Sex steroids and breast cancer metastasis
Sex steroids, particularly estrogen and progesterone, promote normal breast tissue growth and differentiation. Prolonged exposure of estrogen and/or progesterone is considered a risk factor for breast cancer carcinogenesis, and the effects of sex steroids on breast cancer metastasis are controversia...
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E-Artikel |
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| Erschienen: |
Walter de Gruyter ; 2010 |
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7 |
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Walter de Gruyter Online Zeitschriften |
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Enthalten in: Hormone molecular biology and clinical investigation - Berlin : de Gruyter, 2010, 3(2010), 2 vom: 9. Dez., Seite 383-389 |
| Übergeordnetes Werk: |
volume:3 ; year:2010 ; number:2 ; day:9 ; month:12 ; pages:383-389 ; extent:7 |
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10.1515/HMBCI.2010.058 |
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| 520 | |a Sex steroids, particularly estrogen and progesterone, promote normal breast tissue growth and differentiation. Prolonged exposure of estrogen and/or progesterone is considered a risk factor for breast cancer carcinogenesis, and the effects of sex steroids on breast cancer metastasis are controversial. Emerging evidence indicates that sex steroids regulate breast cancer metastatic processes via nongenomic and genomic mechanisms. Through the regulation of actin-binding proteins estrogen and progesterone rapidly provoke actin cytoskeleton reorganization in breast cancer cells, leading to formation of membrane structures facilitating breast cancer cell migration and invasion. In addition, steroid receptors interact and trans-activate receptor tyrosine kinases (including epidermal growth factor receptor and insulin-like growth factor receptor), resulting in growth factor-like effects that promote cancer cell invasive behavior. Moreover, sex steroids regulate the expression of metastasis-associated molecules, such as E-cadherin, matrix metalloproteinases, growth factors, chemokines and their receptors, leading to epithelial-to-mesenchymal-like transition. However, there is also evidence that sex steroids and their receptors protect against breast cancer cell invasiveness through distinct mechanisms. Here, we present an overview of the currently identified actions of sex steroids on breast cancer metastasis and their potential clinical implications. | ||
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10.1515/HMBCI.2010.058 doi artikel_Grundlieferung.pp (DE-627)NLEJ246930438 DE-627 ger DE-627 rakwb Sex steroids and breast cancer metastasis Walter de Gruyter 2010 7 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Sex steroids, particularly estrogen and progesterone, promote normal breast tissue growth and differentiation. Prolonged exposure of estrogen and/or progesterone is considered a risk factor for breast cancer carcinogenesis, and the effects of sex steroids on breast cancer metastasis are controversial. Emerging evidence indicates that sex steroids regulate breast cancer metastatic processes via nongenomic and genomic mechanisms. Through the regulation of actin-binding proteins estrogen and progesterone rapidly provoke actin cytoskeleton reorganization in breast cancer cells, leading to formation of membrane structures facilitating breast cancer cell migration and invasion. In addition, steroid receptors interact and trans-activate receptor tyrosine kinases (including epidermal growth factor receptor and insulin-like growth factor receptor), resulting in growth factor-like effects that promote cancer cell invasive behavior. Moreover, sex steroids regulate the expression of metastasis-associated molecules, such as E-cadherin, matrix metalloproteinases, growth factors, chemokines and their receptors, leading to epithelial-to-mesenchymal-like transition. However, there is also evidence that sex steroids and their receptors protect against breast cancer cell invasiveness through distinct mechanisms. Here, we present an overview of the currently identified actions of sex steroids on breast cancer metastasis and their potential clinical implications. Walter de Gruyter Online Zeitschriften breast cancer metastasis sex steroids sex steroid receptors Fu, Xiao-Dong oth Russo, Eleonora oth Zullino, Sara oth Genazzani, Andrea R. oth Simoncini, Tommaso oth Enthalten in Hormone molecular biology and clinical investigation Berlin : de Gruyter, 2010 3(2010), 2 vom: 9. Dez., Seite 383-389 (DE-627)NLEJ248235699 (DE-600)2536635-X 1868-1891 nnns volume:3 year:2010 number:2 day:9 month:12 pages:383-389 extent:7 https://doi.org/10.1515/HMBCI.2010.058 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 3 2010 2 9 12 383-389 7 |
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10.1515/HMBCI.2010.058 doi artikel_Grundlieferung.pp (DE-627)NLEJ246930438 DE-627 ger DE-627 rakwb Sex steroids and breast cancer metastasis Walter de Gruyter 2010 7 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Sex steroids, particularly estrogen and progesterone, promote normal breast tissue growth and differentiation. Prolonged exposure of estrogen and/or progesterone is considered a risk factor for breast cancer carcinogenesis, and the effects of sex steroids on breast cancer metastasis are controversial. Emerging evidence indicates that sex steroids regulate breast cancer metastatic processes via nongenomic and genomic mechanisms. Through the regulation of actin-binding proteins estrogen and progesterone rapidly provoke actin cytoskeleton reorganization in breast cancer cells, leading to formation of membrane structures facilitating breast cancer cell migration and invasion. In addition, steroid receptors interact and trans-activate receptor tyrosine kinases (including epidermal growth factor receptor and insulin-like growth factor receptor), resulting in growth factor-like effects that promote cancer cell invasive behavior. Moreover, sex steroids regulate the expression of metastasis-associated molecules, such as E-cadherin, matrix metalloproteinases, growth factors, chemokines and their receptors, leading to epithelial-to-mesenchymal-like transition. However, there is also evidence that sex steroids and their receptors protect against breast cancer cell invasiveness through distinct mechanisms. Here, we present an overview of the currently identified actions of sex steroids on breast cancer metastasis and their potential clinical implications. Walter de Gruyter Online Zeitschriften breast cancer metastasis sex steroids sex steroid receptors Fu, Xiao-Dong oth Russo, Eleonora oth Zullino, Sara oth Genazzani, Andrea R. oth Simoncini, Tommaso oth Enthalten in Hormone molecular biology and clinical investigation Berlin : de Gruyter, 2010 3(2010), 2 vom: 9. Dez., Seite 383-389 (DE-627)NLEJ248235699 (DE-600)2536635-X 1868-1891 nnns volume:3 year:2010 number:2 day:9 month:12 pages:383-389 extent:7 https://doi.org/10.1515/HMBCI.2010.058 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 3 2010 2 9 12 383-389 7 |
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10.1515/HMBCI.2010.058 doi artikel_Grundlieferung.pp (DE-627)NLEJ246930438 DE-627 ger DE-627 rakwb Sex steroids and breast cancer metastasis Walter de Gruyter 2010 7 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Sex steroids, particularly estrogen and progesterone, promote normal breast tissue growth and differentiation. Prolonged exposure of estrogen and/or progesterone is considered a risk factor for breast cancer carcinogenesis, and the effects of sex steroids on breast cancer metastasis are controversial. Emerging evidence indicates that sex steroids regulate breast cancer metastatic processes via nongenomic and genomic mechanisms. Through the regulation of actin-binding proteins estrogen and progesterone rapidly provoke actin cytoskeleton reorganization in breast cancer cells, leading to formation of membrane structures facilitating breast cancer cell migration and invasion. In addition, steroid receptors interact and trans-activate receptor tyrosine kinases (including epidermal growth factor receptor and insulin-like growth factor receptor), resulting in growth factor-like effects that promote cancer cell invasive behavior. Moreover, sex steroids regulate the expression of metastasis-associated molecules, such as E-cadherin, matrix metalloproteinases, growth factors, chemokines and their receptors, leading to epithelial-to-mesenchymal-like transition. However, there is also evidence that sex steroids and their receptors protect against breast cancer cell invasiveness through distinct mechanisms. Here, we present an overview of the currently identified actions of sex steroids on breast cancer metastasis and their potential clinical implications. Walter de Gruyter Online Zeitschriften breast cancer metastasis sex steroids sex steroid receptors Fu, Xiao-Dong oth Russo, Eleonora oth Zullino, Sara oth Genazzani, Andrea R. oth Simoncini, Tommaso oth Enthalten in Hormone molecular biology and clinical investigation Berlin : de Gruyter, 2010 3(2010), 2 vom: 9. Dez., Seite 383-389 (DE-627)NLEJ248235699 (DE-600)2536635-X 1868-1891 nnns volume:3 year:2010 number:2 day:9 month:12 pages:383-389 extent:7 https://doi.org/10.1515/HMBCI.2010.058 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 3 2010 2 9 12 383-389 7 |
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10.1515/HMBCI.2010.058 doi artikel_Grundlieferung.pp (DE-627)NLEJ246930438 DE-627 ger DE-627 rakwb Sex steroids and breast cancer metastasis Walter de Gruyter 2010 7 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Sex steroids, particularly estrogen and progesterone, promote normal breast tissue growth and differentiation. Prolonged exposure of estrogen and/or progesterone is considered a risk factor for breast cancer carcinogenesis, and the effects of sex steroids on breast cancer metastasis are controversial. Emerging evidence indicates that sex steroids regulate breast cancer metastatic processes via nongenomic and genomic mechanisms. Through the regulation of actin-binding proteins estrogen and progesterone rapidly provoke actin cytoskeleton reorganization in breast cancer cells, leading to formation of membrane structures facilitating breast cancer cell migration and invasion. In addition, steroid receptors interact and trans-activate receptor tyrosine kinases (including epidermal growth factor receptor and insulin-like growth factor receptor), resulting in growth factor-like effects that promote cancer cell invasive behavior. Moreover, sex steroids regulate the expression of metastasis-associated molecules, such as E-cadherin, matrix metalloproteinases, growth factors, chemokines and their receptors, leading to epithelial-to-mesenchymal-like transition. However, there is also evidence that sex steroids and their receptors protect against breast cancer cell invasiveness through distinct mechanisms. Here, we present an overview of the currently identified actions of sex steroids on breast cancer metastasis and their potential clinical implications. Walter de Gruyter Online Zeitschriften breast cancer metastasis sex steroids sex steroid receptors Fu, Xiao-Dong oth Russo, Eleonora oth Zullino, Sara oth Genazzani, Andrea R. oth Simoncini, Tommaso oth Enthalten in Hormone molecular biology and clinical investigation Berlin : de Gruyter, 2010 3(2010), 2 vom: 9. Dez., Seite 383-389 (DE-627)NLEJ248235699 (DE-600)2536635-X 1868-1891 nnns volume:3 year:2010 number:2 day:9 month:12 pages:383-389 extent:7 https://doi.org/10.1515/HMBCI.2010.058 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 3 2010 2 9 12 383-389 7 |
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10.1515/HMBCI.2010.058 doi artikel_Grundlieferung.pp (DE-627)NLEJ246930438 DE-627 ger DE-627 rakwb Sex steroids and breast cancer metastasis Walter de Gruyter 2010 7 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Sex steroids, particularly estrogen and progesterone, promote normal breast tissue growth and differentiation. Prolonged exposure of estrogen and/or progesterone is considered a risk factor for breast cancer carcinogenesis, and the effects of sex steroids on breast cancer metastasis are controversial. Emerging evidence indicates that sex steroids regulate breast cancer metastatic processes via nongenomic and genomic mechanisms. Through the regulation of actin-binding proteins estrogen and progesterone rapidly provoke actin cytoskeleton reorganization in breast cancer cells, leading to formation of membrane structures facilitating breast cancer cell migration and invasion. In addition, steroid receptors interact and trans-activate receptor tyrosine kinases (including epidermal growth factor receptor and insulin-like growth factor receptor), resulting in growth factor-like effects that promote cancer cell invasive behavior. Moreover, sex steroids regulate the expression of metastasis-associated molecules, such as E-cadherin, matrix metalloproteinases, growth factors, chemokines and their receptors, leading to epithelial-to-mesenchymal-like transition. However, there is also evidence that sex steroids and their receptors protect against breast cancer cell invasiveness through distinct mechanisms. Here, we present an overview of the currently identified actions of sex steroids on breast cancer metastasis and their potential clinical implications. Walter de Gruyter Online Zeitschriften breast cancer metastasis sex steroids sex steroid receptors Fu, Xiao-Dong oth Russo, Eleonora oth Zullino, Sara oth Genazzani, Andrea R. oth Simoncini, Tommaso oth Enthalten in Hormone molecular biology and clinical investigation Berlin : de Gruyter, 2010 3(2010), 2 vom: 9. Dez., Seite 383-389 (DE-627)NLEJ248235699 (DE-600)2536635-X 1868-1891 nnns volume:3 year:2010 number:2 day:9 month:12 pages:383-389 extent:7 https://doi.org/10.1515/HMBCI.2010.058 Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-DGR GBV_NL_ARTICLE AR 3 2010 2 9 12 383-389 7 |
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Sex steroids, particularly estrogen and progesterone, promote normal breast tissue growth and differentiation. Prolonged exposure of estrogen and/or progesterone is considered a risk factor for breast cancer carcinogenesis, and the effects of sex steroids on breast cancer metastasis are controversial. Emerging evidence indicates that sex steroids regulate breast cancer metastatic processes via nongenomic and genomic mechanisms. Through the regulation of actin-binding proteins estrogen and progesterone rapidly provoke actin cytoskeleton reorganization in breast cancer cells, leading to formation of membrane structures facilitating breast cancer cell migration and invasion. In addition, steroid receptors interact and trans-activate receptor tyrosine kinases (including epidermal growth factor receptor and insulin-like growth factor receptor), resulting in growth factor-like effects that promote cancer cell invasive behavior. Moreover, sex steroids regulate the expression of metastasis-associated molecules, such as E-cadherin, matrix metalloproteinases, growth factors, chemokines and their receptors, leading to epithelial-to-mesenchymal-like transition. However, there is also evidence that sex steroids and their receptors protect against breast cancer cell invasiveness through distinct mechanisms. Here, we present an overview of the currently identified actions of sex steroids on breast cancer metastasis and their potential clinical implications. |
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Sex steroids, particularly estrogen and progesterone, promote normal breast tissue growth and differentiation. Prolonged exposure of estrogen and/or progesterone is considered a risk factor for breast cancer carcinogenesis, and the effects of sex steroids on breast cancer metastasis are controversial. Emerging evidence indicates that sex steroids regulate breast cancer metastatic processes via nongenomic and genomic mechanisms. Through the regulation of actin-binding proteins estrogen and progesterone rapidly provoke actin cytoskeleton reorganization in breast cancer cells, leading to formation of membrane structures facilitating breast cancer cell migration and invasion. In addition, steroid receptors interact and trans-activate receptor tyrosine kinases (including epidermal growth factor receptor and insulin-like growth factor receptor), resulting in growth factor-like effects that promote cancer cell invasive behavior. Moreover, sex steroids regulate the expression of metastasis-associated molecules, such as E-cadherin, matrix metalloproteinases, growth factors, chemokines and their receptors, leading to epithelial-to-mesenchymal-like transition. However, there is also evidence that sex steroids and their receptors protect against breast cancer cell invasiveness through distinct mechanisms. Here, we present an overview of the currently identified actions of sex steroids on breast cancer metastasis and their potential clinical implications. |
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Sex steroids, particularly estrogen and progesterone, promote normal breast tissue growth and differentiation. Prolonged exposure of estrogen and/or progesterone is considered a risk factor for breast cancer carcinogenesis, and the effects of sex steroids on breast cancer metastasis are controversial. Emerging evidence indicates that sex steroids regulate breast cancer metastatic processes via nongenomic and genomic mechanisms. Through the regulation of actin-binding proteins estrogen and progesterone rapidly provoke actin cytoskeleton reorganization in breast cancer cells, leading to formation of membrane structures facilitating breast cancer cell migration and invasion. In addition, steroid receptors interact and trans-activate receptor tyrosine kinases (including epidermal growth factor receptor and insulin-like growth factor receptor), resulting in growth factor-like effects that promote cancer cell invasive behavior. Moreover, sex steroids regulate the expression of metastasis-associated molecules, such as E-cadherin, matrix metalloproteinases, growth factors, chemokines and their receptors, leading to epithelial-to-mesenchymal-like transition. However, there is also evidence that sex steroids and their receptors protect against breast cancer cell invasiveness through distinct mechanisms. Here, we present an overview of the currently identified actions of sex steroids on breast cancer metastasis and their potential clinical implications. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ246930438</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20220820024941.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">220814s2010 xx |||||o 00| ||und c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1515/HMBCI.2010.058</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">artikel_Grundlieferung.pp</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ246930438</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Sex steroids and breast cancer metastasis</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="b">Walter de Gruyter</subfield><subfield code="c">2010</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">7</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Sex steroids, particularly estrogen and progesterone, promote normal breast tissue growth and differentiation. Prolonged exposure of estrogen and/or progesterone is considered a risk factor for breast cancer carcinogenesis, and the effects of sex steroids on breast cancer metastasis are controversial. Emerging evidence indicates that sex steroids regulate breast cancer metastatic processes via nongenomic and genomic mechanisms. Through the regulation of actin-binding proteins estrogen and progesterone rapidly provoke actin cytoskeleton reorganization in breast cancer cells, leading to formation of membrane structures facilitating breast cancer cell migration and invasion. In addition, steroid receptors interact and trans-activate receptor tyrosine kinases (including epidermal growth factor receptor and insulin-like growth factor receptor), resulting in growth factor-like effects that promote cancer cell invasive behavior. Moreover, sex steroids regulate the expression of metastasis-associated molecules, such as E-cadherin, matrix metalloproteinases, growth factors, chemokines and their receptors, leading to epithelial-to-mesenchymal-like transition. However, there is also evidence that sex steroids and their receptors protect against breast cancer cell invasiveness through distinct mechanisms. 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