We are analyzing https://link.springer.com/article/10.1007/s10585-009-9267-6.

Title:
An improved model to study tumor cell autonomous metastasis programs using MTLn3 cells and the Rag2−/− γc−/− mouse | Clinical & Experimental Metastasis
Description:
The occurrence of metastases is a critical determinant of the prognosis for breast cancer patients. Effective treatment of breast cancer metastases is hampered by a poor understanding of the mechanisms involved in the formation of these secondary tumor deposits. To study the processes of metastasis, valid in vivo tumor metastasis models are required. Here, we show that increased expression of the EGF receptor in the MTLn3 rat mammary tumor cell-line is essential for efficient lung metastasis formation in the Rag mouse model. EGFR expression resulted in delayed orthotopic tumor growth but at the same time strongly enhanced intravasation and lung metastasis. Previously, we demonstrated the critical role of NK cells in a lung metastasis model using MTLn3 cells in syngenic F344 rats. However, this model is incompatible with human EGFR. Using the highly metastatic EGFR-overexpressing MTLn3 cell-line, we report that only Rag2−/−γc−/− mice, which lack NK cells, allow efficient lung metastasis from primary tumors in the mammary gland. In contrast, in nude and SCID mice, the remaining innate immune cells reduce MTLn3 lung metastasis formation. Furthermore, we confirm this finding with the orthotopic transplantation of the 4T1 mouse mammary tumor cell-line. Thus, we have established an improved in vivo model using a Rag2−/− γc−/− mouse strain together with MTLn3 cells that have increased levels of the EGF receptor, which enables us to study EGFR-dependent tumor cell autonomous mechanisms underlying lung metastasis formation. This improved model can be used for drug target validation and development of new therapeutic strategies against breast cancer metastasis formation.
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Keywords {🔍}

cells, tumor, mice, metastasis, cancer, lung, cell, google, scholar, rag, pubmed, article, cas, growth, mouse, metastases, breast, mtln, model, formation, primary, mtlngfperbb, scid, fig, erbb, mammary, mtlngfp, spontaneous, models, tumors, number, study, beige, increased, expression, intravasation, human, assay, nude, immune, orthotopic, results, injected, weight, lungs, blood, balbc, cellline, weeks, van,

Topics {✒️}

mtln3-gfp-erbb1 versus mtln3-gfp mtln3-gfp versus mtln3-gfp-erbb1 scid [cb17/lcr-prkdcscid/crl] gfp-labeled mtln3 cell-lines mtln3-gfp-erbb1 cell-line mtln3-gfp-erbb1 cell line control cell-line mtln3-gfp mtln3-gfp-erbb1 cell-lines fluorescence-activated cell sorting mtln3-gfp-erbb1 transplanted group parental mb-mda-231 cells highly metastatic cell-line 4t1-luc cell-line mtln3-gfp-erbb1 inoculated mouse goat anti-mouse apc mtln3-gfp-erbb1 cells show mtln3-gfp cell-lines rabbit anti-human erbb1 article download pdf c-abl proto-oncogene immune-deficient scid mice tail vein developed mtln3-gfp-erbb1 group marginating pulmonary-nk activity lateral tail vein doxorubicin-induced mitochondrial dysfunction mtln3-gfp-erbb1 cells 000 mtln3-gfp-erbb1 cells gfp-mtln3-erbb1 cells breast/tumor metastasis model mtln3-gfp control cells animals receiving mtln3-gfp open access light-tight specimen box deficient cellular immunity—finding scid beige [cb17/lcr mtln3-gfp inoculated mouse van de water mtln3 cell line study nk-independent mechanisms gfp-positive lung metastases tumor cell line breast cancer research mammary fat pad breast cancer models nonconditioned nod/scid mice human breast carcinomas full access related subjects mammary fat pads

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WebPage:
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         headline:An improved model to study tumor cell autonomous metastasis programs using MTLn3 cells and the Rag2−/− γc−/− mouse
         description:The occurrence of metastases is a critical determinant of the prognosis for breast cancer patients. Effective treatment of breast cancer metastases is hampered by a poor understanding of the mechanisms involved in the formation of these secondary tumor deposits. To study the processes of metastasis, valid in vivo tumor metastasis models are required. Here, we show that increased expression of the EGF receptor in the MTLn3 rat mammary tumor cell-line is essential for efficient lung metastasis formation in the Rag mouse model. EGFR expression resulted in delayed orthotopic tumor growth but at the same time strongly enhanced intravasation and lung metastasis. Previously, we demonstrated the critical role of NK cells in a lung metastasis model using MTLn3 cells in syngenic F344 rats. However, this model is incompatible with human EGFR. Using the highly metastatic EGFR-overexpressing MTLn3 cell-line, we report that only Rag2−/−γc−/− mice, which lack NK cells, allow efficient lung metastasis from primary tumors in the mammary gland. In contrast, in nude and SCID mice, the remaining innate immune cells reduce MTLn3 lung metastasis formation. Furthermore, we confirm this finding with the orthotopic transplantation of the 4T1 mouse mammary tumor cell-line. Thus, we have established an improved in vivo model using a Rag2−/− γc−/− mouse strain together with MTLn3 cells that have increased levels of the EGF receptor, which enables us to study EGFR-dependent tumor cell autonomous mechanisms underlying lung metastasis formation. This improved model can be used for drug target validation and development of new therapeutic strategies against breast cancer metastasis formation.
         datePublished:2009-05-24T00:00:00Z
         dateModified:2009-05-24T00:00:00Z
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      headline:An improved model to study tumor cell autonomous metastasis programs using MTLn3 cells and the Rag2−/− γc−/− mouse
      description:The occurrence of metastases is a critical determinant of the prognosis for breast cancer patients. Effective treatment of breast cancer metastases is hampered by a poor understanding of the mechanisms involved in the formation of these secondary tumor deposits. To study the processes of metastasis, valid in vivo tumor metastasis models are required. Here, we show that increased expression of the EGF receptor in the MTLn3 rat mammary tumor cell-line is essential for efficient lung metastasis formation in the Rag mouse model. EGFR expression resulted in delayed orthotopic tumor growth but at the same time strongly enhanced intravasation and lung metastasis. Previously, we demonstrated the critical role of NK cells in a lung metastasis model using MTLn3 cells in syngenic F344 rats. However, this model is incompatible with human EGFR. Using the highly metastatic EGFR-overexpressing MTLn3 cell-line, we report that only Rag2−/−γc−/− mice, which lack NK cells, allow efficient lung metastasis from primary tumors in the mammary gland. In contrast, in nude and SCID mice, the remaining innate immune cells reduce MTLn3 lung metastasis formation. Furthermore, we confirm this finding with the orthotopic transplantation of the 4T1 mouse mammary tumor cell-line. Thus, we have established an improved in vivo model using a Rag2−/− γc−/− mouse strain together with MTLn3 cells that have increased levels of the EGF receptor, which enables us to study EGFR-dependent tumor cell autonomous mechanisms underlying lung metastasis formation. This improved model can be used for drug target validation and development of new therapeutic strategies against breast cancer metastasis formation.
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      dateModified:2009-05-24T00:00:00Z
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         EGF receptor
         ErbB1
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         MTLn3 cells
         4T1 cells
         Immune deficient mice
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         general
         Oncology
         Hematology
         Surgical Oncology
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      name:Division of Toxicology, Leiden Amsterdam Center for Drug Research (LACDR), Leiden University, Leiden, The Netherlands
      name:Division of Toxicology, Leiden Amsterdam Center for Drug Research (LACDR), Leiden University, Leiden, The Netherlands
      name:Division of Toxicology, Leiden Amsterdam Center for Drug Research (LACDR), Leiden University, Leiden, The Netherlands
      name:Division of Toxicology, Leiden Amsterdam Center for Drug Research (LACDR), Leiden University, Leiden, The Netherlands

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