Loss of heterozygosity in the RAD51 and BRCA2 regions in breast cancer
Abstract Background : Loss of heterozygosity (LOH) in the 15q14-21 and 13q12-13 regions can contribute to the inactivation of RAD51 and BRCA2 genes implicated in the pathogenesis of breast cancer. We investigated allelic losses in microsatellites in the RAD51 and BRCA2 regions, and their association...
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| Veröffentlicht in: | Cancer detection and prevention 2008-01, Vol.32 (2), p.144-148 |
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| creator | Nowacka-Zawisza, Maria, MSc Bryś, Magdalena, PhD Romanowicz-Makowska, Hanna, MD, PhD Kulig, Andrzej, MD, PhD Krajewska, Wanda M., PhD, DSc |
| description | Abstract Background : Loss of heterozygosity (LOH) in the 15q14-21 and 13q12-13 regions can contribute to the inactivation of RAD51 and BRCA2 genes implicated in the pathogenesis of breast cancer. We investigated allelic losses in microsatellites in the RAD51 and BRCA2 regions, and their association with clinicopathological parameters in breast cancer. Methods : The LOH analysis was performed by amplifying DNA by PCR, using D15S118, D15S214, D15S1006 polymorphic markers in the 15q14-21 region and D13S260, D13S290 polymorphic markers in the 13q12-13 region in 36 sporadic breast cancer cases. Results : LOH in the RAD51 region ranged from 29% to 46% and in the BRCA2 region from 38% to 43% of informative cases. Eleven percent of the breast cancer cases displayed LOH for at least one studied marker in the RAD51 region exclusively. On the other hand, 44% of cases manifested statistically significant LOH for at least one microsatellite marker concomitantly in the RAD51 and BRCA2 regions. LOH in the RAD51 region similarly as in the BRCA2 region appeared to correlate with steroid receptors content and lymph node status. Discussion : The obtained results indicate that alteration in RAD51 region may contribute to the disturbances of DNA repair involving RAD51 and/or BRCA2 penetration and thus enhance the risk of breast cancer development. |
| doi_str_mv | 10.1016/j.cdp.2008.06.005 |
| format | Article |
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We investigated allelic losses in microsatellites in the RAD51 and BRCA2 regions, and their association with clinicopathological parameters in breast cancer. Methods : The LOH analysis was performed by amplifying DNA by PCR, using D15S118, D15S214, D15S1006 polymorphic markers in the 15q14-21 region and D13S260, D13S290 polymorphic markers in the 13q12-13 region in 36 sporadic breast cancer cases. Results : LOH in the RAD51 region ranged from 29% to 46% and in the BRCA2 region from 38% to 43% of informative cases. Eleven percent of the breast cancer cases displayed LOH for at least one studied marker in the RAD51 region exclusively. On the other hand, 44% of cases manifested statistically significant LOH for at least one microsatellite marker concomitantly in the RAD51 and BRCA2 regions. LOH in the RAD51 region similarly as in the BRCA2 region appeared to correlate with steroid receptors content and lymph node status. Discussion : The obtained results indicate that alteration in RAD51 region may contribute to the disturbances of DNA repair involving RAD51 and/or BRCA2 penetration and thus enhance the risk of breast cancer development.</description><identifier>ISSN: 0361-090X</identifier><identifier>ISSN: 1877-7821</identifier><identifier>EISSN: 1873-443X</identifier><identifier>EISSN: 1525-1500</identifier><identifier>EISSN: 1877-783X</identifier><identifier>DOI: 10.1016/j.cdp.2008.06.005</identifier><identifier>PMID: 18632222</identifier><identifier>CODEN: CDPRD4</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Adult ; Age ; Aged ; Amino acids ; BRCA2 ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Cancer ; Clinicopathological parameters ; Deoxyribonucleic acid ; DNA ; Epidemiology ; Female ; Genes, BRCA2 ; Genomes ; Hematology, Oncology and Palliative Medicine ; Heterozygous alleles ; Humans ; Loss of heterozygosity (LOH) ; Loss of Heterozygosity - genetics ; Microsatelite markers ; Microsatellite Repeats ; Middle Aged ; Molecular weight ; Polymerase Chain Reaction ; Proteins ; RAD51 ; Rad51 Recombinase - genetics ; Receptors, Estrogen - metabolism ; Receptors, Progesterone - metabolism ; Risk Factors ; Statistical analysis ; Tumors</subject><ispartof>Cancer detection and prevention, 2008-01, Vol.32 (2), p.144-148</ispartof><rights>International Society for Preventive Oncology</rights><rights>2008 International Society for Preventive Oncology</rights><rights>Copyright Elsevier Limited 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c465t-4910604107e0c24adf3c73b5ecb21fd6a85cbbb77fed4e4b12f6b35197d9fdf23</citedby><cites>FETCH-LOGICAL-c465t-4910604107e0c24adf3c73b5ecb21fd6a85cbbb77fed4e4b12f6b35197d9fdf23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18632222$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nowacka-Zawisza, Maria, MSc</creatorcontrib><creatorcontrib>Bryś, Magdalena, PhD</creatorcontrib><creatorcontrib>Romanowicz-Makowska, Hanna, MD, PhD</creatorcontrib><creatorcontrib>Kulig, Andrzej, MD, PhD</creatorcontrib><creatorcontrib>Krajewska, Wanda M., PhD, DSc</creatorcontrib><title>Loss of heterozygosity in the RAD51 and BRCA2 regions in breast cancer</title><title>Cancer detection and prevention</title><addtitle>Cancer Detect Prev</addtitle><description>Abstract Background : Loss of heterozygosity (LOH) in the 15q14-21 and 13q12-13 regions can contribute to the inactivation of RAD51 and BRCA2 genes implicated in the pathogenesis of breast cancer. We investigated allelic losses in microsatellites in the RAD51 and BRCA2 regions, and their association with clinicopathological parameters in breast cancer. Methods : The LOH analysis was performed by amplifying DNA by PCR, using D15S118, D15S214, D15S1006 polymorphic markers in the 15q14-21 region and D13S260, D13S290 polymorphic markers in the 13q12-13 region in 36 sporadic breast cancer cases. Results : LOH in the RAD51 region ranged from 29% to 46% and in the BRCA2 region from 38% to 43% of informative cases. Eleven percent of the breast cancer cases displayed LOH for at least one studied marker in the RAD51 region exclusively. On the other hand, 44% of cases manifested statistically significant LOH for at least one microsatellite marker concomitantly in the RAD51 and BRCA2 regions. LOH in the RAD51 region similarly as in the BRCA2 region appeared to correlate with steroid receptors content and lymph node status. Discussion : The obtained results indicate that alteration in RAD51 region may contribute to the disturbances of DNA repair involving RAD51 and/or BRCA2 penetration and thus enhance the risk of breast cancer development.</description><subject>Adult</subject><subject>Age</subject><subject>Aged</subject><subject>Amino acids</subject><subject>BRCA2</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cancer</subject><subject>Clinicopathological parameters</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Genes, BRCA2</subject><subject>Genomes</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>Heterozygous alleles</subject><subject>Humans</subject><subject>Loss of heterozygosity (LOH)</subject><subject>Loss of Heterozygosity - genetics</subject><subject>Microsatelite markers</subject><subject>Microsatellite Repeats</subject><subject>Middle Aged</subject><subject>Molecular weight</subject><subject>Polymerase Chain Reaction</subject><subject>Proteins</subject><subject>RAD51</subject><subject>Rad51 Recombinase - genetics</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Receptors, Progesterone - metabolism</subject><subject>Risk Factors</subject><subject>Statistical analysis</subject><subject>Tumors</subject><issn>0361-090X</issn><issn>1877-7821</issn><issn>1873-443X</issn><issn>1525-1500</issn><issn>1877-783X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kdFqFDEUhoModq0-gDcSEHo348kkk8wgCOtqtbBQqAq9C5nkpM06O7Mms4X16c2wC4VemJtc5Pt_cr5DyFsGJQMmP2xK63ZlBdCUIEuA-hlZsEbxQgh--5wsgEtWQAu3Z-RVShvImZbLl-SMNZJX-SzI5XpMiY6e3uOEcfx7uBtTmA40DHS6R3qz_FIzagZHP9-slhWNeBfGIc3PXUSTJmrNYDG-Ji-86RO-Od3n5Nfl15-r78X6-tvVarkurJD1VIiWgQTBQCHYShjnuVW8q9F2FfNOmqa2Xdcp5dEJFB2rvOx4zVrlWu98xc_JxbF3F8c_e0yT3oZkse_NgOM-6Uy2slIz-P4JuBn3cch_00zk8WXNVJMpdqRszBoier2LYWviQTPQs2K90VmxnhVrkDorzpl3p-Z9t0X3mDg5zcDHI4BZxEPAqJMNmC25ENFO2o3hv_WfnqRtH4ZgTf8bD5gep9Cp0qB_zDueVwwNACjV8n_-Kp7g</recordid><startdate>20080101</startdate><enddate>20080101</enddate><creator>Nowacka-Zawisza, Maria, MSc</creator><creator>Bryś, Magdalena, PhD</creator><creator>Romanowicz-Makowska, Hanna, MD, PhD</creator><creator>Kulig, Andrzej, MD, PhD</creator><creator>Krajewska, Wanda M., PhD, DSc</creator><general>Elsevier Ltd</general><general>Elsevier Limited</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>7RV</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88C</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>KB0</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20080101</creationdate><title>Loss of heterozygosity in the RAD51 and BRCA2 regions in breast cancer</title><author>Nowacka-Zawisza, Maria, MSc ; Bryś, Magdalena, PhD ; Romanowicz-Makowska, Hanna, MD, PhD ; Kulig, Andrzej, MD, PhD ; Krajewska, Wanda M., PhD, DSc</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c465t-4910604107e0c24adf3c73b5ecb21fd6a85cbbb77fed4e4b12f6b35197d9fdf23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult</topic><topic>Age</topic><topic>Aged</topic><topic>Amino acids</topic><topic>BRCA2</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Cancer</topic><topic>Clinicopathological parameters</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Epidemiology</topic><topic>Female</topic><topic>Genes, BRCA2</topic><topic>Genomes</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>Heterozygous alleles</topic><topic>Humans</topic><topic>Loss of heterozygosity (LOH)</topic><topic>Loss of Heterozygosity - genetics</topic><topic>Microsatelite markers</topic><topic>Microsatellite Repeats</topic><topic>Middle Aged</topic><topic>Molecular weight</topic><topic>Polymerase Chain Reaction</topic><topic>Proteins</topic><topic>RAD51</topic><topic>Rad51 Recombinase - genetics</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Receptors, Progesterone - metabolism</topic><topic>Risk Factors</topic><topic>Statistical analysis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nowacka-Zawisza, Maria, MSc</creatorcontrib><creatorcontrib>Bryś, Magdalena, PhD</creatorcontrib><creatorcontrib>Romanowicz-Makowska, Hanna, MD, PhD</creatorcontrib><creatorcontrib>Kulig, Andrzej, MD, PhD</creatorcontrib><creatorcontrib>Krajewska, Wanda M., PhD, DSc</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>Proquest Nursing & Allied Health Source</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Healthcare Administration Database (Alumni)</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</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>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Cancer detection and prevention</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nowacka-Zawisza, Maria, MSc</au><au>Bryś, Magdalena, PhD</au><au>Romanowicz-Makowska, Hanna, MD, PhD</au><au>Kulig, Andrzej, MD, PhD</au><au>Krajewska, Wanda M., PhD, DSc</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Loss of heterozygosity in the RAD51 and BRCA2 regions in breast cancer</atitle><jtitle>Cancer detection and prevention</jtitle><addtitle>Cancer Detect Prev</addtitle><date>2008-01-01</date><risdate>2008</risdate><volume>32</volume><issue>2</issue><spage>144</spage><epage>148</epage><pages>144-148</pages><issn>0361-090X</issn><issn>1877-7821</issn><eissn>1873-443X</eissn><eissn>1525-1500</eissn><eissn>1877-783X</eissn><coden>CDPRD4</coden><abstract>Abstract Background : Loss of heterozygosity (LOH) in the 15q14-21 and 13q12-13 regions can contribute to the inactivation of RAD51 and BRCA2 genes implicated in the pathogenesis of breast cancer. We investigated allelic losses in microsatellites in the RAD51 and BRCA2 regions, and their association with clinicopathological parameters in breast cancer. Methods : The LOH analysis was performed by amplifying DNA by PCR, using D15S118, D15S214, D15S1006 polymorphic markers in the 15q14-21 region and D13S260, D13S290 polymorphic markers in the 13q12-13 region in 36 sporadic breast cancer cases. Results : LOH in the RAD51 region ranged from 29% to 46% and in the BRCA2 region from 38% to 43% of informative cases. Eleven percent of the breast cancer cases displayed LOH for at least one studied marker in the RAD51 region exclusively. On the other hand, 44% of cases manifested statistically significant LOH for at least one microsatellite marker concomitantly in the RAD51 and BRCA2 regions. LOH in the RAD51 region similarly as in the BRCA2 region appeared to correlate with steroid receptors content and lymph node status. Discussion : The obtained results indicate that alteration in RAD51 region may contribute to the disturbances of DNA repair involving RAD51 and/or BRCA2 penetration and thus enhance the risk of breast cancer development.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>18632222</pmid><doi>10.1016/j.cdp.2008.06.005</doi><tpages>5</tpages></addata></record> |
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| subjects | Adult Age Aged Amino acids BRCA2 Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Cancer Clinicopathological parameters Deoxyribonucleic acid DNA Epidemiology Female Genes, BRCA2 Genomes Hematology, Oncology and Palliative Medicine Heterozygous alleles Humans Loss of heterozygosity (LOH) Loss of Heterozygosity - genetics Microsatelite markers Microsatellite Repeats Middle Aged Molecular weight Polymerase Chain Reaction Proteins RAD51 Rad51 Recombinase - genetics Receptors, Estrogen - metabolism Receptors, Progesterone - metabolism Risk Factors Statistical analysis Tumors |
| title | Loss of heterozygosity in the RAD51 and BRCA2 regions in breast cancer |
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