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We began analyzing https://breast-cancer-research.biomedcentral.com/articles/10.1186/bcr1395, but it redirected us to https://breast-cancer-research.biomedcentral.com/articles/10.1186/bcr1395. The analysis below is for the second page.

Title[redir]:
Effect of a farnesyl transferase inhibitor (R115777) on ductal carcinoma in situ of the breast in a human xenograft model and on breast and ovarian cancer cell growth in vitro and in vivo | Breast Cancer Research | Full Text
Description:
Introduction The ras pathway is essential for cell growth and proliferation. The effects of R115777, a farnesyl transferase inhibitor, were investigated in cancer cell lines expressing varying levels of growth factor receptors and with differing ras status. Effects on tumour xenografts and human ductal carcinoma in situ (DCIS) of the breast in a xenograft mouse model were also tested. Method In vitro, the concentrations required to reduce cell numbers by 50% (50% inhibitory concentration) were established (MDA-MB231, MCF-7, MCF-7/HER2-18, BT-474, SK-BR3 and SKOV3). Human DCIS was implanted in nude mice or, in separate experiments, cultured cells were injected (MDA-MB231, MCF-7/HER2-18, SKOV3) and allowed to form tumours. Proliferation and apoptosis were determined by immunohistochemistry in xenografts and cell tumours. Results The 50% inhibitory concentrations varied a hundred-fold, from 39 nmol/l (± 26 nmol/l) for SKBR3 to 5.9 μmol/l(± 0.8 μmol/l) for MDA-MB231. In MCF-7/HER2-18 and SKOV3 cells the levels of tumour growth inhibition were approximately 85% and 40%, respectively. There was a significant decrease in the cell turnover index (CTI; proliferation/apoptosis). In MDA-MB 231 with activated k-ras no inhibition was observed. In treated DCIS xenografts proliferation decreased and apoptosis increased. The CTI ratio between the start and 1 and 2 weeks of treatment were 1.99 and 1.50, respectively, for controls and 0.85 (P = 0.005) and 0.75 (P = 0.08) for treated xenografts. Conclusion Treatment with the farnesyl transferase inhibitor reduced cell growth in vitro and cell tumour growth in vivo. In DCIS treatment resulted in a reduced CTI. R115777 is a promising treatment for breast cancer but the relation between effect and growth factor receptor and ras status has to be established.

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Keywords {🔍}

cell, cancer, tumours, growth, breast, ras, pubmed, google, scholar, treated, cas, tumour, dcis, article, treatment, mgkg, xenografts, experiments, human, inhibition, study, control, transferase, effect, farnesyl, proliferation, protein, vitro, day, cells, vivo, fti, mcfher, res, apoptosis, cti, lines, index, table, inhibitor, mice, line, carcinoma, reduced, authors, data, pathway, factor, results, controls,

Topics {✒️}

springer nature carboxyl-terminal tetrapeptide caax expressed wild-type k-ras tamoxifen-resistant tumorigenic growth eosin stained sections final tumour volume 1309/4ncm-qj9w-qm0j-6qje mda-mb231 cell lines mda-mb231 cell line mitogen-activated protein kinase authors scientific editing proliferation index/apoptotic index materials body weight loss/gain activated wild-type ras wild-type ras proteins authors’ original file wild-type ras cancer final histopathological report farnesyl transferase inhibitor mouse received tissue farnesyl transferase inhibition privacy choices/manage cookies comedo-type ductal carcinoma median tumour volume de klerk gj enzyme farnesyl transferase cell turnover index bmc farnesyl transferase inhibitors final manuscript dose-ranging pharmacodynamic study unchanged apoptotic index ras proto-oncogene activation treated mcf-7/her2-18 tumours mutated k-ras protein transferase blocks cell lines considered skov3 cell tumours farnesyl tranferase inhibition mcf-7/her2-18 cells treated author correspondence mcf-7/her2-18 control tumours mcf-7 cell line mcf-7/her2-18 tumours grown 1465-542x contact activated k-ras k-rasbv12 proteins wild-type ras [11–13] wild-type ras

Schema {🗺️}

WebPage:
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         headline:Effect of a farnesyl transferase inhibitor (R115777) on ductal carcinoma in situ of the breast in a human xenograft model and on breast and ovarian cancer cell growth in vitro and in vivo
         description:The ras pathway is essential for cell growth and proliferation. The effects of R115777, a farnesyl transferase inhibitor, were investigated in cancer cell lines expressing varying levels of growth factor receptors and with differing ras status. Effects on tumour xenografts and human ductal carcinoma in situ (DCIS) of the breast in a xenograft mouse model were also tested. In vitro, the concentrations required to reduce cell numbers by 50% (50% inhibitory concentration) were established (MDA-MB231, MCF-7, MCF-7/HER2-18, BT-474, SK-BR3 and SKOV3). Human DCIS was implanted in nude mice or, in separate experiments, cultured cells were injected (MDA-MB231, MCF-7/HER2-18, SKOV3) and allowed to form tumours. Proliferation and apoptosis were determined by immunohistochemistry in xenografts and cell tumours. The 50% inhibitory concentrations varied a hundred-fold, from 39 nmol/l (± 26 nmol/l) for SKBR3 to 5.9 μmol/l(± 0.8 μmol/l) for MDA-MB231. In MCF-7/HER2-18 and SKOV3 cells the levels of tumour growth inhibition were approximately 85% and 40%, respectively. There was a significant decrease in the cell turnover index (CTI; proliferation/apoptosis). In MDA-MB 231 with activated k-ras no inhibition was observed. In treated DCIS xenografts proliferation decreased and apoptosis increased. The CTI ratio between the start and 1 and 2 weeks of treatment were 1.99 and 1.50, respectively, for controls and 0.85 (P = 0.005) and 0.75 (P = 0.08) for treated xenografts. Treatment with the farnesyl transferase inhibitor reduced cell growth in vitro and cell tumour growth in vivo. In DCIS treatment resulted in a reduced CTI. R115777 is a promising treatment for breast cancer but the relation between effect and growth factor receptor and ras status has to be established.
         datePublished:2006-04-12T00:00:00Z
         dateModified:2006-04-12T00:00:00Z
         pageStart:1
         pageEnd:10
         license:http://creativecommons.org/licenses/by/2.0/
         sameAs:https://doi.org/10.1186/bcr1395
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            SKOV3 Cell
            Farnesyl Transferase Inhibition
            R115777 Treatment
            Final Tumour Volume
            Cancer Research
            Oncology
            Surgical Oncology
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                        name:Department of Medical Statistics, South Manchester University Hospital, Manchester, UK
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                     address:
                        name:Department of Pathology, South Manchester University Hospital, Manchester, UK
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ScholarlyArticle:
      headline:Effect of a farnesyl transferase inhibitor (R115777) on ductal carcinoma in situ of the breast in a human xenograft model and on breast and ovarian cancer cell growth in vitro and in vivo
      description:The ras pathway is essential for cell growth and proliferation. The effects of R115777, a farnesyl transferase inhibitor, were investigated in cancer cell lines expressing varying levels of growth factor receptors and with differing ras status. Effects on tumour xenografts and human ductal carcinoma in situ (DCIS) of the breast in a xenograft mouse model were also tested. In vitro, the concentrations required to reduce cell numbers by 50% (50% inhibitory concentration) were established (MDA-MB231, MCF-7, MCF-7/HER2-18, BT-474, SK-BR3 and SKOV3). Human DCIS was implanted in nude mice or, in separate experiments, cultured cells were injected (MDA-MB231, MCF-7/HER2-18, SKOV3) and allowed to form tumours. Proliferation and apoptosis were determined by immunohistochemistry in xenografts and cell tumours. The 50% inhibitory concentrations varied a hundred-fold, from 39 nmol/l (± 26 nmol/l) for SKBR3 to 5.9 μmol/l(± 0.8 μmol/l) for MDA-MB231. In MCF-7/HER2-18 and SKOV3 cells the levels of tumour growth inhibition were approximately 85% and 40%, respectively. There was a significant decrease in the cell turnover index (CTI; proliferation/apoptosis). In MDA-MB 231 with activated k-ras no inhibition was observed. In treated DCIS xenografts proliferation decreased and apoptosis increased. The CTI ratio between the start and 1 and 2 weeks of treatment were 1.99 and 1.50, respectively, for controls and 0.85 (P = 0.005) and 0.75 (P = 0.08) for treated xenografts. Treatment with the farnesyl transferase inhibitor reduced cell growth in vitro and cell tumour growth in vivo. In DCIS treatment resulted in a reduced CTI. R115777 is a promising treatment for breast cancer but the relation between effect and growth factor receptor and ras status has to be established.
      datePublished:2006-04-12T00:00:00Z
      dateModified:2006-04-12T00:00:00Z
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      pageEnd:10
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      sameAs:https://doi.org/10.1186/bcr1395
      keywords:
         Apoptotic Index
         SKOV3 Cell
         Farnesyl Transferase Inhibition
         R115777 Treatment
         Final Tumour Volume
         Cancer Research
         Oncology
         Surgical Oncology
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         name:BioMed Central
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            type:ImageObject
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      author:
            name:Fredrik Wärnberg
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                     type:PostalAddress
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            type:Person
            name:Julie Morris
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                  address:
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         name:Breast Biology Group, Christie Hospital NHS Trust, Manchester, UK
         type:PostalAddress
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         name:Department of Medical Statistics, South Manchester University Hospital, Manchester, UK
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               type:PostalAddress
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            name:Breast Biology Group, Christie Hospital NHS Trust
            address:
               name:Breast Biology Group, Christie Hospital NHS Trust, Manchester, UK
               type:PostalAddress
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      name:Elizabeth Anderson
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            name:Breast Biology Group, Christie Hospital NHS Trust
            address:
               name:Breast Biology Group, Christie Hospital NHS Trust, Manchester, UK
               type:PostalAddress
            type:Organization
      name:Fiona Knox
      affiliation:
            name:South Manchester University Hospital
            address:
               name:Department of Surgery, South Manchester University Hospital, Manchester, UK
               type:PostalAddress
            type:Organization
      name:Robert B Clarke
      affiliation:
            name:Breast Biology Group, Christie Hospital NHS Trust
            address:
               name:Breast Biology Group, Christie Hospital NHS Trust, Manchester, UK
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            name:South Manchester University Hospital
            address:
               name:Department of Pathology, South Manchester University Hospital, Manchester, UK
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Breast Biology Group, Christie Hospital NHS Trust, Manchester, UK
      name:Department of Pathology, South Manchester University Hospital, Manchester, UK
      name:Breast Biology Group, Christie Hospital NHS Trust, Manchester, UK
      name:Breast Biology Group, Christie Hospital NHS Trust, Manchester, UK
      name:Department of Surgery, South Manchester University Hospital, Manchester, UK
      name:Breast Biology Group, Christie Hospital NHS Trust, Manchester, UK
      name:Department of Medical Statistics, South Manchester University Hospital, Manchester, UK
      name:Department of Pathology, South Manchester University Hospital, Manchester, UK

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