Loss of heterozygosity at chromosome 9p in ductal carcinoma in situ and invasive carcinoma of the breast
Twenty-three cases of ductal carcinoma in situ (DCIS), ten of which had an associated invasive component, were studied for loss of heterozygosity (LOH) of microsatellite markers on chromosome 9p and the results compared with a panel of 20 invasive breast carcinomas. In addition to the gene encoding...
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Veröffentlicht in: | British journal of cancer 1998-05, Vol.77 (9), p.1439-1447 |
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description | Twenty-three cases of ductal carcinoma in situ (DCIS), ten of which had an associated invasive component, were studied for loss of heterozygosity (LOH) of microsatellite markers on chromosome 9p and the results compared with a panel of 20 invasive breast carcinomas. In addition to the gene encoding p16, chromosome 9p is also thought to contain other putative tumour-suppressor genes. If the three panels of breast tumours showed LOH of markers in this region this would suggest that such putative genes were important in breast carcinogenesis. By studying both preinvasive and invasive breast tumours, it should also be possible to gain further information about the relationship between lesions of a different stage and to determine whether DCIS is indeed a precursor of invasive ductal carcinoma. Levels of LOH were low in the invasive-only set of tumours. Surprisingly, considerably higher levels of loss were observed in the tumours with an in situ component. Also, much heterogeneity was observed between different DCIS ducts or invasive tumour and DCIS from the same case. |
doi_str_mv | 10.1038/bjc.1998.237 |
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In addition to the gene encoding p16, chromosome 9p is also thought to contain other putative tumour-suppressor genes. If the three panels of breast tumours showed LOH of markers in this region this would suggest that such putative genes were important in breast carcinogenesis. By studying both preinvasive and invasive breast tumours, it should also be possible to gain further information about the relationship between lesions of a different stage and to determine whether DCIS is indeed a precursor of invasive ductal carcinoma. Levels of LOH were low in the invasive-only set of tumours. Surprisingly, considerably higher levels of loss were observed in the tumours with an in situ component. Also, much heterogeneity was observed between different DCIS ducts or invasive tumour and DCIS from the same case.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/bjc.1998.237</identifier><identifier>PMID: 9652759</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cancer Research ; Carcinoma in Situ - genetics ; Carcinoma in Situ - secondary ; Carcinoma, Ductal, Breast - genetics ; Carcinoma, Ductal, Breast - secondary ; Chromosomes, Human, Pair 9 - genetics ; DNA, Neoplasm - genetics ; Drug Resistance ; Epidemiology ; experimental-oncology ; Female ; Genetic Markers - genetics ; Gynecology. Andrology. Obstetrics ; Humans ; Loss of Heterozygosity - genetics ; Mammary gland diseases ; Medical sciences ; Molecular Medicine ; Neoplasm Invasiveness - genetics ; Oncology ; Tumors</subject><ispartof>British journal of cancer, 1998-05, Vol.77 (9), p.1439-1447</ispartof><rights>Cancer Research Campaign 1998</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-7efa8098290fadf2372fb4d35a296913afb4a5fdee6b66cc9e2a1015efe0b0723</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2150179/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2150179/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,2727,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2224577$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9652759$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marsh, KL</creatorcontrib><creatorcontrib>Varley, JM</creatorcontrib><title>Loss of heterozygosity at chromosome 9p in ductal carcinoma in situ and invasive carcinoma of the breast</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Twenty-three cases of ductal carcinoma in situ (DCIS), ten of which had an associated invasive component, were studied for loss of heterozygosity (LOH) of microsatellite markers on chromosome 9p and the results compared with a panel of 20 invasive breast carcinomas. In addition to the gene encoding p16, chromosome 9p is also thought to contain other putative tumour-suppressor genes. If the three panels of breast tumours showed LOH of markers in this region this would suggest that such putative genes were important in breast carcinogenesis. By studying both preinvasive and invasive breast tumours, it should also be possible to gain further information about the relationship between lesions of a different stage and to determine whether DCIS is indeed a precursor of invasive ductal carcinoma. Levels of LOH were low in the invasive-only set of tumours. Surprisingly, considerably higher levels of loss were observed in the tumours with an in situ component. Also, much heterogeneity was observed between different DCIS ducts or invasive tumour and DCIS from the same case.</description><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer Research</subject><subject>Carcinoma in Situ - genetics</subject><subject>Carcinoma in Situ - secondary</subject><subject>Carcinoma, Ductal, Breast - genetics</subject><subject>Carcinoma, Ductal, Breast - secondary</subject><subject>Chromosomes, Human, Pair 9 - genetics</subject><subject>DNA, Neoplasm - genetics</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>experimental-oncology</subject><subject>Female</subject><subject>Genetic Markers - genetics</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Loss of Heterozygosity - genetics</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Molecular Medicine</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Oncology</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMFr2zAUxsXYaNNut10LOvQ4Z5IcW9ZlMMrWFgK9bGfxLD_FDrEUJDmQ_vWTSQjtYSe9p--n7-l9hHzlbMlZ2Xxvt2bJlWqWopQfyIJXpSh4I-RHsmCMyYIpwa7JTYzb3CrWyCtypepKyEotSL_2MVJvaY8Jg389bnwc0pFCoqYPfvTRj0jVng6OdpNJsKMGghmcH2G-y_BEwXW5PkAcDvhGzq6pR9oGhJg-k08WdhG_nM9b8vf3rz8PT8X65fH54ee6MCvJUyHRQsNUIxSz0Nm8krDtqisrEKpWvITcQWU7xLqta2MUCuCMV2iRtUyK8pb8OPnup3bEzqBLAXZ6H4YRwlF7GPR7xQ293viDFrxiXKps8O1kYEKOJqC9vOVMz4HrHLieA9f5dxm_ezvvAp8Tzvr9WYdoYGcDODPECyaEWFVytilOWMyK22DQWz8Fl5P631h64h2kKeDFL0MzMyP_AA_Xpfg</recordid><startdate>19980501</startdate><enddate>19980501</enddate><creator>Marsh, KL</creator><creator>Varley, JM</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>5PM</scope></search><sort><creationdate>19980501</creationdate><title>Loss of heterozygosity at chromosome 9p in ductal carcinoma in situ and invasive carcinoma of the breast</title><author>Marsh, KL ; Varley, JM</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-7efa8098290fadf2372fb4d35a296913afb4a5fdee6b66cc9e2a1015efe0b0723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer Research</topic><topic>Carcinoma in Situ - genetics</topic><topic>Carcinoma in Situ - secondary</topic><topic>Carcinoma, Ductal, Breast - genetics</topic><topic>Carcinoma, Ductal, Breast - secondary</topic><topic>Chromosomes, Human, Pair 9 - genetics</topic><topic>DNA, Neoplasm - genetics</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>experimental-oncology</topic><topic>Female</topic><topic>Genetic Markers - genetics</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Loss of Heterozygosity - genetics</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Molecular Medicine</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Oncology</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marsh, KL</creatorcontrib><creatorcontrib>Varley, JM</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>PubMed Central (Full Participant titles)</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marsh, KL</au><au>Varley, JM</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of heterozygosity at chromosome 9p in ductal carcinoma in situ and invasive carcinoma of the breast</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>1998-05-01</date><risdate>1998</risdate><volume>77</volume><issue>9</issue><spage>1439</spage><epage>1447</epage><pages>1439-1447</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Twenty-three cases of ductal carcinoma in situ (DCIS), ten of which had an associated invasive component, were studied for loss of heterozygosity (LOH) of microsatellite markers on chromosome 9p and the results compared with a panel of 20 invasive breast carcinomas. In addition to the gene encoding p16, chromosome 9p is also thought to contain other putative tumour-suppressor genes. If the three panels of breast tumours showed LOH of markers in this region this would suggest that such putative genes were important in breast carcinogenesis. By studying both preinvasive and invasive breast tumours, it should also be possible to gain further information about the relationship between lesions of a different stage and to determine whether DCIS is indeed a precursor of invasive ductal carcinoma. Levels of LOH were low in the invasive-only set of tumours. Surprisingly, considerably higher levels of loss were observed in the tumours with an in situ component. Also, much heterogeneity was observed between different DCIS ducts or invasive tumour and DCIS from the same case.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>9652759</pmid><doi>10.1038/bjc.1998.237</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Biological and medical sciences Biomedical and Life Sciences Biomedicine Breast Neoplasms - genetics Breast Neoplasms - pathology Cancer Research Carcinoma in Situ - genetics Carcinoma in Situ - secondary Carcinoma, Ductal, Breast - genetics Carcinoma, Ductal, Breast - secondary Chromosomes, Human, Pair 9 - genetics DNA, Neoplasm - genetics Drug Resistance Epidemiology experimental-oncology Female Genetic Markers - genetics Gynecology. Andrology. Obstetrics Humans Loss of Heterozygosity - genetics Mammary gland diseases Medical sciences Molecular Medicine Neoplasm Invasiveness - genetics Oncology Tumors |
title | Loss of heterozygosity at chromosome 9p in ductal carcinoma in situ and invasive carcinoma of the breast |
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