Loss of expression of chromosome 16q genes DPEP1 and CTCF in lobular carcinoma in situ of the breast
Background Loss of the chromosomal material at 16q is the most frequent genetic event in invasive and in situ (LCIS) lobular carcinoma of the breast. However, the smallest region of overlap at 16q is not restricted to just the CDH1 locus harbouring E-cadherin, suggesting that neighbouring genes migh...
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description | Background Loss of the chromosomal material at 16q is the most frequent genetic event in invasive and in situ (LCIS) lobular carcinoma of the breast. However, the smallest region of overlap at 16q is not restricted to just the CDH1 locus harbouring E-cadherin, suggesting that neighbouring genes might be involved in the development and progression of these tumours. Potential novel tumour suppressor genes (TSG) at 16q include CCCTC-binding factor (CTCF), Decreased Expression in Renal and Prostate Cancer (DERPC) and Dipeptidase 1 (DPEP1). The aim of this study is to assess the expression of these genes in LCIS and compare them with normal breast, using CDH1 as a control, in order to evaluate their role as TSGs. Methods Cells from LCIS cases and normal breast lobules were microdissected and expression of target genes were quantified using real-time PCR. In addition, immunohistochemistry (IHC) for E-cadherin and CTCF was performed on paraffin processed LCIS (n = 49) and normal breast cases. Results All LCIS showed negative expression of E-cadherin. Similar to CDH1, CTCF and DPEP1 gene expression was significantly lower in LCIS cases compared with normal cases (P < 0.05). CTCF IHC expression showed significant reduction in LCIS compared to normal parenchymal cells. However, there was no difference in expression of DERPC between LCIS and normal breast tissue. Conclusions In addition to CDH1, loss of CTCF and DPEP1 gene expression suggest they are possible TSG in breast cancer and may, similar to CDH1, be potentially utilised as markers of predisposition of women diagnosed with LCIS. |
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Claire ; Powe, Desmond G ; Ellis, Ian O</creator><creatorcontrib>Green, Andrew R ; Krivinskas, Sophie ; Young, Peter ; Rakha, Emad A ; Paish, E. Claire ; Powe, Desmond G ; Ellis, Ian O</creatorcontrib><description>Background Loss of the chromosomal material at 16q is the most frequent genetic event in invasive and in situ (LCIS) lobular carcinoma of the breast. However, the smallest region of overlap at 16q is not restricted to just the CDH1 locus harbouring E-cadherin, suggesting that neighbouring genes might be involved in the development and progression of these tumours. Potential novel tumour suppressor genes (TSG) at 16q include CCCTC-binding factor (CTCF), Decreased Expression in Renal and Prostate Cancer (DERPC) and Dipeptidase 1 (DPEP1). The aim of this study is to assess the expression of these genes in LCIS and compare them with normal breast, using CDH1 as a control, in order to evaluate their role as TSGs. Methods Cells from LCIS cases and normal breast lobules were microdissected and expression of target genes were quantified using real-time PCR. In addition, immunohistochemistry (IHC) for E-cadherin and CTCF was performed on paraffin processed LCIS (n = 49) and normal breast cases. Results All LCIS showed negative expression of E-cadherin. Similar to CDH1, CTCF and DPEP1 gene expression was significantly lower in LCIS cases compared with normal cases (P < 0.05). CTCF IHC expression showed significant reduction in LCIS compared to normal parenchymal cells. However, there was no difference in expression of DERPC between LCIS and normal breast tissue. Conclusions In addition to CDH1, loss of CTCF and DPEP1 gene expression suggest they are possible TSG in breast cancer and may, similar to CDH1, be potentially utilised as markers of predisposition of women diagnosed with LCIS.</description><identifier>ISSN: 0167-6806</identifier><identifier>EISSN: 1573-7217</identifier><identifier>DOI: 10.1007/s10549-008-9905-8</identifier><identifier>PMID: 18213475</identifier><identifier>CODEN: BCTRD6</identifier><language>eng</language><publisher>Boston: Boston : Springer US</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Breast cancer ; Breast Neoplasms - genetics ; Cancer research ; Cancer therapies ; Carcinoma in Situ - genetics ; Carcinoma, Lobular - genetics ; CCCTC-Binding Factor ; Chromosome Deletion ; Chromosome Mapping ; Chromosomes, Human, Pair 16 ; Comparative studies ; DNA Primers ; DNA-Binding Proteins - genetics ; Female ; Gene Expression Regulation, Neoplastic ; Genetics ; Gynecology. Andrology. Obstetrics ; Humans ; Immunohistochemistry ; Mammary gland diseases ; Medical sciences ; Medicine ; Medicine & Public Health ; Middle Aged ; Oligonucleotide Array Sequence Analysis ; Oncology ; Preclinical Study ; Repressor Proteins - genetics ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Neoplasm - genetics ; RNA, Neoplasm - isolation & purification ; RNA, Ribosomal, 18S - genetics ; Tumors</subject><ispartof>Breast cancer research and treatment, 2009-01, Vol.113 (1), p.59-66</ispartof><rights>Springer Science+Business Media, LLC. 2008</rights><rights>2009 INIST-CNRS</rights><rights>Springer Science+Business Media, LLC. 2009</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-e75452e9874e7002699fda22ae3c3b5cc4a1ffd46c8813688d956de099149b4a3</citedby><cites>FETCH-LOGICAL-c488t-e75452e9874e7002699fda22ae3c3b5cc4a1ffd46c8813688d956de099149b4a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10549-008-9905-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10549-008-9905-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,778,782,883,27907,27908,41471,42540,51302</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21190292$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18213475$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00478302$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Green, Andrew R</creatorcontrib><creatorcontrib>Krivinskas, Sophie</creatorcontrib><creatorcontrib>Young, Peter</creatorcontrib><creatorcontrib>Rakha, Emad A</creatorcontrib><creatorcontrib>Paish, E. Claire</creatorcontrib><creatorcontrib>Powe, Desmond G</creatorcontrib><creatorcontrib>Ellis, Ian O</creatorcontrib><title>Loss of expression of chromosome 16q genes DPEP1 and CTCF in lobular carcinoma in situ of the breast</title><title>Breast cancer research and treatment</title><addtitle>Breast Cancer Res Treat</addtitle><addtitle>Breast Cancer Res Treat</addtitle><description>Background Loss of the chromosomal material at 16q is the most frequent genetic event in invasive and in situ (LCIS) lobular carcinoma of the breast. However, the smallest region of overlap at 16q is not restricted to just the CDH1 locus harbouring E-cadherin, suggesting that neighbouring genes might be involved in the development and progression of these tumours. Potential novel tumour suppressor genes (TSG) at 16q include CCCTC-binding factor (CTCF), Decreased Expression in Renal and Prostate Cancer (DERPC) and Dipeptidase 1 (DPEP1). The aim of this study is to assess the expression of these genes in LCIS and compare them with normal breast, using CDH1 as a control, in order to evaluate their role as TSGs. Methods Cells from LCIS cases and normal breast lobules were microdissected and expression of target genes were quantified using real-time PCR. In addition, immunohistochemistry (IHC) for E-cadherin and CTCF was performed on paraffin processed LCIS (n = 49) and normal breast cases. Results All LCIS showed negative expression of E-cadherin. Similar to CDH1, CTCF and DPEP1 gene expression was significantly lower in LCIS cases compared with normal cases (P < 0.05). CTCF IHC expression showed significant reduction in LCIS compared to normal parenchymal cells. However, there was no difference in expression of DERPC between LCIS and normal breast tissue. Conclusions In addition to CDH1, loss of CTCF and DPEP1 gene expression suggest they are possible TSG in breast cancer and may, similar to CDH1, be potentially utilised as markers of predisposition of women diagnosed with LCIS.</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Cancer research</subject><subject>Cancer therapies</subject><subject>Carcinoma in Situ - genetics</subject><subject>Carcinoma, Lobular - genetics</subject><subject>CCCTC-Binding Factor</subject><subject>Chromosome Deletion</subject><subject>Chromosome Mapping</subject><subject>Chromosomes, Human, Pair 16</subject><subject>Comparative studies</subject><subject>DNA Primers</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetics</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Oncology</subject><subject>Preclinical Study</subject><subject>Repressor Proteins - genetics</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Neoplasm - genetics</subject><subject>RNA, Neoplasm - isolation & purification</subject><subject>RNA, Ribosomal, 18S - genetics</subject><subject>Tumors</subject><issn>0167-6806</issn><issn>1573-7217</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkktr3DAUhUVpaaZpf0A3rSi00IXbq4f1WIZJ0gQGGmiyFrIszzjY1kSyS_LvI-MhgS6aldDVd4_O1RFCHwn8IADyZyJQcl0AqEJrKAv1Cq1IKVkhKZGv0QqIkIVQII7Qu5RuAUBL0G_REVGUMC7LFao3ISUcGuzv99Gn1IZh3rldDH1IofeYiDu89YNP-PTq7IpgO9R4fb0-x-2Au1BNnY3Y2ejaIfR2LqZ2nGaNcedxFb1N43v0prFd8h8O6zG6OT-7Xl8Um9-_Ltcnm8JxpcbCy5KX1GsluZcAVGjd1JZS65ljVekct6Rpai6cUoQJpWpditqD1oTrilt2jL4vujvbmX1sexsfTLCtuTjZmLkGwKViQP-SzH5b2H0Md5NPo-nb5HzX2cGHKRkhJOdZ-UWQgmSMkhn88g94G6Y45IENJZRLSZXMEFkgF_PDR988-SRg5lDNEmq2qswcqlG559NBeKp6Xz93HFLMwNcDYJOzXRPt4Nr0xGVzGqimmaMLl_LRsPXx2eH_bv-8NDU2GLuNWfjmDwXCIH81DnnwRwWWvsw</recordid><startdate>20090101</startdate><enddate>20090101</enddate><creator>Green, Andrew R</creator><creator>Krivinskas, Sophie</creator><creator>Young, Peter</creator><creator>Rakha, Emad A</creator><creator>Paish, E. Claire</creator><creator>Powe, Desmond G</creator><creator>Ellis, Ian O</creator><general>Boston : Springer US</general><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><general>Springer Verlag</general><scope>FBQ</scope><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>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope></search><sort><creationdate>20090101</creationdate><title>Loss of expression of chromosome 16q genes DPEP1 and CTCF in lobular carcinoma in situ of the breast</title><author>Green, Andrew R ; Krivinskas, Sophie ; Young, Peter ; Rakha, Emad A ; Paish, E. Claire ; Powe, Desmond G ; Ellis, Ian O</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-e75452e9874e7002699fda22ae3c3b5cc4a1ffd46c8813688d956de099149b4a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Cancer research</topic><topic>Cancer therapies</topic><topic>Carcinoma in Situ - genetics</topic><topic>Carcinoma, Lobular - genetics</topic><topic>CCCTC-Binding Factor</topic><topic>Chromosome Deletion</topic><topic>Chromosome Mapping</topic><topic>Chromosomes, Human, Pair 16</topic><topic>Comparative studies</topic><topic>DNA Primers</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetics</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Oncology</topic><topic>Preclinical Study</topic><topic>Repressor Proteins - genetics</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Neoplasm - genetics</topic><topic>RNA, Neoplasm - isolation & purification</topic><topic>RNA, Ribosomal, 18S - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Green, Andrew R</creatorcontrib><creatorcontrib>Krivinskas, Sophie</creatorcontrib><creatorcontrib>Young, Peter</creatorcontrib><creatorcontrib>Rakha, Emad A</creatorcontrib><creatorcontrib>Paish, E. Claire</creatorcontrib><creatorcontrib>Powe, Desmond G</creatorcontrib><creatorcontrib>Ellis, Ian O</creatorcontrib><collection>AGRIS</collection><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>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><jtitle>Breast cancer research and treatment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Green, Andrew R</au><au>Krivinskas, Sophie</au><au>Young, Peter</au><au>Rakha, Emad A</au><au>Paish, E. Claire</au><au>Powe, Desmond G</au><au>Ellis, Ian O</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of expression of chromosome 16q genes DPEP1 and CTCF in lobular carcinoma in situ of the breast</atitle><jtitle>Breast cancer research and treatment</jtitle><stitle>Breast Cancer Res Treat</stitle><addtitle>Breast Cancer Res Treat</addtitle><date>2009-01-01</date><risdate>2009</risdate><volume>113</volume><issue>1</issue><spage>59</spage><epage>66</epage><pages>59-66</pages><issn>0167-6806</issn><eissn>1573-7217</eissn><coden>BCTRD6</coden><abstract>Background Loss of the chromosomal material at 16q is the most frequent genetic event in invasive and in situ (LCIS) lobular carcinoma of the breast. However, the smallest region of overlap at 16q is not restricted to just the CDH1 locus harbouring E-cadherin, suggesting that neighbouring genes might be involved in the development and progression of these tumours. Potential novel tumour suppressor genes (TSG) at 16q include CCCTC-binding factor (CTCF), Decreased Expression in Renal and Prostate Cancer (DERPC) and Dipeptidase 1 (DPEP1). The aim of this study is to assess the expression of these genes in LCIS and compare them with normal breast, using CDH1 as a control, in order to evaluate their role as TSGs. Methods Cells from LCIS cases and normal breast lobules were microdissected and expression of target genes were quantified using real-time PCR. In addition, immunohistochemistry (IHC) for E-cadherin and CTCF was performed on paraffin processed LCIS (n = 49) and normal breast cases. Results All LCIS showed negative expression of E-cadherin. Similar to CDH1, CTCF and DPEP1 gene expression was significantly lower in LCIS cases compared with normal cases (P < 0.05). CTCF IHC expression showed significant reduction in LCIS compared to normal parenchymal cells. However, there was no difference in expression of DERPC between LCIS and normal breast tissue. Conclusions In addition to CDH1, loss of CTCF and DPEP1 gene expression suggest they are possible TSG in breast cancer and may, similar to CDH1, be potentially utilised as markers of predisposition of women diagnosed with LCIS.</abstract><cop>Boston</cop><pub>Boston : Springer US</pub><pmid>18213475</pmid><doi>10.1007/s10549-008-9905-8</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adult Aged Biological and medical sciences Breast cancer Breast Neoplasms - genetics Cancer research Cancer therapies Carcinoma in Situ - genetics Carcinoma, Lobular - genetics CCCTC-Binding Factor Chromosome Deletion Chromosome Mapping Chromosomes, Human, Pair 16 Comparative studies DNA Primers DNA-Binding Proteins - genetics Female Gene Expression Regulation, Neoplastic Genetics Gynecology. Andrology. Obstetrics Humans Immunohistochemistry Mammary gland diseases Medical sciences Medicine Medicine & Public Health Middle Aged Oligonucleotide Array Sequence Analysis Oncology Preclinical Study Repressor Proteins - genetics Reverse Transcriptase Polymerase Chain Reaction RNA, Neoplasm - genetics RNA, Neoplasm - isolation & purification RNA, Ribosomal, 18S - genetics Tumors |
title | Loss of expression of chromosome 16q genes DPEP1 and CTCF in lobular carcinoma in situ of the breast |
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