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We are analyzing https://www.nature.com/articles/onc200979.

Title:
Reversibility and recurrence of IGF-IR-induced mammary tumors | Oncogene
Description:
The type-I insulin-like growth factor receptor (IGF-IR) is frequently overexpressed in breast cancer and therapeutic agents targeting IGF-IR are currently in development. The ultimate success of anti-IGF-IR therapies will depend on the extent to which established tumors remain dependent upon IGF-IR signaling for sustained growth. To investigate the potential benefits and pitfalls of targeting IGF-IR, we used a doxycycline inducible mouse model of IGF-IR initiated breast cancer. We found that downregulation of IGF-IR results in tumor-size-dependent regression to an undetectable state. Partially regressed tumors almost always resumed growth in the absence of doxycycline and a proportion of tumors that regressed to an undetectable state ultimately recurred. This re-emergence of tumor growth in the absence of doxycycline was facilitated by IGF-IR-dependent and IGF-IR-independent mechanisms. Tumor escape from IGF-IR dependence was associated with an epithelial to mesenchymal transition and upregulation of transcriptional repressors of E-cadherin. These results suggest that tumors initiated by IGF-IR have the ability to become independent of this initiating oncogene, and IGF-IR independence is associated with characteristics consistent with an epithelial to mesenchymal transition.
Website Age:
30 years and 10 months (reg. 1994-08-11).

Matching Content Categories {πŸ“š}

  • Education
  • Health & Fitness
  • Science

Content Management System {πŸ“}

What CMS is nature.com built with?

Custom-built

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

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of nature.com 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.
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How Does Nature.com Make Money? {πŸ’Έ}


Display Ads {🎯}


The website utilizes display ads within its content to generate revenue. Check the next section for further revenue estimates.

Ads are managed by yourbow.com. Particular relationships are as follows:

Direct Advertisers (10)
google.com, pmc.com, doceree.com, yourbow.com, audienciad.com, onlinemediasolutions.com, advibe.media, aps.amazon.com, getmediamx.com, onomagic.com

Reseller Advertisers (38)
conversantmedia.com, rubiconproject.com, pubmatic.com, appnexus.com, openx.com, smartadserver.com, lijit.com, sharethrough.com, video.unrulymedia.com, google.com, yahoo.com, triplelift.com, onetag.com, sonobi.com, contextweb.com, 33across.com, indexexchange.com, media.net, themediagrid.com, adform.com, richaudience.com, sovrn.com, improvedigital.com, freewheel.tv, smaato.com, yieldmo.com, amxrtb.com, adyoulike.com, adpone.com, criteo.com, smilewanted.com, 152media.info, e-planning.net, smartyads.com, loopme.com, opera.com, mediafuse.com, betweendigital.com

How Much Does Nature.com Make? {πŸ’°}


Display Ads {🎯}

$63,100 per month
Our analysis indicates Nature.com generates between $42,042 and $115,616 monthly online from display ads.

Keywords {πŸ”}

cancer, article, google, scholar, cas, growth, breast, insulinlike, receptor, factor, res, nature, oncogene, mammary, tumor, human, igfir, access, tumors, expression, cell, content, research, cookies, recurrence, jones, campbell, moorehead, transgenic, privacy, function, signaling, mouse, epithelial, transition, open, nat, type, monoclonal, antibody, pubmed, tumorigenesis, moody, ontario, data, petrik, targeting, development, model, transcriptional,

Topics {βœ’οΈ}

nature portfolio permissions reprints privacy policy nature formalin-fixed paraffin-embedded tissues cancer research society tgf-beta-induced collagen expression c-myc-induced mammary adenocarcinomas advertising igf-ir-induced mammary tumors social media health research p19arf/p53 pathway lesions author information authors mammary gland development anti-igf-ir therapies real-time pcr primer conditional wnt-induced tumorigenesis targeting igf-ir author correspondence tumor-size-dependent regression endocrine-responsive breast cancer springerlink instant access personal data recombinant humanized anti-insulin tumor development igf-ir-independent mechanisms signal transduction function regulates epithelial plasticity data protection permissions invasive breast cancers transgenic mouse model igf-ir-dependent e-cadherin gene expression accelerates mammary tumorigenesis breast cancer cells kinase activity human breast cancer igf-ir dependence igf-ir independence human lung tumors igf-ir signaling igf-ir results growth factor receptor breast cancer panagiotis induces tumor formation metastasizing mammary carcinomas igf-ii mrna privacy

Questions {❓}

  • Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype?

Schema {πŸ—ΊοΈ}

WebPage:
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         headline:Reversibility and recurrence of IGF-IR-induced mammary tumors
         description:The type-I insulin-like growth factor receptor (IGF-IR) is frequently overexpressed in breast cancer and therapeutic agents targeting IGF-IR are currently in development. The ultimate success of anti-IGF-IR therapies will depend on the extent to which established tumors remain dependent upon IGF-IR signaling for sustained growth. To investigate the potential benefits and pitfalls of targeting IGF-IR, we used a doxycycline inducible mouse model of IGF-IR initiated breast cancer. We found that downregulation of IGF-IR results in tumor-size-dependent regression to an undetectable state. Partially regressed tumors almost always resumed growth in the absence of doxycycline and a proportion of tumors that regressed to an undetectable state ultimately recurred. This re-emergence of tumor growth in the absence of doxycycline was facilitated by IGF-IR-dependent and IGF-IR-independent mechanisms. Tumor escape from IGF-IR dependence was associated with an epithelial to mesenchymal transition and upregulation of transcriptional repressors of E-cadherin. These results suggest that tumors initiated by IGF-IR have the ability to become independent of this initiating oncogene, and IGF-IR independence is associated with characteristics consistent with an epithelial to mesenchymal transition.
         datePublished:2009-04-20T00:00:00Z
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      headline:Reversibility and recurrence of IGF-IR-induced mammary tumors
      description:The type-I insulin-like growth factor receptor (IGF-IR) is frequently overexpressed in breast cancer and therapeutic agents targeting IGF-IR are currently in development. The ultimate success of anti-IGF-IR therapies will depend on the extent to which established tumors remain dependent upon IGF-IR signaling for sustained growth. To investigate the potential benefits and pitfalls of targeting IGF-IR, we used a doxycycline inducible mouse model of IGF-IR initiated breast cancer. We found that downregulation of IGF-IR results in tumor-size-dependent regression to an undetectable state. Partially regressed tumors almost always resumed growth in the absence of doxycycline and a proportion of tumors that regressed to an undetectable state ultimately recurred. This re-emergence of tumor growth in the absence of doxycycline was facilitated by IGF-IR-dependent and IGF-IR-independent mechanisms. Tumor escape from IGF-IR dependence was associated with an epithelial to mesenchymal transition and upregulation of transcriptional repressors of E-cadherin. These results suggest that tumors initiated by IGF-IR have the ability to become independent of this initiating oncogene, and IGF-IR independence is associated with characteristics consistent with an epithelial to mesenchymal transition.
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         Cell Biology
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            name:C I Campbell
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                  name:Ontario Veterinary College, University of Guelph
                  address:
                     name:Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Canada
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Social Networks {πŸ‘}(1)

External Links {πŸ”—}(127)

Analytics and Tracking {πŸ“Š}

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Libraries {πŸ“š}

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Emails and Hosting {βœ‰οΈ}

Mail Servers:

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6.42s.