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Radial scars of the breast and breast carcinomas have similar alterations in expression of factors involved in vascular stroma formation
We recently reported that radial scars are an independent histologic risk factor for breast cancer. The reason for this association is not known. Given the importance of stromal–epithelial interactions in the pathogenesis of breast cancer, we studied radial scars for the expression of a number of fa...
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Published in: | Human pathology 2002-01, Vol.33 (1), p.29-38 |
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description | We recently reported that radial scars are an independent histologic risk factor for breast cancer. The reason for this association is not known. Given the importance of stromal–epithelial interactions in the pathogenesis of breast cancer, we studied radial scars for the expression of a number of factors known to be involved in the formation of vascular stroma in breast cancer. In situ hybridization was performed on formalin-fixed paraffin sections using 35S-labeled riboprobes for collagen type 1, total fibronectin, extra domain A (ED-A)+ fibronectin, thrombospondin 1, vascular permeability factor (VPF)/vascular endothelial growth factor (VEGF), and one of its endothelial receptors, kinase insert domain–containing receptor (KDR) (vascular endothelial growth factor receptor [VEGFR-2]). Expression levels in radial scars (9 cases) were compared with those in normal breast tissue (15 cases) and infiltrating ductal breast carcinoma (4 cases). Factor VIII–related antigen immunostaining was used to define the distribution of microvessels in radial scars, carcinoma, and normal breast tissue. Compared with normal breast tissue, the radial scars showed focally increased numbers of blood vessels and focally increased expression of messenger RNA (mRNA) for collagen type 1, total fibronectin, ED-A+ fibronectin, thrombospondin 1, VPF/VEGF, and KDR. This pattern of mRNA overexpression was similar to that seen in the 4 invasive cancers. We conclude that there are similarities between radial scars and invasive breast cancers with regard to the level of mRNA expression for several factors involved in the formation of vascular stroma. These results suggest that a similar disturbance in stromal–epithelial interactions is present in both lesions. HUM PATHOL 33:29-38. Copyright © 2002 by W.B. Saunders Company |
doi_str_mv | 10.1053/hupa.2002.30190 |
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The reason for this association is not known. Given the importance of stromal–epithelial interactions in the pathogenesis of breast cancer, we studied radial scars for the expression of a number of factors known to be involved in the formation of vascular stroma in breast cancer. In situ hybridization was performed on formalin-fixed paraffin sections using 35S-labeled riboprobes for collagen type 1, total fibronectin, extra domain A (ED-A)+ fibronectin, thrombospondin 1, vascular permeability factor (VPF)/vascular endothelial growth factor (VEGF), and one of its endothelial receptors, kinase insert domain–containing receptor (KDR) (vascular endothelial growth factor receptor [VEGFR-2]). Expression levels in radial scars (9 cases) were compared with those in normal breast tissue (15 cases) and infiltrating ductal breast carcinoma (4 cases). Factor VIII–related antigen immunostaining was used to define the distribution of microvessels in radial scars, carcinoma, and normal breast tissue. Compared with normal breast tissue, the radial scars showed focally increased numbers of blood vessels and focally increased expression of messenger RNA (mRNA) for collagen type 1, total fibronectin, ED-A+ fibronectin, thrombospondin 1, VPF/VEGF, and KDR. This pattern of mRNA overexpression was similar to that seen in the 4 invasive cancers. We conclude that there are similarities between radial scars and invasive breast cancers with regard to the level of mRNA expression for several factors involved in the formation of vascular stroma. These results suggest that a similar disturbance in stromal–epithelial interactions is present in both lesions. HUM PATHOL 33:29-38. Copyright © 2002 by W.B. Saunders Company</description><identifier>ISSN: 0046-8177</identifier><identifier>EISSN: 1532-8392</identifier><identifier>DOI: 10.1053/hupa.2002.30190</identifier><identifier>PMID: 11823971</identifier><identifier>CODEN: HPCQA4</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Aged ; angiogenesis ; benign breast disease ; Biological and medical sciences ; Breast - anatomy & histology ; Breast - blood supply ; Breast - metabolism ; Breast - pathology ; breast cancer ; Breast Neoplasms - blood supply ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Carcinoma, Intraductal, Noninfiltrating - blood supply ; Carcinoma, Intraductal, Noninfiltrating - metabolism ; Carcinoma, Intraductal, Noninfiltrating - secondary ; Cicatrix - metabolism ; Cicatrix - pathology ; Collagen Type I - genetics ; Collagen Type I - metabolism ; Ectodysplasins ; Endothelial Growth Factors - genetics ; Endothelial Growth Factors - metabolism ; Female ; Fibronectins - genetics ; Fibronectins - metabolism ; Gynecology. Andrology. Obstetrics ; Humans ; In Situ Hybridization ; Lymphokines - genetics ; Lymphokines - metabolism ; Mammary gland diseases ; Medical sciences ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Microcirculation - anatomy & histology ; Microcirculation - metabolism ; Microcirculation - pathology ; Middle Aged ; Neovascularization, Pathologic - metabolism ; Neovascularization, Pathologic - pathology ; radial scar ; Receptor Protein-Tyrosine Kinases - genetics ; Receptor Protein-Tyrosine Kinases - metabolism ; Receptors, Growth Factor - genetics ; Receptors, Growth Factor - metabolism ; Receptors, Vascular Endothelial Growth Factor ; RNA - metabolism ; RNA, Neoplasm - analysis ; stroma ; Stromal Cells - metabolism ; Stromal Cells - pathology ; Thrombospondin 1 - genetics ; Thrombospondin 1 - metabolism ; Tumors ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors</subject><ispartof>Human pathology, 2002-01, Vol.33 (1), p.29-38</ispartof><rights>2002 W.B. Saunders Company</rights><rights>2002 INIST-CNRS</rights><rights>Copyright 2002 by W.B. Saunders Company</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c373t-767abb39c9ec58e67241a6af378ff26702fd6212a2d9f6b8c4a97e85946617e23</citedby><cites>FETCH-LOGICAL-c373t-767abb39c9ec58e67241a6af378ff26702fd6212a2d9f6b8c4a97e85946617e23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13467775$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11823971$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jacobs, Timothy W.</creatorcontrib><creatorcontrib>Schnitt, Stuart J.</creatorcontrib><creatorcontrib>Tan, Xiaolian</creatorcontrib><creatorcontrib>Brown, Lawrence F.</creatorcontrib><title>Radial scars of the breast and breast carcinomas have similar alterations in expression of factors involved in vascular stroma formation</title><title>Human pathology</title><addtitle>Hum Pathol</addtitle><description>We recently reported that radial scars are an independent histologic risk factor for breast cancer. The reason for this association is not known. Given the importance of stromal–epithelial interactions in the pathogenesis of breast cancer, we studied radial scars for the expression of a number of factors known to be involved in the formation of vascular stroma in breast cancer. In situ hybridization was performed on formalin-fixed paraffin sections using 35S-labeled riboprobes for collagen type 1, total fibronectin, extra domain A (ED-A)+ fibronectin, thrombospondin 1, vascular permeability factor (VPF)/vascular endothelial growth factor (VEGF), and one of its endothelial receptors, kinase insert domain–containing receptor (KDR) (vascular endothelial growth factor receptor [VEGFR-2]). Expression levels in radial scars (9 cases) were compared with those in normal breast tissue (15 cases) and infiltrating ductal breast carcinoma (4 cases). Factor VIII–related antigen immunostaining was used to define the distribution of microvessels in radial scars, carcinoma, and normal breast tissue. Compared with normal breast tissue, the radial scars showed focally increased numbers of blood vessels and focally increased expression of messenger RNA (mRNA) for collagen type 1, total fibronectin, ED-A+ fibronectin, thrombospondin 1, VPF/VEGF, and KDR. This pattern of mRNA overexpression was similar to that seen in the 4 invasive cancers. We conclude that there are similarities between radial scars and invasive breast cancers with regard to the level of mRNA expression for several factors involved in the formation of vascular stroma. These results suggest that a similar disturbance in stromal–epithelial interactions is present in both lesions. HUM PATHOL 33:29-38. Copyright © 2002 by W.B. Saunders Company</description><subject>Adult</subject><subject>Aged</subject><subject>angiogenesis</subject><subject>benign breast disease</subject><subject>Biological and medical sciences</subject><subject>Breast - anatomy & histology</subject><subject>Breast - blood supply</subject><subject>Breast - metabolism</subject><subject>Breast - pathology</subject><subject>breast cancer</subject><subject>Breast Neoplasms - blood supply</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Carcinoma, Intraductal, Noninfiltrating - blood supply</subject><subject>Carcinoma, Intraductal, Noninfiltrating - metabolism</subject><subject>Carcinoma, Intraductal, Noninfiltrating - secondary</subject><subject>Cicatrix - metabolism</subject><subject>Cicatrix - pathology</subject><subject>Collagen Type I - genetics</subject><subject>Collagen Type I - metabolism</subject><subject>Ectodysplasins</subject><subject>Endothelial Growth Factors - genetics</subject><subject>Endothelial Growth Factors - metabolism</subject><subject>Female</subject><subject>Fibronectins - genetics</subject><subject>Fibronectins - metabolism</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>In Situ Hybridization</subject><subject>Lymphokines - genetics</subject><subject>Lymphokines - metabolism</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Microcirculation - anatomy & histology</subject><subject>Microcirculation - metabolism</subject><subject>Microcirculation - pathology</subject><subject>Middle Aged</subject><subject>Neovascularization, Pathologic - metabolism</subject><subject>Neovascularization, Pathologic - pathology</subject><subject>radial scar</subject><subject>Receptor Protein-Tyrosine Kinases - genetics</subject><subject>Receptor Protein-Tyrosine Kinases - metabolism</subject><subject>Receptors, Growth Factor - genetics</subject><subject>Receptors, Growth Factor - metabolism</subject><subject>Receptors, Vascular Endothelial Growth Factor</subject><subject>RNA - metabolism</subject><subject>RNA, Neoplasm - analysis</subject><subject>stroma</subject><subject>Stromal Cells - metabolism</subject><subject>Stromal Cells - pathology</subject><subject>Thrombospondin 1 - genetics</subject><subject>Thrombospondin 1 - metabolism</subject><subject>Tumors</subject><subject>Vascular Endothelial Growth Factor A</subject><subject>Vascular Endothelial Growth Factors</subject><issn>0046-8177</issn><issn>1532-8392</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNp1kMuO1DAQRS0EYpqBNTvkDezS40diJ0s0Gh7SSEgI1lbFKauNkrhxpSP4Az4bZ7rRrFiVS3XulXUYey3FXopG3xxOR9grIdReC9mJJ2wnG62qVnfqKdsJUZuqldZesRdEP4SQsqmb5-xKylbpzsod-_MVhggjJw-ZeAp8OSDvMwItHObh37NcfZzTBMQPsCKnOMURModxwQxLTDPxOHP8dcxIVNatKoBfUt4OaxpXHDZiBfKnLUlLLnU8pDw95F-yZwFGwleXec2-f7j7dvupuv_y8fPt-_vKa6uXyhoLfa8736FvWjRW1RIMBG3bEJSxQoXBKKlADV0wfetr6Cy2TVcbIy0qfc3enXuPOf08IS1uiuRxHGHGdCJnZS2bUlvAmzPocyLKGNwxxwnybyeF2-S7Tb7b5LsH-SXx5lJ96iccHvmL7QK8vQDFAowhw-wjPXK6NtbapnDdmcMiYo2YHfmIs8chZvSLG1L87yf-ArSFo0k</recordid><startdate>200201</startdate><enddate>200201</enddate><creator>Jacobs, Timothy W.</creator><creator>Schnitt, Stuart J.</creator><creator>Tan, Xiaolian</creator><creator>Brown, Lawrence F.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200201</creationdate><title>Radial scars of the breast and breast carcinomas have similar alterations in expression of factors involved in vascular stroma formation</title><author>Jacobs, Timothy W. ; Schnitt, Stuart J. ; Tan, Xiaolian ; Brown, Lawrence F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c373t-767abb39c9ec58e67241a6af378ff26702fd6212a2d9f6b8c4a97e85946617e23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adult</topic><topic>Aged</topic><topic>angiogenesis</topic><topic>benign breast disease</topic><topic>Biological and medical sciences</topic><topic>Breast - anatomy & histology</topic><topic>Breast - blood supply</topic><topic>Breast - metabolism</topic><topic>Breast - pathology</topic><topic>breast cancer</topic><topic>Breast Neoplasms - blood supply</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Carcinoma, Intraductal, Noninfiltrating - blood supply</topic><topic>Carcinoma, Intraductal, Noninfiltrating - metabolism</topic><topic>Carcinoma, Intraductal, Noninfiltrating - secondary</topic><topic>Cicatrix - metabolism</topic><topic>Cicatrix - pathology</topic><topic>Collagen Type I - genetics</topic><topic>Collagen Type I - metabolism</topic><topic>Ectodysplasins</topic><topic>Endothelial Growth Factors - genetics</topic><topic>Endothelial Growth Factors - metabolism</topic><topic>Female</topic><topic>Fibronectins - genetics</topic><topic>Fibronectins - metabolism</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>In Situ Hybridization</topic><topic>Lymphokines - genetics</topic><topic>Lymphokines - metabolism</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Microcirculation - anatomy & histology</topic><topic>Microcirculation - metabolism</topic><topic>Microcirculation - pathology</topic><topic>Middle Aged</topic><topic>Neovascularization, Pathologic - metabolism</topic><topic>Neovascularization, Pathologic - pathology</topic><topic>radial scar</topic><topic>Receptor Protein-Tyrosine Kinases - genetics</topic><topic>Receptor Protein-Tyrosine Kinases - metabolism</topic><topic>Receptors, Growth Factor - genetics</topic><topic>Receptors, Growth Factor - metabolism</topic><topic>Receptors, Vascular Endothelial Growth Factor</topic><topic>RNA - metabolism</topic><topic>RNA, Neoplasm - analysis</topic><topic>stroma</topic><topic>Stromal Cells - metabolism</topic><topic>Stromal Cells - pathology</topic><topic>Thrombospondin 1 - genetics</topic><topic>Thrombospondin 1 - metabolism</topic><topic>Tumors</topic><topic>Vascular Endothelial Growth Factor A</topic><topic>Vascular Endothelial Growth Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jacobs, Timothy W.</creatorcontrib><creatorcontrib>Schnitt, Stuart J.</creatorcontrib><creatorcontrib>Tan, Xiaolian</creatorcontrib><creatorcontrib>Brown, Lawrence F.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Human pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jacobs, Timothy W.</au><au>Schnitt, Stuart J.</au><au>Tan, Xiaolian</au><au>Brown, Lawrence F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Radial scars of the breast and breast carcinomas have similar alterations in expression of factors involved in vascular stroma formation</atitle><jtitle>Human pathology</jtitle><addtitle>Hum Pathol</addtitle><date>2002-01</date><risdate>2002</risdate><volume>33</volume><issue>1</issue><spage>29</spage><epage>38</epage><pages>29-38</pages><issn>0046-8177</issn><eissn>1532-8392</eissn><coden>HPCQA4</coden><abstract>We recently reported that radial scars are an independent histologic risk factor for breast cancer. The reason for this association is not known. Given the importance of stromal–epithelial interactions in the pathogenesis of breast cancer, we studied radial scars for the expression of a number of factors known to be involved in the formation of vascular stroma in breast cancer. In situ hybridization was performed on formalin-fixed paraffin sections using 35S-labeled riboprobes for collagen type 1, total fibronectin, extra domain A (ED-A)+ fibronectin, thrombospondin 1, vascular permeability factor (VPF)/vascular endothelial growth factor (VEGF), and one of its endothelial receptors, kinase insert domain–containing receptor (KDR) (vascular endothelial growth factor receptor [VEGFR-2]). Expression levels in radial scars (9 cases) were compared with those in normal breast tissue (15 cases) and infiltrating ductal breast carcinoma (4 cases). Factor VIII–related antigen immunostaining was used to define the distribution of microvessels in radial scars, carcinoma, and normal breast tissue. Compared with normal breast tissue, the radial scars showed focally increased numbers of blood vessels and focally increased expression of messenger RNA (mRNA) for collagen type 1, total fibronectin, ED-A+ fibronectin, thrombospondin 1, VPF/VEGF, and KDR. This pattern of mRNA overexpression was similar to that seen in the 4 invasive cancers. We conclude that there are similarities between radial scars and invasive breast cancers with regard to the level of mRNA expression for several factors involved in the formation of vascular stroma. These results suggest that a similar disturbance in stromal–epithelial interactions is present in both lesions. HUM PATHOL 33:29-38. Copyright © 2002 by W.B. Saunders Company</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>11823971</pmid><doi>10.1053/hupa.2002.30190</doi><tpages>10</tpages></addata></record> |
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subjects | Adult Aged angiogenesis benign breast disease Biological and medical sciences Breast - anatomy & histology Breast - blood supply Breast - metabolism Breast - pathology breast cancer Breast Neoplasms - blood supply Breast Neoplasms - metabolism Breast Neoplasms - pathology Carcinoma, Intraductal, Noninfiltrating - blood supply Carcinoma, Intraductal, Noninfiltrating - metabolism Carcinoma, Intraductal, Noninfiltrating - secondary Cicatrix - metabolism Cicatrix - pathology Collagen Type I - genetics Collagen Type I - metabolism Ectodysplasins Endothelial Growth Factors - genetics Endothelial Growth Factors - metabolism Female Fibronectins - genetics Fibronectins - metabolism Gynecology. Andrology. Obstetrics Humans In Situ Hybridization Lymphokines - genetics Lymphokines - metabolism Mammary gland diseases Medical sciences Membrane Proteins - genetics Membrane Proteins - metabolism Microcirculation - anatomy & histology Microcirculation - metabolism Microcirculation - pathology Middle Aged Neovascularization, Pathologic - metabolism Neovascularization, Pathologic - pathology radial scar Receptor Protein-Tyrosine Kinases - genetics Receptor Protein-Tyrosine Kinases - metabolism Receptors, Growth Factor - genetics Receptors, Growth Factor - metabolism Receptors, Vascular Endothelial Growth Factor RNA - metabolism RNA, Neoplasm - analysis stroma Stromal Cells - metabolism Stromal Cells - pathology Thrombospondin 1 - genetics Thrombospondin 1 - metabolism Tumors Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factors |
title | Radial scars of the breast and breast carcinomas have similar alterations in expression of factors involved in vascular stroma formation |
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