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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. Schema
  9. External Links
  10. Analytics And Tracking
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We are analyzing https://link.springer.com/article/10.1007/s10549-005-6939-z.

Title:
Nordihydroguaiaretic Acid (NDGA) Inhibits the IGF-1 and c-erbB2/HER2/neu Receptors and Suppresses Growth in Breast Cancer Cells | Breast Cancer Research and Treatment
Description:
Nordihydroguaiaretic acid (NDGA) is a phenolic compound isolated from the creosote bush Larrea divaricatta that has anti-cancer activities both in vitro and in vivo. We can now attribute certain of these anti-cancer properties in breast cancer cells to the ability of NDGA to directly inhibit the function of two receptor tyrosine kinases (RTKs), the insulin-like growth factor receptor (IGF-1R) and the c-erbB2/HER2/neu (HER2/neu) receptor. In MCF-7 human breast cancer cells, low micromolar concentrations of NDGA inhibited activation of the IGF-1R, and downstream phosphorylation of both the Akt/PKB serine kinase and the pro-apoptotic protein BAD. In mouse MCNeuA cells, NDGA also inhibited ligand independent phosphorylation of HER2/neu. To study whether this inhibitory effect in cells was due to a direct action on these receptors, we studied the IGF-1-stimulated tyrosine kinase activity of isolated IGF-1R, which was inhibited by NDGA at 10 μM or less. NDGA was also effective at inhibiting autophosphorylation of the isolated HER2/neu receptor at similar concentrations. In addition, NDGA inhibited IGF-1 specific growth of cultured breast cancer cells with an IC50 of approximately 30 μM. NDGA treatment (intraperitoneal injection 3 times per week) also decreased the activity of the IGF-1R and the HER2/neu receptor in MCNeuA cells implanted into mice. This inhibition of RTK activity was associated with decreased growth rates of MCNeuA cells in vivo. These studies indicate that the anti-breast cancer properties of NDGA are related to the inhibition of two important RTKs. Agents of this class may therefore provide new insights into potential therapies for this disease.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Education
  • Science
  • 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 7,643,078 visitors per month in the current month.

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

We see no obvious way the site makes money.

Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Link.springer.com might be making money, but it's not detectable how they're doing it.

Keywords {🔍}

google, scholar, cas, pubmed, cancer, article, growth, breast, receptor, cells, cell, insulinlike, factor, human, kinase, res, ndga, acid, tyrosine, apoptosis, nordihydroguaiaretic, inhibition, mice, inhibitors, research, receptors, access, biol, treatment, igf, herneu, activity, factors, pancreatic, oncogene, privacy, cookies, content, inhibits, youngren, activation, protein, expression, usa, transgenic, lipoxygenase, san, publish, search, goldfine,

Topics {✒️}

c-erbb2/her2/neu receptors month download article/chapter growth factor receptors lipoxygenase inhibitor-induced apoptosis pro-apoptotic protein bad physiologically relevant target mmtv/neu transgenic mouse garcia-echeverria ma pearson fujita-yamaguchi js miller cardiff wj muller c-erbb2/her2/neu sbraccia id goldfine triple-negative breast cancer igf2-id1-igf2 circuit high-performance liquid chromatography anti-breast cancer properties cozens db evans full article pdf akt/pkb serine kinase lobo lj esserman protein tyrosine phosphorylation isolated her2/neu receptor antiapoptotic signalling tyrosine kinase inhibitors san francisco/mt human breast cancer breast cancer cells colorectal tumor cells klippel mj weber seufferlein mj seckl mouse mcneua cells growth factor receptor transgenic mice expressing transgenic mice carrying arteaga receptor tyrosine kinases protein kinase article youngren breast cancer stem molecular ullrich wl mcguire normoglycemic pima indians receptors anti-cancer properties privacy choices/manage cookies malignant glioma cells dyal1mxlvvyhs7c%3d 10 dyal1mxmt1kjs78%3d 10 dyak1cxksfkksrk%3d 10 malkinson jl mulshine

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Nordihydroguaiaretic Acid (NDGA) Inhibits the IGF-1 and c-erbB2/HER2/neu Receptors and Suppresses Growth in Breast Cancer Cells
         description:Nordihydroguaiaretic acid (NDGA) is a phenolic compound isolated from the creosote bush Larrea divaricatta that has anti-cancer activities both in vitro and in vivo. We can now attribute certain of these anti-cancer properties in breast cancer cells to the ability of NDGA to directly inhibit the function of two receptor tyrosine kinases (RTKs), the insulin-like growth factor receptor (IGF-1R) and the c-erbB2/HER2/neu (HER2/neu) receptor. In MCF-7 human breast cancer cells, low micromolar concentrations of NDGA inhibited activation of the IGF-1R, and downstream phosphorylation of both the Akt/PKB serine kinase and the pro-apoptotic protein BAD. In mouse MCNeuA cells, NDGA also inhibited ligand independent phosphorylation of HER2/neu. To study whether this inhibitory effect in cells was due to a direct action on these receptors, we studied the IGF-1-stimulated tyrosine kinase activity of isolated IGF-1R, which was inhibited by NDGA at 10 μM or less. NDGA was also effective at inhibiting autophosphorylation of the isolated HER2/neu receptor at similar concentrations. In addition, NDGA inhibited IGF-1 specific growth of cultured breast cancer cells with an IC50 of approximately 30 μM. NDGA treatment (intraperitoneal injection 3 times per week) also decreased the activity of the IGF-1R and the HER2/neu receptor in MCNeuA cells implanted into mice. This inhibition of RTK activity was associated with decreased growth rates of MCNeuA cells in vivo. These studies indicate that the anti-breast cancer properties of NDGA are related to the inhibition of two important RTKs. Agents of this class may therefore provide new insights into potential therapies for this disease.
         datePublished:
         dateModified:
         pageStart:37
         pageEnd:46
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            proliferation
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            syngeneic mouse model
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ScholarlyArticle:
      headline:Nordihydroguaiaretic Acid (NDGA) Inhibits the IGF-1 and c-erbB2/HER2/neu Receptors and Suppresses Growth in Breast Cancer Cells
      description:Nordihydroguaiaretic acid (NDGA) is a phenolic compound isolated from the creosote bush Larrea divaricatta that has anti-cancer activities both in vitro and in vivo. We can now attribute certain of these anti-cancer properties in breast cancer cells to the ability of NDGA to directly inhibit the function of two receptor tyrosine kinases (RTKs), the insulin-like growth factor receptor (IGF-1R) and the c-erbB2/HER2/neu (HER2/neu) receptor. In MCF-7 human breast cancer cells, low micromolar concentrations of NDGA inhibited activation of the IGF-1R, and downstream phosphorylation of both the Akt/PKB serine kinase and the pro-apoptotic protein BAD. In mouse MCNeuA cells, NDGA also inhibited ligand independent phosphorylation of HER2/neu. To study whether this inhibitory effect in cells was due to a direct action on these receptors, we studied the IGF-1-stimulated tyrosine kinase activity of isolated IGF-1R, which was inhibited by NDGA at 10 μM or less. NDGA was also effective at inhibiting autophosphorylation of the isolated HER2/neu receptor at similar concentrations. In addition, NDGA inhibited IGF-1 specific growth of cultured breast cancer cells with an IC50 of approximately 30 μM. NDGA treatment (intraperitoneal injection 3 times per week) also decreased the activity of the IGF-1R and the HER2/neu receptor in MCNeuA cells implanted into mice. This inhibition of RTK activity was associated with decreased growth rates of MCNeuA cells in vivo. These studies indicate that the anti-breast cancer properties of NDGA are related to the inhibition of two important RTKs. Agents of this class may therefore provide new insights into potential therapies for this disease.
      datePublished:
      dateModified:
      pageStart:37
      pageEnd:46
      sameAs:https://doi.org/10.1007/s10549-005-6939-z
      keywords:
         MCF-7 cells
         proliferation
         small molecule inhibitor
         syngeneic mouse model
         tyrosine kinase
         Oncology
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      isPartOf:
         name:Breast Cancer Research and Treatment
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            1573-7217
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            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
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                     name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
                     type:PostalAddress
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                     type:PostalAddress
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                  address:
                     name:Department of Surgery, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
                     type:PostalAddress
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                  name:University of California
                  address:
                     name:Department of Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, USA
                     type:PostalAddress
                  type:Organization
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            name:Ira D. Goldfine
            affiliation:
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                  address:
                     name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
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      address:
         name:Department of Surgery, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
         type:PostalAddress
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      address:
         name:Department of Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, USA
         type:PostalAddress
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      address:
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            name:University of California
            address:
               name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
               type:PostalAddress
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      affiliation:
            name:University of California
            address:
               name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
               type:PostalAddress
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      name:Cristina Penaranda
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            name:University of California
            address:
               name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
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               name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
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            address:
               name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
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      name:Margaret Lobo
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            name:University of California
            address:
               name:Department of Surgery, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
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      name:Michael Campbell
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            name:University of California
            address:
               name:Department of Surgery, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
               type:PostalAddress
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      name:John Kerner
      affiliation:
            name:University of California
            address:
               name:Department of Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, USA
               type:PostalAddress
            type:Organization
      name:Ira D. Goldfine
      affiliation:
            name:University of California
            address:
               name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
      name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
      name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
      name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
      name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
      name:Department of Surgery, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
      name:Department of Surgery, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
      name:Department of Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, USA
      name:Division of Diabetes and Endocrine Research, San Francisco/Mt. Zion Medical Center, University of California, San Francisco, USA
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External Links {🔗}(201)

Analytics and Tracking {📊}

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Libraries {📚}

  • Clipboard.js
  • Prism.js

CDN Services {📦}

  • Crossref

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