We are analyzing https://link.springer.com/article/10.1007/bf01961241.

Title:
Estrogen-dependent, tamoxifen-resistant tumorigenic growth of MCF-7 cells transfected with HER2/neu | Breast Cancer Research and Treatment
Description:
Since the poor prognosis associated with HER2 amplified breast cancers might be explained by a mechanistic association between p185HER2 overexpression and therapeutic resistance, we assessed the chemo-endocrine sensitivity of estrogen receptor (ER) containing MCF-7 breast cancer cells transfected with full-length HER2 cDNA. Of the 36 isolated MCF/HER2 subclones, 7 were found to overexpress p185HER2 surface receptor at levels 3 to 45-fold greater than parental or control transfected cells (MCF/neo). The overexpressing transfectants possessed increased inositol-1,4,5-trisphosphate-3
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 7,603,474 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? {💸}

We see no obvious way the site makes money.

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 {🔍}

cancer, google, scholar, breast, pubmed, cells, human, growth, article, mcf, benz, mcfher, tumors, tumor, research, resistance, usa, content, scott, sarup, johnson, shepard, osborne, pher, receptor, cell, tamoxifen, access, oncogene, res, privacy, cookies, treatment, sensitivity, transfectants, expression, ovarian, publish, search, tamoxifenresistant, transfected, coronado, cancers, overexpression, monoclonal, antibody, mice, ullrich, biol, cerbb,

Topics {✒️}

estrogen-induced post-transcriptional modulation c-erbb-2 protein enhances c-myc proto-oncogene expression tamoxifen-resistant tumorigenic growth month download article/chapter her2/neu report published c-erbb-2 proto-oncogenes mcf/her2–18 cells contained tam-resistant growth exhibited receptor-specific partial agonist full-length her2 cdna transient induction ofc-myc human breast cancers mcf/her2–18 tumors grew mcf/her2–18 tumors continued anti-p185her2 monoclonal antibody breast cancer cells 5-trisphosphate-3'-kinase activity comparable long-term antiestrogen therapy long-term antiestrogen administration human breast cancer acquired tamoxifen resistance c-erbb-2 oncogene advanced breast cancer related subjects mcf/her2–18 cells thein vitro sensitivity therapeutic resistance tumor suppressor genes mcf-7 cells transfected human breast tumors tumor necrosis factor hormone-dependent tumorigenicity full article pdf tamoxifen-stimulated growth mcf/her2–18 tumors privacy choices/manage cookies scott gk c-haras oncogene control transfected cells tyrosine kinase receptor c-ha-ras1 trans-4-hydroxy-tamoxifen estrogenic tamoxifen metabolites athymic nude mouse antiproliferative effectsin vitro highly overexpressing transfectants advanced ovarian carcinomas stimulates receptor functions c-myc overexpression

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Estrogen-dependent, tamoxifen-resistant tumorigenic growth of MCF-7 cells transfected with HER2/neu
         description:Since the poor prognosis associated with HER2 amplified breast cancers might be explained by a mechanistic association between p185HER2 overexpression and therapeutic resistance, we assessed the chemo-endocrine sensitivity of estrogen receptor (ER) containing MCF-7 breast cancer cells transfected with full-length HER2 cDNA. Of the 36 isolated MCF/HER2 subclones, 7 were found to overexpress p185HER2 surface receptor at levels 3 to 45-fold greater than parental or control transfected cells (MCF/neo). The overexpressing transfectants possessed increased inositol-1,4,5-trisphosphate-3'-kinase activity comparable to enzyme activity in the endogenously HER2 amplified breast cancer cell lines SK-Br-3 and BT-474. The anti-p185HER2 monoclonal antibody and receptor-specific partial agonist, muMAb4D5 (4D5), known to inhibit growth of SK-Br-3 and BT-474 cells, produced no significant growth inhibitory effect on any of the transfectants including the 45-fold overexpressing MCF/HER2–18 cells which were studied in greater detail. MCF/HER2–18 cells contained at least partially functioning exogenous receptor since 4D5 (3µg/ml) specifically stimulated phosphorylation of p185HER2 and its co-precipitating ptyr56 substrate within 5 min, and this was followed at 1 h by a transient induction ofc-myc but notc-fos mRNA. ER content and thein vitro sensitivity of MCF/HER2–18 cells to 5-fluorouracil and adriamycin were identical to those of control transfectants and parental cells. However, these highly overexpressing transfectants had acquired low level (2 to 4-fold) resistance to cisplatin and were no longer sensitive to the antiestrogen tamoxifen (TAM). To compare the hormone-dependent tumorigenicity of the HER2 transfectants, MCF/HER2–18 and control cells (MCF, MCF/neo-3) were implanted into ovariectomized athymic nude mice. No tumors were produced in the absence of estradiol (E2) administration. In E2 supplemented mice, MCF/HER2–18 tumors grew most rapidly. When E2 treatment was stopped and daily TAM injections were initiated, MCF-7 and MCF/neo-3 tumor growth ceased immediately, while MCF/HER2–18 tumors continued to show an accelerated growth rate lasting weeks. This pattern of hormone-dependent, TAM-resistant growth exhibited by the MCF/HER2–18 tumors in nude mice supports the possibility that p185HER2 overexpression in human breast cancers may be linked to therapeutic resistance.
         datePublished:
         dateModified:
         pageStart:85
         pageEnd:95
         sameAs:https://doi.org/10.1007/BF01961241
         keywords:
            chemotherapy
            HER2/c-erbB-2/neu
            MCF-7
            resistance
            tamoxifen
            transfection
            Oncology
         image:
         isPartOf:
            name:Breast Cancer Research and Treatment
            issn:
               1573-7217
               0167-6806
            volumeNumber:24
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Kluwer Academic Publishers
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Christopher C. Benz
               affiliation:
                     name:University of California
                     address:
                        name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Gary K. Scott
               affiliation:
                     name:University of California
                     address:
                        name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Jay C. Sarup
               affiliation:
                     name:Genetech, Inc.
                     address:
                        name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Randolph M. Johnson
               affiliation:
                     name:Genetech, Inc.
                     address:
                        name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Debasish Tripathy
               affiliation:
                     name:University of California
                     address:
                        name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Ester Coronado
               affiliation:
                     name:University of Texas Health Science Center
                     address:
                        name:Department of Medicine, University of Texas Health Science Center, San Antonio, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:H. Michael Shepard
               affiliation:
                     name:Genetech, Inc.
                     address:
                        name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
                        type:PostalAddress
                     type:Organization
               type:Person
               name:C. Kent Osborne
               affiliation:
                     name:University of Texas Health Science Center
                     address:
                        name:Department of Medicine, University of Texas Health Science Center, San Antonio, USA
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Estrogen-dependent, tamoxifen-resistant tumorigenic growth of MCF-7 cells transfected with HER2/neu
      description:Since the poor prognosis associated with HER2 amplified breast cancers might be explained by a mechanistic association between p185HER2 overexpression and therapeutic resistance, we assessed the chemo-endocrine sensitivity of estrogen receptor (ER) containing MCF-7 breast cancer cells transfected with full-length HER2 cDNA. Of the 36 isolated MCF/HER2 subclones, 7 were found to overexpress p185HER2 surface receptor at levels 3 to 45-fold greater than parental or control transfected cells (MCF/neo). The overexpressing transfectants possessed increased inositol-1,4,5-trisphosphate-3'-kinase activity comparable to enzyme activity in the endogenously HER2 amplified breast cancer cell lines SK-Br-3 and BT-474. The anti-p185HER2 monoclonal antibody and receptor-specific partial agonist, muMAb4D5 (4D5), known to inhibit growth of SK-Br-3 and BT-474 cells, produced no significant growth inhibitory effect on any of the transfectants including the 45-fold overexpressing MCF/HER2–18 cells which were studied in greater detail. MCF/HER2–18 cells contained at least partially functioning exogenous receptor since 4D5 (3µg/ml) specifically stimulated phosphorylation of p185HER2 and its co-precipitating ptyr56 substrate within 5 min, and this was followed at 1 h by a transient induction ofc-myc but notc-fos mRNA. ER content and thein vitro sensitivity of MCF/HER2–18 cells to 5-fluorouracil and adriamycin were identical to those of control transfectants and parental cells. However, these highly overexpressing transfectants had acquired low level (2 to 4-fold) resistance to cisplatin and were no longer sensitive to the antiestrogen tamoxifen (TAM). To compare the hormone-dependent tumorigenicity of the HER2 transfectants, MCF/HER2–18 and control cells (MCF, MCF/neo-3) were implanted into ovariectomized athymic nude mice. No tumors were produced in the absence of estradiol (E2) administration. In E2 supplemented mice, MCF/HER2–18 tumors grew most rapidly. When E2 treatment was stopped and daily TAM injections were initiated, MCF-7 and MCF/neo-3 tumor growth ceased immediately, while MCF/HER2–18 tumors continued to show an accelerated growth rate lasting weeks. This pattern of hormone-dependent, TAM-resistant growth exhibited by the MCF/HER2–18 tumors in nude mice supports the possibility that p185HER2 overexpression in human breast cancers may be linked to therapeutic resistance.
      datePublished:
      dateModified:
      pageStart:85
      pageEnd:95
      sameAs:https://doi.org/10.1007/BF01961241
      keywords:
         chemotherapy
         HER2/c-erbB-2/neu
         MCF-7
         resistance
         tamoxifen
         transfection
         Oncology
      image:
      isPartOf:
         name:Breast Cancer Research and Treatment
         issn:
            1573-7217
            0167-6806
         volumeNumber:24
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Kluwer Academic Publishers
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Christopher C. Benz
            affiliation:
                  name:University of California
                  address:
                     name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Gary K. Scott
            affiliation:
                  name:University of California
                  address:
                     name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jay C. Sarup
            affiliation:
                  name:Genetech, Inc.
                  address:
                     name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Randolph M. Johnson
            affiliation:
                  name:Genetech, Inc.
                  address:
                     name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Debasish Tripathy
            affiliation:
                  name:University of California
                  address:
                     name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Ester Coronado
            affiliation:
                  name:University of Texas Health Science Center
                  address:
                     name:Department of Medicine, University of Texas Health Science Center, San Antonio, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:H. Michael Shepard
            affiliation:
                  name:Genetech, Inc.
                  address:
                     name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
                     type:PostalAddress
                  type:Organization
            type:Person
            name:C. Kent Osborne
            affiliation:
                  name:University of Texas Health Science Center
                  address:
                     name:Department of Medicine, University of Texas Health Science Center, San Antonio, USA
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Breast Cancer Research and Treatment
      issn:
         1573-7217
         0167-6806
      volumeNumber:24
Organization:
      name:Kluwer Academic Publishers
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of California
      address:
         name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
         type:PostalAddress
      name:University of California
      address:
         name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
         type:PostalAddress
      name:Genetech, Inc.
      address:
         name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
         type:PostalAddress
      name:Genetech, Inc.
      address:
         name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
         type:PostalAddress
      name:University of California
      address:
         name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
         type:PostalAddress
      name:University of Texas Health Science Center
      address:
         name:Department of Medicine, University of Texas Health Science Center, San Antonio, USA
         type:PostalAddress
      name:Genetech, Inc.
      address:
         name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
         type:PostalAddress
      name:University of Texas Health Science Center
      address:
         name:Department of Medicine, University of Texas Health Science Center, San Antonio, USA
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Christopher C. Benz
      affiliation:
            name:University of California
            address:
               name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Gary K. Scott
      affiliation:
            name:University of California
            address:
               name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Jay C. Sarup
      affiliation:
            name:Genetech, Inc.
            address:
               name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Randolph M. Johnson
      affiliation:
            name:Genetech, Inc.
            address:
               name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Debasish Tripathy
      affiliation:
            name:University of California
            address:
               name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Ester Coronado
      affiliation:
            name:University of Texas Health Science Center
            address:
               name:Department of Medicine, University of Texas Health Science Center, San Antonio, USA
               type:PostalAddress
            type:Organization
      name:H. Michael Shepard
      affiliation:
            name:Genetech, Inc.
            address:
               name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
               type:PostalAddress
            type:Organization
      name:C. Kent Osborne
      affiliation:
            name:University of Texas Health Science Center
            address:
               name:Department of Medicine, University of Texas Health Science Center, San Antonio, USA
               type:PostalAddress
            type:Organization
PostalAddress:
      name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
      name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
      name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
      name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
      name:M-1282 Cancer Research Institute, University of California, San Francisco, USA
      name:Department of Medicine, University of Texas Health Science Center, San Antonio, USA
      name:Department of Developmental Biology, Genetech, Inc., South San Francisco, USA
      name:Department of Medicine, University of Texas Health Science Center, San Antonio, USA
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(91)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.06s.

LINK . SPRINGER . COM {}