Here's how LINK.SPRINGER.COM makes money* and how much!

*Please read our disclaimer before using our estimates.
Loading...

LINK . SPRINGER . COM {}

  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
  8. Questions
  9. Schema
  10. External Links
  11. Analytics And Tracking
  12. Libraries
  13. CDN Services

We are analyzing https://link.springer.com/article/10.1186/1476-4598-6-27.

Title:
Some facts and thoughts: p73 as a tumor suppressor gene in the network of tumor suppressors | Molecular Cancer
Description:
The question of whether p73 is a tumor suppressor gene, is not yet answered with full confidence. The lack of spontaneous tumor formation in p73 null mice and infrequent p73 mutations seen in a variety of cancers analyzed would straightaway negate its role as a primary tumor suppressor gene. However, accumulating evidence suggest that p73 gene and its target genes are hypermethylated in the cancer of lymphoid origin. Here I discuss some facts and thoughts that support the idea that p73 could still be a tumor suppressor gene. The tumor suppressor network in which p73 appears to be a participant involves E2F1, JunB, INK4a/p16, ARF/p19, p57kip2 and BRCA1. Knock out of each gene in E2F-1-p73-JunB-p16INK4a network of tumor suppressor proteins result in lymphoma/leukemia formation. Further, I tried to explain why lymphomas are not seen in p73 null mice and why p73 gene is not prone to frequent mutation.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Education
  • Science
  • Telecommunications

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

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


Based on our best estimate, this website will receive around 5,000,016 visitors per month in the current month.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {πŸ’Έ}

We're unsure how the site profits.

Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Link.springer.com might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {πŸ”}

tumor, pubmed, article, gene, google, scholar, cas, suppressor, expression, mice, cell, shown, cancer, cells, null, junb, lymphoma, tumors, promoter, leukemia, adenosine, figure, proliferation, target, pkip, apoptosis, methylation, myeloid, human, sigma, develop, function, functions, pathway, transcriptional, genes, dna, network, formation, suggest, cpg, hypermethylation, res, central, access, brca, oncogene, growth, inactivation, increased,

Topics {βœ’οΈ}

transactivation-deficient deltata-p73 acts open access article t-cell tumour suppressor antigen-induced t-cell proliferation article download pdf ccaat/enhancer binding proteins expressing wild-type p53 expressing wild-type p73 acute lymphocytic leukemia cell-cycle regulatory pathway coiled-coil-mediated interaction human hepatoma li-7a chronic myeloid leukemia splenic t-cells isolated e2f1-/+e2f2-/- mice developed cisplatin-induced dna damage related subjects aberrantly expressd c-jun p73/p63 null mice elicit anti-proliferative effect authors’ original file acute nonlymphocytic leukemia acute promyelocytic leukemia[34] cell death differ acute lymphoblastic leukemia e2f-1-p73-junb-p16ink4a network acute lymphoplastic leukemia privacy choices/manage cookies e2f1-deficient mice ubiquitin-dependent degradation tumor suppressor pathway sumo-1 interaction motif myeloid hyperplasia/leukemia article boominathan p73 null mice tumor cell types derived cell lines[16] p73-deficient mice dna damage signals antioncogenic response triggered sumo-1-interacting proteins tumor suppressor gene tumor suppressor gene[46] p73 splicing products t-cell receptors suppresses tumor growth human cancer cells dna methyl transfereases dna damaging drugs aberrant dna methylation

Questions {❓}

  • How can we explain this tumor paradox?
  • If indeed p73 is a tumor suppressor gene, then why p73 null mice failed to develop lymphoma?
  • Stiewe T, Putzer BM: Role of p73 in malignancy: tumor suppressor or oncogene?
  • Why do p73 mutations are infrequent in tumors?

Schema {πŸ—ΊοΈ}

WebPage:
      mainEntity:
         headline:Some facts and thoughts: p73 as a tumor suppressor gene in the network of tumor suppressors
         description:The question of whether p73 is a tumor suppressor gene, is not yet answered with full confidence. The lack of spontaneous tumor formation in p73 null mice and infrequent p73 mutations seen in a variety of cancers analyzed would straightaway negate its role as a primary tumor suppressor gene. However, accumulating evidence suggest that p73 gene and its target genes are hypermethylated in the cancer of lymphoid origin. Here I discuss some facts and thoughts that support the idea that p73 could still be a tumor suppressor gene. The tumor suppressor network in which p73 appears to be a participant involves E2F1, JunB, INK4a/p16, ARF/p19, p57kip2 and BRCA1. Knock out of each gene in E2F-1-p73-JunB-p16INK4a network of tumor suppressor proteins result in lymphoma/leukemia formation. Further, I tried to explain why lymphomas are not seen in p73 null mice and why p73 gene is not prone to frequent mutation.
         datePublished:2007-04-03T00:00:00Z
         dateModified:2007-04-03T00:00:00Z
         pageStart:1
         pageEnd:8
         license:https://creativecommons.org/licenses/by/2.0
         sameAs:https://doi.org/10.1186/1476-4598-6-27
         keywords:
            Acute Lymphocytic Leukemia
            Tumor Suppressor Gene
            Chronic Myeloid Leukemia
            Null Mouse
            Intraductal Papillary Mucinous Neoplasm
            Cancer Research
            Oncology
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1476-4598-6-27/MediaObjects/12943_2007_Article_235_Fig1_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1476-4598-6-27/MediaObjects/12943_2007_Article_235_Fig2_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1476-4598-6-27/MediaObjects/12943_2007_Article_235_Fig3_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1476-4598-6-27/MediaObjects/12943_2007_Article_235_Fig4_HTML.jpg
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1476-4598-6-27/MediaObjects/12943_2007_Article_235_Fig5_HTML.jpg
         isPartOf:
            name:Molecular Cancer
            issn:
               1476-4598
            volumeNumber:6
            type:
               Periodical
               PublicationVolume
         publisher:
            name:BioMed Central
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Lakshmanane Boominathan
               affiliation:
                     name:
                     address:
                        name:Pondicherry-4, India
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Some facts and thoughts: p73 as a tumor suppressor gene in the network of tumor suppressors
      description:The question of whether p73 is a tumor suppressor gene, is not yet answered with full confidence. The lack of spontaneous tumor formation in p73 null mice and infrequent p73 mutations seen in a variety of cancers analyzed would straightaway negate its role as a primary tumor suppressor gene. However, accumulating evidence suggest that p73 gene and its target genes are hypermethylated in the cancer of lymphoid origin. Here I discuss some facts and thoughts that support the idea that p73 could still be a tumor suppressor gene. The tumor suppressor network in which p73 appears to be a participant involves E2F1, JunB, INK4a/p16, ARF/p19, p57kip2 and BRCA1. Knock out of each gene in E2F-1-p73-JunB-p16INK4a network of tumor suppressor proteins result in lymphoma/leukemia formation. Further, I tried to explain why lymphomas are not seen in p73 null mice and why p73 gene is not prone to frequent mutation.
      datePublished:2007-04-03T00:00:00Z
      dateModified:2007-04-03T00:00:00Z
      pageStart:1
      pageEnd:8
      license:https://creativecommons.org/licenses/by/2.0
      sameAs:https://doi.org/10.1186/1476-4598-6-27
      keywords:
         Acute Lymphocytic Leukemia
         Tumor Suppressor Gene
         Chronic Myeloid Leukemia
         Null Mouse
         Intraductal Papillary Mucinous Neoplasm
         Cancer Research
         Oncology
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1476-4598-6-27/MediaObjects/12943_2007_Article_235_Fig1_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1476-4598-6-27/MediaObjects/12943_2007_Article_235_Fig2_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1476-4598-6-27/MediaObjects/12943_2007_Article_235_Fig3_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1476-4598-6-27/MediaObjects/12943_2007_Article_235_Fig4_HTML.jpg
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1186%2F1476-4598-6-27/MediaObjects/12943_2007_Article_235_Fig5_HTML.jpg
      isPartOf:
         name:Molecular Cancer
         issn:
            1476-4598
         volumeNumber:6
         type:
            Periodical
            PublicationVolume
      publisher:
         name:BioMed Central
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Lakshmanane Boominathan
            affiliation:
                  name:
                  address:
                     name:Pondicherry-4, India
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Molecular Cancer
      issn:
         1476-4598
      volumeNumber:6
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:
      address:
         name:Pondicherry-4, India
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Lakshmanane Boominathan
      affiliation:
            name:
            address:
               name:Pondicherry-4, India
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Pondicherry-4, India

External Links {πŸ”—}(185)

Analytics and Tracking {πŸ“Š}

  • Google Tag Manager

Libraries {πŸ“š}

  • Clipboard.js
  • Prism.js

CDN Services {πŸ“¦}

  • Crossref

4.58s.