We are analyzing https://link.springer.com/article/10.1186/bcr723.

Title:
Models of breast cancer: quo vadis, animal modeling? | Breast Cancer Research
Description:
Rodent models for breast cancer have for many decades provided unparalleled insights into cellular and molecular aspects of neoplastic transformation and tumorigenesis. Despite recent improvements in the fidelity of genetically engineered mice, rodent models are still being criticized by many colleagues for not being
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Science
Education
Health & Fitness

Content Management System {📝}

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 {📈}

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

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We don't see any clear sign of profit-making.

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 could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

cells, cancer, breast, human, models, mammary, pubmed, article, google, scholar, cas, model, mice, epithelial, mouse, tumorigenesis, xenograft, cell, gem, tumor, colleagues, transformation, tert, neoplastic, gene, telomerase, oncogene, genetic, tumors, expression, central, disease, gland, genes, hahn, important, normal, stem, stroma, function, animal, humans, pathways, murine, kim, growth, factors, genetically, development, cancers,

Topics {✒️}

kay-uwe wagner prolactin induces eralpha-positive kluwer academic/plenum publishers mmtv/c-myc genes mmtv/v-ha-ras yeast-based screening assay central database http cre-lox-mediated deletion eralpha-negative mammary cancer cancer-initiating epithelial subtypes k14-positive myoepithelial cells ionizing radiation-induced models breast cancer research cre-mediated gene deletion correct epithelial–stromal interaction telomere length-independent mechanism p53-deficient mice succumb conditional wnt-induced tumorigenesis mammary-specific model demonstrates chemical carcinogen-induced tumorigenesis genetically engineered mice metastatic breast cancer privacy choices/manage cookies article wagner reflect species-related incompatibilities rudland ps natl cancer inst utilize fibroblasts derived untransformed epithelial cells luminal epithelial cells human stroma–epithelia graft k14-cre mice blunted ductal morphogenesis newly developed strains multiple genetic defects transform human cells breast tumor subtypes borresen-dale al human breast cancers diverse epithelial subtypes multiple genetic alterations breast cancer risk cell biological concept telomere dysfunction promotes gene expression induced defined genetic elements mammary epithelial cells tumors arose solely cancer-prone mouse sv40 early region

Questions {❓}

Another important question remains: how different are these pathways in human versus murine cells?
But does each step toward neoplastic transformation recapitulate the morphology, pathology, and etiology of the progressing disease?
Kim JB, O'Hare MJ, Stein R: Models of breast cancer: is merging human and animal models the future?
Models of breast cancer: quo vadis, animal modeling?
Models of breast cancer: quo vadis, animal modeling?
When can we expect to have an authentic mouse model for breast cancer?
Without TERT expression how do they otherwise maintain their replicative potential?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Models of breast cancer: quo vadis, animal modeling?
         description:Rodent models for breast cancer have for many decades provided unparalleled insights into cellular and molecular aspects of neoplastic transformation and tumorigenesis. Despite recent improvements in the fidelity of genetically engineered mice, rodent models are still being criticized by many colleagues for not being 'authentic' enough to the human disease. Motives for this criticism are manifold and range from a very general antipathy against the rodent model system to well-founded arguments that highlight physiological variations between species. Newly proposed differences in genetic pathways that cause cancer in humans and mice invigorated the ongoing discussion about the legitimacy of the murine system to model the human disease. The present commentary intends to stimulate a debate on this subject by providing the background about new developments in animal modeling, by disputing suggested limitations of genetically engineered mice, and by discussing improvements but also ambiguous expectations on the authenticity of xenograft models to faithfully mimic the human disease.
         datePublished:2003-10-31T00:00:00Z
         dateModified:2003-10-31T00:00:00Z
         pageStart:1
         pageEnd:8
         sameAs:https://doi.org/10.1186/bcr723
         keywords:
            breast neoplasms
            gene targeting
            genetically engineered mice
            genetic models
            genetic techniques
            xenograft
            Cancer Research
            Oncology
            Surgical Oncology
         image:
         isPartOf:
            name:Breast Cancer Research
            issn:
               1465-542X
            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:Kay-Uwe Wagner
               affiliation:
                     name:University of Nebraska Medical Center
                     address:
                        name:University of Nebraska Medical Center, Omaha, USA
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Models of breast cancer: quo vadis, animal modeling?
      description:Rodent models for breast cancer have for many decades provided unparalleled insights into cellular and molecular aspects of neoplastic transformation and tumorigenesis. Despite recent improvements in the fidelity of genetically engineered mice, rodent models are still being criticized by many colleagues for not being 'authentic' enough to the human disease. Motives for this criticism are manifold and range from a very general antipathy against the rodent model system to well-founded arguments that highlight physiological variations between species. Newly proposed differences in genetic pathways that cause cancer in humans and mice invigorated the ongoing discussion about the legitimacy of the murine system to model the human disease. The present commentary intends to stimulate a debate on this subject by providing the background about new developments in animal modeling, by disputing suggested limitations of genetically engineered mice, and by discussing improvements but also ambiguous expectations on the authenticity of xenograft models to faithfully mimic the human disease.
      datePublished:2003-10-31T00:00:00Z
      dateModified:2003-10-31T00:00:00Z
      pageStart:1
      pageEnd:8
      sameAs:https://doi.org/10.1186/bcr723
      keywords:
         breast neoplasms
         gene targeting
         genetically engineered mice
         genetic models
         genetic techniques
         xenograft
         Cancer Research
         Oncology
         Surgical Oncology
      image:
      isPartOf:
         name:Breast Cancer Research
         issn:
            1465-542X
         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:Kay-Uwe Wagner
            affiliation:
                  name:University of Nebraska Medical Center
                  address:
                     name:University of Nebraska Medical Center, Omaha, USA
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Breast Cancer Research
      issn:
         1465-542X
      volumeNumber:6
Organization:
      name:BioMed Central
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Nebraska Medical Center
      address:
         name:University of Nebraska Medical Center, Omaha, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Kay-Uwe Wagner
      affiliation:
            name:University of Nebraska Medical Center
            address:
               name:University of Nebraska Medical Center, Omaha, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:University of Nebraska Medical Center, Omaha, USA

External Links {🔗}(179)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.56s.

LINK . SPRINGER . COM {}