🗺️}

WebPage:
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Social Networks {👍}(2)

External Links {🔗}(709)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

  • Prism.js

Emails and Hosting {✉️}

Mail Servers:

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

Name Servers:

  • josh.ns.cloudflare.com
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