Clinical and histomolecular endometrial tumor characterization of patients at-risk for Lynch syndrome in South of Brazil
Lynch syndrome is an autosomal dominant cancer predisposition syndrome caused by germline mutations in one of the mismatch repair (MMR) genes: MLH1 , MSH2 , MSH6 and PMS2 . Clinically, Lynch syndrome is characterized by early onset (45 years) of colorectal cancer (CRC), as well as extra-colonic canc...
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creator | Cossio, Silvia Liliana Koehler-Santos, Patricia Pessini, Suzana Arenhart Mónego, Heleuza Edelweiss, Maria Isabel Meurer, Luise Errami, Abdellatif Coffa, Jordy Bock, Hugo Saraiva-Pereira, Maria Luiza Ashton-Prolla, Patricia Prolla, João Carlos |
description | Lynch syndrome is an autosomal dominant cancer predisposition syndrome caused by germline mutations in one of the mismatch repair (MMR) genes:
MLH1
,
MSH2
,
MSH6
and
PMS2
. Clinically, Lynch syndrome is characterized by early onset (45 years) of colorectal cancer (CRC), as well as extra-colonic cancer. Male and female carriers of Lynch syndrome-associated mutations have different lifetime risks for CRC and in women endometrial cancer (EC) may be the most common tumor. Whenever Amsterdam criteria are not fulfilled, the currently recommended laboratory screening strategies involve microsatellite instability testing and immunohistochemistry staining of the tumor for the major MMR proteins. The aim of this study was to estimate the frequency of MMR deficiencies in women diagnosed with EC who are at-risk for Lynch syndrome. Thirty women diagnosed with EC under the age of 50 years and/or women with EC and a first degree relative diagnosed with a Lynch syndrome-associated tumor were included. To assess MMR deficiencies four methods were used: multiplex PCR, Single Strand Conformation Polymorphism, Immunohistochemistry and Methylation Specific–Multiplex Ligation-dependent Probe Amplification. Twelve (40%) patients with EC fulfilling one of the inclusion criteria had results indicative of MMR deficiency. The identification of 5 women with clear evidence of MMR deficiency and absence of either Amsterdam or Bethesda criteria among 10 diagnosed with EC under the age of 50 years reinforces previous suggestions by some authors that these women should be considered at risk and always screened for Lynch syndrome after informed consent. |
doi_str_mv | 10.1007/s10689-009-9297-x |
format | Article |
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MLH1
,
MSH2
,
MSH6
and
PMS2
. Clinically, Lynch syndrome is characterized by early onset (45 years) of colorectal cancer (CRC), as well as extra-colonic cancer. Male and female carriers of Lynch syndrome-associated mutations have different lifetime risks for CRC and in women endometrial cancer (EC) may be the most common tumor. Whenever Amsterdam criteria are not fulfilled, the currently recommended laboratory screening strategies involve microsatellite instability testing and immunohistochemistry staining of the tumor for the major MMR proteins. The aim of this study was to estimate the frequency of MMR deficiencies in women diagnosed with EC who are at-risk for Lynch syndrome. Thirty women diagnosed with EC under the age of 50 years and/or women with EC and a first degree relative diagnosed with a Lynch syndrome-associated tumor were included. To assess MMR deficiencies four methods were used: multiplex PCR, Single Strand Conformation Polymorphism, Immunohistochemistry and Methylation Specific–Multiplex Ligation-dependent Probe Amplification. Twelve (40%) patients with EC fulfilling one of the inclusion criteria had results indicative of MMR deficiency. The identification of 5 women with clear evidence of MMR deficiency and absence of either Amsterdam or Bethesda criteria among 10 diagnosed with EC under the age of 50 years reinforces previous suggestions by some authors that these women should be considered at risk and always screened for Lynch syndrome after informed consent.</description><identifier>ISSN: 1389-9600</identifier><identifier>EISSN: 1573-7292</identifier><identifier>DOI: 10.1007/s10689-009-9297-x</identifier><identifier>PMID: 19821155</identifier><identifier>CODEN: FCAAAJ</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Biomedical and Life Sciences ; Biomedicine ; Brazil - epidemiology ; Cancer Research ; Colorectal Neoplasms - epidemiology ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - physiopathology ; Colorectal Neoplasms, Hereditary Nonpolyposis - diagnosis ; Colorectal Neoplasms, Hereditary Nonpolyposis - etiology ; Colorectal Neoplasms, Hereditary Nonpolyposis - genetics ; DNA Methylation - genetics ; DNA Mismatch Repair - genetics ; DNA Repair ; DNA-Binding Proteins - genetics ; Endometrial Neoplasms - complications ; Endometrial Neoplasms - epidemiology ; Endometrial Neoplasms - genetics ; Epidemiology ; Female ; Human Genetics ; Humans ; Immunohistochemistry ; Male ; Microsatellite Instability ; MutS Homolog 2 Protein - genetics ; Risk</subject><ispartof>Familial cancer, 2010-06, Vol.9 (2), p.131-139</ispartof><rights>Springer Science+Business Media B.V. 2009</rights><rights>Springer Science+Business Media B.V. 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c370t-ec9ca99db029cb6419475eb5a389ceeff585e1a44438a2cf909e7968f3cdf4ac3</citedby><cites>FETCH-LOGICAL-c370t-ec9ca99db029cb6419475eb5a389ceeff585e1a44438a2cf909e7968f3cdf4ac3</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/s10689-009-9297-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10689-009-9297-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19821155$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cossio, Silvia Liliana</creatorcontrib><creatorcontrib>Koehler-Santos, Patricia</creatorcontrib><creatorcontrib>Pessini, Suzana Arenhart</creatorcontrib><creatorcontrib>Mónego, Heleuza</creatorcontrib><creatorcontrib>Edelweiss, Maria Isabel</creatorcontrib><creatorcontrib>Meurer, Luise</creatorcontrib><creatorcontrib>Errami, Abdellatif</creatorcontrib><creatorcontrib>Coffa, Jordy</creatorcontrib><creatorcontrib>Bock, Hugo</creatorcontrib><creatorcontrib>Saraiva-Pereira, Maria Luiza</creatorcontrib><creatorcontrib>Ashton-Prolla, Patricia</creatorcontrib><creatorcontrib>Prolla, João Carlos</creatorcontrib><title>Clinical and histomolecular endometrial tumor characterization of patients at-risk for Lynch syndrome in South of Brazil</title><title>Familial cancer</title><addtitle>Familial Cancer</addtitle><addtitle>Fam Cancer</addtitle><description>Lynch syndrome is an autosomal dominant cancer predisposition syndrome caused by germline mutations in one of the mismatch repair (MMR) genes:
MLH1
,
MSH2
,
MSH6
and
PMS2
. Clinically, Lynch syndrome is characterized by early onset (45 years) of colorectal cancer (CRC), as well as extra-colonic cancer. Male and female carriers of Lynch syndrome-associated mutations have different lifetime risks for CRC and in women endometrial cancer (EC) may be the most common tumor. Whenever Amsterdam criteria are not fulfilled, the currently recommended laboratory screening strategies involve microsatellite instability testing and immunohistochemistry staining of the tumor for the major MMR proteins. The aim of this study was to estimate the frequency of MMR deficiencies in women diagnosed with EC who are at-risk for Lynch syndrome. Thirty women diagnosed with EC under the age of 50 years and/or women with EC and a first degree relative diagnosed with a Lynch syndrome-associated tumor were included. To assess MMR deficiencies four methods were used: multiplex PCR, Single Strand Conformation Polymorphism, Immunohistochemistry and Methylation Specific–Multiplex Ligation-dependent Probe Amplification. Twelve (40%) patients with EC fulfilling one of the inclusion criteria had results indicative of MMR deficiency. The identification of 5 women with clear evidence of MMR deficiency and absence of either Amsterdam or Bethesda criteria among 10 diagnosed with EC under the age of 50 years reinforces previous suggestions by some authors that these women should be considered at risk and always screened for Lynch syndrome after informed consent.</description><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brazil - epidemiology</subject><subject>Cancer Research</subject><subject>Colorectal Neoplasms - epidemiology</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - physiopathology</subject><subject>Colorectal Neoplasms, Hereditary Nonpolyposis - diagnosis</subject><subject>Colorectal Neoplasms, Hereditary Nonpolyposis - etiology</subject><subject>Colorectal Neoplasms, Hereditary Nonpolyposis - genetics</subject><subject>DNA Methylation - genetics</subject><subject>DNA Mismatch Repair - genetics</subject><subject>DNA Repair</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Endometrial Neoplasms - complications</subject><subject>Endometrial Neoplasms - epidemiology</subject><subject>Endometrial Neoplasms - genetics</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Microsatellite Instability</subject><subject>MutS Homolog 2 Protein - genetics</subject><subject>Risk</subject><issn>1389-9600</issn><issn>1573-7292</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</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>eNp1kU2vEyEUhonReD_0B7gxxI2r0QMMZVhqo16TJi7UNaHMwXKdgQpM0t5fL02b3MTEFSd5n_MCeQh5xeAdA1DvC4PVoDsA3WmuVXd4Qq6ZVKJTXPOnbRYt1SuAK3JTyj0ABy7Uc3LF9MAZk_KaHNZTiMHZido40l0oNc1pQrdMNlOMY5qx5tDiuswpU7ez2bqKOTzYGlKkydN9mzDWQm3tcii_qW_g5hjdjpZjHHOroCHS72mpuxP_MduHML0gz7ydCr68nLfk5-dPP9Z33ebbl6_rD5vOCQW1Q6ed1XrcAtduu-qZ7pXErbTtaw7RezlIZLbvezFY7rwGjUqvBi_c6HvrxC15e-7d5_RnwVLNHIrDabIR01KMEkJyqXvWyDf_kPdpybE9znAmOTBgukHsDLmcSsnozT6H2eajYWBOUsxZimlSzEmKObSd15fiZTvj-LhxsdAAfgZKi-IvzI83_7_1Lx-LmpY</recordid><startdate>20100601</startdate><enddate>20100601</enddate><creator>Cossio, Silvia Liliana</creator><creator>Koehler-Santos, Patricia</creator><creator>Pessini, Suzana Arenhart</creator><creator>Mónego, Heleuza</creator><creator>Edelweiss, Maria Isabel</creator><creator>Meurer, Luise</creator><creator>Errami, Abdellatif</creator><creator>Coffa, Jordy</creator><creator>Bock, Hugo</creator><creator>Saraiva-Pereira, Maria Luiza</creator><creator>Ashton-Prolla, Patricia</creator><creator>Prolla, João Carlos</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20100601</creationdate><title>Clinical and histomolecular endometrial tumor characterization of patients at-risk for Lynch syndrome in South of Brazil</title><author>Cossio, Silvia Liliana ; Koehler-Santos, Patricia ; Pessini, Suzana Arenhart ; Mónego, Heleuza ; Edelweiss, Maria Isabel ; Meurer, Luise ; Errami, Abdellatif ; Coffa, Jordy ; Bock, Hugo ; Saraiva-Pereira, Maria Luiza ; Ashton-Prolla, Patricia ; Prolla, João Carlos</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c370t-ec9ca99db029cb6419475eb5a389ceeff585e1a44438a2cf909e7968f3cdf4ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brazil - epidemiology</topic><topic>Cancer Research</topic><topic>Colorectal Neoplasms - epidemiology</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - physiopathology</topic><topic>Colorectal Neoplasms, Hereditary Nonpolyposis - diagnosis</topic><topic>Colorectal Neoplasms, Hereditary Nonpolyposis - etiology</topic><topic>Colorectal Neoplasms, Hereditary Nonpolyposis - genetics</topic><topic>DNA Methylation - genetics</topic><topic>DNA Mismatch Repair - genetics</topic><topic>DNA Repair</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Endometrial Neoplasms - complications</topic><topic>Endometrial Neoplasms - epidemiology</topic><topic>Endometrial Neoplasms - genetics</topic><topic>Epidemiology</topic><topic>Female</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Microsatellite Instability</topic><topic>MutS Homolog 2 Protein - genetics</topic><topic>Risk</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cossio, Silvia Liliana</creatorcontrib><creatorcontrib>Koehler-Santos, Patricia</creatorcontrib><creatorcontrib>Pessini, Suzana Arenhart</creatorcontrib><creatorcontrib>Mónego, Heleuza</creatorcontrib><creatorcontrib>Edelweiss, Maria Isabel</creatorcontrib><creatorcontrib>Meurer, Luise</creatorcontrib><creatorcontrib>Errami, Abdellatif</creatorcontrib><creatorcontrib>Coffa, Jordy</creatorcontrib><creatorcontrib>Bock, Hugo</creatorcontrib><creatorcontrib>Saraiva-Pereira, Maria Luiza</creatorcontrib><creatorcontrib>Ashton-Prolla, Patricia</creatorcontrib><creatorcontrib>Prolla, João Carlos</creatorcontrib><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research 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>Engineering Research Database</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>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>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Familial cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cossio, Silvia Liliana</au><au>Koehler-Santos, Patricia</au><au>Pessini, Suzana Arenhart</au><au>Mónego, Heleuza</au><au>Edelweiss, Maria Isabel</au><au>Meurer, Luise</au><au>Errami, Abdellatif</au><au>Coffa, Jordy</au><au>Bock, Hugo</au><au>Saraiva-Pereira, Maria Luiza</au><au>Ashton-Prolla, Patricia</au><au>Prolla, João Carlos</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinical and histomolecular endometrial tumor characterization of patients at-risk for Lynch syndrome in South of Brazil</atitle><jtitle>Familial cancer</jtitle><stitle>Familial Cancer</stitle><addtitle>Fam Cancer</addtitle><date>2010-06-01</date><risdate>2010</risdate><volume>9</volume><issue>2</issue><spage>131</spage><epage>139</epage><pages>131-139</pages><issn>1389-9600</issn><eissn>1573-7292</eissn><coden>FCAAAJ</coden><abstract>Lynch syndrome is an autosomal dominant cancer predisposition syndrome caused by germline mutations in one of the mismatch repair (MMR) genes:
MLH1
,
MSH2
,
MSH6
and
PMS2
. Clinically, Lynch syndrome is characterized by early onset (45 years) of colorectal cancer (CRC), as well as extra-colonic cancer. Male and female carriers of Lynch syndrome-associated mutations have different lifetime risks for CRC and in women endometrial cancer (EC) may be the most common tumor. Whenever Amsterdam criteria are not fulfilled, the currently recommended laboratory screening strategies involve microsatellite instability testing and immunohistochemistry staining of the tumor for the major MMR proteins. The aim of this study was to estimate the frequency of MMR deficiencies in women diagnosed with EC who are at-risk for Lynch syndrome. Thirty women diagnosed with EC under the age of 50 years and/or women with EC and a first degree relative diagnosed with a Lynch syndrome-associated tumor were included. To assess MMR deficiencies four methods were used: multiplex PCR, Single Strand Conformation Polymorphism, Immunohistochemistry and Methylation Specific–Multiplex Ligation-dependent Probe Amplification. Twelve (40%) patients with EC fulfilling one of the inclusion criteria had results indicative of MMR deficiency. The identification of 5 women with clear evidence of MMR deficiency and absence of either Amsterdam or Bethesda criteria among 10 diagnosed with EC under the age of 50 years reinforces previous suggestions by some authors that these women should be considered at risk and always screened for Lynch syndrome after informed consent.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>19821155</pmid><doi>10.1007/s10689-009-9297-x</doi><tpages>9</tpages></addata></record> |
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subjects | Biomedical and Life Sciences Biomedicine Brazil - epidemiology Cancer Research Colorectal Neoplasms - epidemiology Colorectal Neoplasms - genetics Colorectal Neoplasms - physiopathology Colorectal Neoplasms, Hereditary Nonpolyposis - diagnosis Colorectal Neoplasms, Hereditary Nonpolyposis - etiology Colorectal Neoplasms, Hereditary Nonpolyposis - genetics DNA Methylation - genetics DNA Mismatch Repair - genetics DNA Repair DNA-Binding Proteins - genetics Endometrial Neoplasms - complications Endometrial Neoplasms - epidemiology Endometrial Neoplasms - genetics Epidemiology Female Human Genetics Humans Immunohistochemistry Male Microsatellite Instability MutS Homolog 2 Protein - genetics Risk |
title | Clinical and histomolecular endometrial tumor characterization of patients at-risk for Lynch syndrome in South of Brazil |
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