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  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. Schema
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We began analyzing https://www.oncotarget.com/article/12768/text/, but it redirected us to https://www.oncotarget.com/article/12768/text/. The analysis below is for the second page.

Title[redir]:
A role for the vitamin D pathway in non-intestinal lesions in genetic and carcinogen models of colorectal cancer and in familial adenomatous polyposis | Oncotarget
Description:
// Yong-Sik Bong 1, * , Shahin Assefnia 1, * , Therese Tuohy 2 , Deborah W Neklason 2 , Randall W Burt 2 , Jaeil Ahn 3 , Paul J Bueno De Mesquita 1 , Stephen W. Byers 1 1 Georgetown-Lombardi Comprehensive Cancer Center, Department of Oncology, Georgetown University School of Medicine, Washington, DC, United States of America 2 Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, United States of America 3 Department of Biostatistics, Bioinformatics and Biomathematics, Georgetown University School of Medicine, Washington, DC, United States of America * These authors contributed equally to this work Correspondence to: Stephen W, email: [email protected] Keywords: gardner’s syndrome, anal cancer, vitamin D receptor, azoxymethane, colon cancer Received: April 13, 2016      Accepted: October 11, 2016      Published: October 19, 2016 ABSTRACT Vitamin D is implicated in the etiology of cancers of the gastrointestinal tract, usually characterized by alteration in the APC/β-catenin/TCF tumor suppressor pathway. The vitamin D receptor (VDR) is also implicated in cardiovascular and skin diseases as well as in immunity. Activated VDR can indirectly alter β-catenin nuclear localization and directly suppress β-catenin/TCF mediated transcriptional activity. We treated VDR null mice with the carcinogen azoxymethane (AOM) and generated mice bearing a mutated APC (hypomorph) on a VDR null background ( Apc 1638N/+ Vdr −/− ). VDR null mice do not develop GI or extra-colonic tumors but loss of VDR decreased intestinal tumor latency and increased progression to adenocarcinoma in both models. AOM treatment of VDR null mice also caused squamous cell carcinoma of the anus. Although levels and distribution of total or activated β-catenin in the epithelial component of tumors were unaffected by loss of VDR, β-catenin dependent cyclin D1 expression was affected suggesting a direct VDR effect on β-catenin co-activator activity. Extra-colonic mucosa manifestations in Apc 1638N/+ Vdr −/− animals included increased nuclear β-catenin in submucosal stromal cells, spleno- and cardiomegaly and large epidermoid cysts characteristic of the FAP variant, Gardner’s syndrome. Consistent with this, SNPs in the VDR, vitamin D binding protein and CYP24 as well as mutations in APC distal to codon 850 were strongly associated with Gardners syndrome in a cohort of 457 FAP patients, This work suggests that alterations in the vitamin D/VDR axis are important in Gardner’s syndrome, as well as in the etiology of anal cancer.

Matching Content Categories {📚}

  • Science
  • Health & Fitness
  • Education

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 75,489,999 visitors per month in the current month.

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How Does Doi.org Make Money? {💸}

We don’t know how the website earns money.

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 could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

vdr, vitamin, mice, tumor, cancer, βcatenin, apc, apcnvdr, lesions, cell, extracolonic, fap, apcn, figure, colon, tumors, cells, months, receptor, skin, intestinal, patients, left, syndrome, progression, staining, journal, loss, animals, pathway, cyclin, gene, incidence, mouse, representative, model, colorectal, gardners, activity, increased, genes, upper, sections, cysts, mutation, signaling, ablation, bar, models, polyposis,

Topics {✒️}

reduced vdr/β-catenin interactions anti-active β-catenin antibody β-catenin-related neoplasias found parasite-free animal facility wnt/beta-catenin signalling represses β-catenin signaling activate β-catenin signaling β-catenin target gene mediating β-catenin phosphorylation activated β-catenin signaling cardiac renin-angiotensin systems activated β-catenin occurred avidin/biotin blocking kit biotin-conjugated secondary antibodies inflammation-driven tumor progression regulate beta-catenin proteolysis representative hematoxylin/eosin staining inaugural editorial blood-derived genomic dna regulating β-catenin signaling uk/pathology/protocols/alcblue vdr directly regulates tailed chi-square test extra-colonic mucosa manifestations activated β-catenin results vdr-mediated transcriptional regulation anti-active caspase-3 antibody targeted chain-termination mutation publication alerts subscribe aom-induced tumors revealed open-access journal dedicated increasing dna damage epidermal cysts/keratocanthomas prompted free publication β-catenin activates nuclear β-catenin chemically induced tumorigenesis current opinion total β-catenin levels enhancing wnt signaling familial adenomatous polyposis basal cell carcinomas increased tumor multiplicity/progression beta-catenin crossregulation apc1638n/+vdr−/− mice compared squamous cell carcinoma adenomatous polyposis coli familial polyposis coli apcmin/+vdr−/− animals compared active β-catenin

Schema {🗺️}

Article:
      license:https://creativecommons.org/licenses/by/4.0/
      publisher:
         type:Organization
         name:Oncotarget
         logo:
            type:ImageObject
            url:https://www.oncotarget.com/images/oncotarget-logo-square.png
            width:1200
            height:1200
      dateModified:2016-12-06T08:11:12Z
      mainEntityOfPage:
         type:WebPage
         id:https://www.oncotarget.com/article/12768/text/
      headline:A role for the vitamin D pathway in non-intestinal lesions in genetic and carcinogen models of colorectal c
      articleSection:Research Papers
      sameAs:https://doi.org/10.18632/oncotarget.12768
      image:https://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=viewFile&path%5B%5D=12768&path%5B%5D=40456&path%5B%5D=191361
      datePublished:2016-10-19T00:00:00Z
      author:
            type:Person
            name:Bong, Yong-Sik
            type:Person
            name:Assefnia, Shahin
            type:Person
            name:Tuohy, Therese
            type:Person
            name:Neklason, Deborah W
            type:Person
            name:Burt, Randall W
            type:Person
            name:Ahn, Jaeil
            type:Person
            name:Bueno De Mesquita, Paul J
            type:Person
            name:Byers, Stephen W.
Organization:
      name:Oncotarget
      logo:
         type:ImageObject
         url:https://www.oncotarget.com/images/oncotarget-logo-square.png
         width:1200
         height:1200
ImageObject:
      url:https://www.oncotarget.com/images/oncotarget-logo-square.png
      width:1200
      height:1200
WebPage:
      id:https://www.oncotarget.com/article/12768/text/
Person:
      name:Bong, Yong-Sik
      name:Assefnia, Shahin
      name:Tuohy, Therese
      name:Neklason, Deborah W
      name:Burt, Randall W
      name:Ahn, Jaeil
      name:Bueno De Mesquita, Paul J
      name:Byers, Stephen W.

External Links {🔗}(84)

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