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Gene Expression Profiles of BRCA1-Linked, BRCA2-Linked, and Sporadic Ovarian Cancers
Background: Germline mutations in BRCA1 and BRCA2 are responsible for 5%–10% of epithelial ovarian cancers, but the molecular pathways affected by these mutations are unknown. We used complementary DNA (cDNA) microarrays to compare gene expression patterns in ovarian cancers associated with BRCA1 or...
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| Published in: | JNCI : Journal of the National Cancer Institute 2002-07, Vol.94 (13), p.990-1000 |
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| creator | Jazaeri, Amir A. Yee, Cindy J. Sotiriou, Christos Brantley, Kelly R. Boyd, Jeff Liu, Edison T. |
| description | Background: Germline mutations in BRCA1 and BRCA2 are responsible for 5%–10% of epithelial ovarian cancers, but the molecular pathways affected by these mutations are unknown. We used complementary DNA (cDNA) microarrays to compare gene expression patterns in ovarian cancers associated with BRCA1 or BRCA2 mutations with gene expression patterns in sporadic epithelial ovarian cancers and to identify patterns common to both hereditary and sporadic tumors. Methods: Tumor samples from 61 patients with pathologically confirmed epithelial ovarian adenocarcinoma with matched clinicopathologic features were studied, including 18 with BRCA1 founder mutations, 16 with BRCA2 founder mutations, and 27 without either founder mutation (termed sporadic cancers). The cDNA microarrays contained 7651 sequence-verified features. Gene expression data were analyzed with a modified two-sided F test, with P |
| doi_str_mv | 10.1093/jnci/94.13.990 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_18454468</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>18454468</sourcerecordid><originalsourceid>FETCH-LOGICAL-c523t-57ba4239bc5b999dccd9e8ec5922f3fda4dfa933a581d786bea509a101f6c9503</originalsourceid><addsrcrecordid>eNpd0M1LHDEYwOFQWuqqvfZYhoKenDWfM3mPdlG3sMWPKoiXkMkHZJ3NbJNd0f_e6C4KzSW85EkIP4S-EzwmGNjxPJpwDHxM2BgAf0IjwhtcU4LFZzTCmLa1lC3fQbs5z3FZQPlXtEMohgZLPkI35y666vRpmVzOYYjVZRp86F2uBl_9up6ckHoW4oOzR28TfZ90tNXf5ZC0Daa6eNQp6FhNdDQu5X30xes-u2_bfQ_dnp3eTKb17OL89-RkVhtB2aoWbac5ZdAZ0QGANcaCk84IoNQzbzW3XgNjWkhiW9l0TgsMmmDiGwMCsz10uHl3mYZ_a5dXahGycX2voxvWWRHJBeeNLPDnf3A-rFMsf1O0pJAEeFvQeINMGnJOzqtlCgudnhXB6jW2eo2tgCvCVIldLvzYvrruFs5-8G3dAg62QGeje59KnpA_HGeNgDdXb1zIK_f0fq7Tg2pa1go1vbtX-I5RMWVX6g97Af5ZlHc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>220981947</pqid></control><display><type>article</type><title>Gene Expression Profiles of BRCA1-Linked, BRCA2-Linked, and Sporadic Ovarian Cancers</title><source>Oxford Journals Online</source><creator>Jazaeri, Amir A. ; Yee, Cindy J. ; Sotiriou, Christos ; Brantley, Kelly R. ; Boyd, Jeff ; Liu, Edison T.</creator><creatorcontrib>Jazaeri, Amir A. ; Yee, Cindy J. ; Sotiriou, Christos ; Brantley, Kelly R. ; Boyd, Jeff ; Liu, Edison T.</creatorcontrib><description>Background: Germline mutations in BRCA1 and BRCA2 are responsible for 5%–10% of epithelial ovarian cancers, but the molecular pathways affected by these mutations are unknown. We used complementary DNA (cDNA) microarrays to compare gene expression patterns in ovarian cancers associated with BRCA1 or BRCA2 mutations with gene expression patterns in sporadic epithelial ovarian cancers and to identify patterns common to both hereditary and sporadic tumors. Methods: Tumor samples from 61 patients with pathologically confirmed epithelial ovarian adenocarcinoma with matched clinicopathologic features were studied, including 18 with BRCA1 founder mutations, 16 with BRCA2 founder mutations, and 27 without either founder mutation (termed sporadic cancers). The cDNA microarrays contained 7651 sequence-verified features. Gene expression data were analyzed with a modified two-sided F test, with P<.0001 considered statistically significant. The expression level of six genes was also studied with reverse transcription–polymerase chain reaction. Results: The greatest contrast in gene expression was observed between tumors with BRCA1 mutations and those with BRCA2 mutations; 110 genes showed statistically significantly different expression levels (P<.0001). This group of genes could segregate sporadic tumors into two subgroups, “BRCA1-like” and “BRCA2-like,” suggesting that BRCA1-related and BRCA2-related pathways are also involved in sporadic ovarian cancers. Fifty-three genes were differentially expressed between tumors with BRCA1 mutations and sporadic tumors; six of the 53 mapped to Xp11.23 and were expressed at higher levels in tumors with BRCA1 mutations than in sporadic tumors. Compared with the immortalized ovarian surface epithelial cells used as reference, several interferon-inducible genes were overexpressed in the majority of tumors with a BRCA mutation and in sporadic tumors. Conclusions: Mutations in BRCA1 and BRCA2 may lead to carcinogenesis through distinct molecular pathways that also appear to be involved in sporadic cancers. Sporadic carcinogenic pathways may result from epigenetic aberrations of BRCA1 and BRCA2 or their downstream effectors.</description><identifier>ISSN: 0027-8874</identifier><identifier>EISSN: 1460-2105</identifier><identifier>DOI: 10.1093/jnci/94.13.990</identifier><identifier>PMID: 12096084</identifier><identifier>CODEN: JNCIEQ</identifier><language>eng</language><publisher>Cary, NC: Oxford University Press</publisher><subject>Adenocarcinoma, Clear Cell - genetics ; Adenocarcinoma, Clear Cell - metabolism ; Adenocarcinoma, Mucinous - genetics ; Adenocarcinoma, Mucinous - metabolism ; Aged ; Biological and medical sciences ; BRCA1 Protein - genetics ; BRCA2 Protein - genetics ; Carcinoma, Endometrioid - genetics ; Carcinoma, Endometrioid - metabolism ; Cystadenocarcinoma, Serous - genetics ; Cystadenocarcinoma, Serous - metabolism ; DNA Primers - chemistry ; Female ; Female genital diseases ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genotype ; Germ-Line Mutation ; Gynecology. Andrology. Obstetrics ; Humans ; Medical sciences ; Middle Aged ; Oligonucleotide Array Sequence Analysis ; Ovarian Neoplasms - genetics ; Ovarian Neoplasms - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - analysis ; RNA, Messenger - genetics ; RNA, Neoplasm - analysis ; Tumors</subject><ispartof>JNCI : Journal of the National Cancer Institute, 2002-07, Vol.94 (13), p.990-1000</ispartof><rights>2003 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Jul 3, 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c523t-57ba4239bc5b999dccd9e8ec5922f3fda4dfa933a581d786bea509a101f6c9503</citedby><cites>FETCH-LOGICAL-c523t-57ba4239bc5b999dccd9e8ec5922f3fda4dfa933a581d786bea509a101f6c9503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14365984$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12096084$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jazaeri, Amir A.</creatorcontrib><creatorcontrib>Yee, Cindy J.</creatorcontrib><creatorcontrib>Sotiriou, Christos</creatorcontrib><creatorcontrib>Brantley, Kelly R.</creatorcontrib><creatorcontrib>Boyd, Jeff</creatorcontrib><creatorcontrib>Liu, Edison T.</creatorcontrib><title>Gene Expression Profiles of BRCA1-Linked, BRCA2-Linked, and Sporadic Ovarian Cancers</title><title>JNCI : Journal of the National Cancer Institute</title><addtitle>JNCI J Natl Cancer Inst</addtitle><description>Background: Germline mutations in BRCA1 and BRCA2 are responsible for 5%–10% of epithelial ovarian cancers, but the molecular pathways affected by these mutations are unknown. We used complementary DNA (cDNA) microarrays to compare gene expression patterns in ovarian cancers associated with BRCA1 or BRCA2 mutations with gene expression patterns in sporadic epithelial ovarian cancers and to identify patterns common to both hereditary and sporadic tumors. Methods: Tumor samples from 61 patients with pathologically confirmed epithelial ovarian adenocarcinoma with matched clinicopathologic features were studied, including 18 with BRCA1 founder mutations, 16 with BRCA2 founder mutations, and 27 without either founder mutation (termed sporadic cancers). The cDNA microarrays contained 7651 sequence-verified features. Gene expression data were analyzed with a modified two-sided F test, with P<.0001 considered statistically significant. The expression level of six genes was also studied with reverse transcription–polymerase chain reaction. Results: The greatest contrast in gene expression was observed between tumors with BRCA1 mutations and those with BRCA2 mutations; 110 genes showed statistically significantly different expression levels (P<.0001). This group of genes could segregate sporadic tumors into two subgroups, “BRCA1-like” and “BRCA2-like,” suggesting that BRCA1-related and BRCA2-related pathways are also involved in sporadic ovarian cancers. Fifty-three genes were differentially expressed between tumors with BRCA1 mutations and sporadic tumors; six of the 53 mapped to Xp11.23 and were expressed at higher levels in tumors with BRCA1 mutations than in sporadic tumors. Compared with the immortalized ovarian surface epithelial cells used as reference, several interferon-inducible genes were overexpressed in the majority of tumors with a BRCA mutation and in sporadic tumors. Conclusions: Mutations in BRCA1 and BRCA2 may lead to carcinogenesis through distinct molecular pathways that also appear to be involved in sporadic cancers. Sporadic carcinogenic pathways may result from epigenetic aberrations of BRCA1 and BRCA2 or their downstream effectors.</description><subject>Adenocarcinoma, Clear Cell - genetics</subject><subject>Adenocarcinoma, Clear Cell - metabolism</subject><subject>Adenocarcinoma, Mucinous - genetics</subject><subject>Adenocarcinoma, Mucinous - metabolism</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>BRCA1 Protein - genetics</subject><subject>BRCA2 Protein - genetics</subject><subject>Carcinoma, Endometrioid - genetics</subject><subject>Carcinoma, Endometrioid - metabolism</subject><subject>Cystadenocarcinoma, Serous - genetics</subject><subject>Cystadenocarcinoma, Serous - metabolism</subject><subject>DNA Primers - chemistry</subject><subject>Female</subject><subject>Female genital diseases</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genotype</subject><subject>Germ-Line Mutation</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - analysis</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Neoplasm - analysis</subject><subject>Tumors</subject><issn>0027-8874</issn><issn>1460-2105</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNpd0M1LHDEYwOFQWuqqvfZYhoKenDWfM3mPdlG3sMWPKoiXkMkHZJ3NbJNd0f_e6C4KzSW85EkIP4S-EzwmGNjxPJpwDHxM2BgAf0IjwhtcU4LFZzTCmLa1lC3fQbs5z3FZQPlXtEMohgZLPkI35y666vRpmVzOYYjVZRp86F2uBl_9up6ckHoW4oOzR28TfZ90tNXf5ZC0Daa6eNQp6FhNdDQu5X30xes-u2_bfQ_dnp3eTKb17OL89-RkVhtB2aoWbac5ZdAZ0QGANcaCk84IoNQzbzW3XgNjWkhiW9l0TgsMmmDiGwMCsz10uHl3mYZ_a5dXahGycX2voxvWWRHJBeeNLPDnf3A-rFMsf1O0pJAEeFvQeINMGnJOzqtlCgudnhXB6jW2eo2tgCvCVIldLvzYvrruFs5-8G3dAg62QGeje59KnpA_HGeNgDdXb1zIK_f0fq7Tg2pa1go1vbtX-I5RMWVX6g97Af5ZlHc</recordid><startdate>20020703</startdate><enddate>20020703</enddate><creator>Jazaeri, Amir A.</creator><creator>Yee, Cindy J.</creator><creator>Sotiriou, Christos</creator><creator>Brantley, Kelly R.</creator><creator>Boyd, Jeff</creator><creator>Liu, Edison T.</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</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>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope></search><sort><creationdate>20020703</creationdate><title>Gene Expression Profiles of BRCA1-Linked, BRCA2-Linked, and Sporadic Ovarian Cancers</title><author>Jazaeri, Amir A. ; Yee, Cindy J. ; Sotiriou, Christos ; Brantley, Kelly R. ; Boyd, Jeff ; Liu, Edison T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c523t-57ba4239bc5b999dccd9e8ec5922f3fda4dfa933a581d786bea509a101f6c9503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adenocarcinoma, Clear Cell - genetics</topic><topic>Adenocarcinoma, Clear Cell - metabolism</topic><topic>Adenocarcinoma, Mucinous - genetics</topic><topic>Adenocarcinoma, Mucinous - metabolism</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>BRCA1 Protein - genetics</topic><topic>BRCA2 Protein - genetics</topic><topic>Carcinoma, Endometrioid - genetics</topic><topic>Carcinoma, Endometrioid - metabolism</topic><topic>Cystadenocarcinoma, Serous - genetics</topic><topic>Cystadenocarcinoma, Serous - metabolism</topic><topic>DNA Primers - chemistry</topic><topic>Female</topic><topic>Female genital diseases</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genotype</topic><topic>Germ-Line Mutation</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - analysis</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Neoplasm - analysis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jazaeri, Amir A.</creatorcontrib><creatorcontrib>Yee, Cindy J.</creatorcontrib><creatorcontrib>Sotiriou, Christos</creatorcontrib><creatorcontrib>Brantley, Kelly R.</creatorcontrib><creatorcontrib>Boyd, Jeff</creatorcontrib><creatorcontrib>Liu, Edison T.</creatorcontrib><collection>Istex</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>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>JNCI : Journal of the National Cancer Institute</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jazaeri, Amir A.</au><au>Yee, Cindy J.</au><au>Sotiriou, Christos</au><au>Brantley, Kelly R.</au><au>Boyd, Jeff</au><au>Liu, Edison T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gene Expression Profiles of BRCA1-Linked, BRCA2-Linked, and Sporadic Ovarian Cancers</atitle><jtitle>JNCI : Journal of the National Cancer Institute</jtitle><addtitle>JNCI J Natl Cancer Inst</addtitle><date>2002-07-03</date><risdate>2002</risdate><volume>94</volume><issue>13</issue><spage>990</spage><epage>1000</epage><pages>990-1000</pages><issn>0027-8874</issn><eissn>1460-2105</eissn><coden>JNCIEQ</coden><abstract>Background: Germline mutations in BRCA1 and BRCA2 are responsible for 5%–10% of epithelial ovarian cancers, but the molecular pathways affected by these mutations are unknown. We used complementary DNA (cDNA) microarrays to compare gene expression patterns in ovarian cancers associated with BRCA1 or BRCA2 mutations with gene expression patterns in sporadic epithelial ovarian cancers and to identify patterns common to both hereditary and sporadic tumors. Methods: Tumor samples from 61 patients with pathologically confirmed epithelial ovarian adenocarcinoma with matched clinicopathologic features were studied, including 18 with BRCA1 founder mutations, 16 with BRCA2 founder mutations, and 27 without either founder mutation (termed sporadic cancers). The cDNA microarrays contained 7651 sequence-verified features. Gene expression data were analyzed with a modified two-sided F test, with P<.0001 considered statistically significant. The expression level of six genes was also studied with reverse transcription–polymerase chain reaction. Results: The greatest contrast in gene expression was observed between tumors with BRCA1 mutations and those with BRCA2 mutations; 110 genes showed statistically significantly different expression levels (P<.0001). This group of genes could segregate sporadic tumors into two subgroups, “BRCA1-like” and “BRCA2-like,” suggesting that BRCA1-related and BRCA2-related pathways are also involved in sporadic ovarian cancers. Fifty-three genes were differentially expressed between tumors with BRCA1 mutations and sporadic tumors; six of the 53 mapped to Xp11.23 and were expressed at higher levels in tumors with BRCA1 mutations than in sporadic tumors. Compared with the immortalized ovarian surface epithelial cells used as reference, several interferon-inducible genes were overexpressed in the majority of tumors with a BRCA mutation and in sporadic tumors. Conclusions: Mutations in BRCA1 and BRCA2 may lead to carcinogenesis through distinct molecular pathways that also appear to be involved in sporadic cancers. Sporadic carcinogenic pathways may result from epigenetic aberrations of BRCA1 and BRCA2 or their downstream effectors.</abstract><cop>Cary, NC</cop><pub>Oxford University Press</pub><pmid>12096084</pmid><doi>10.1093/jnci/94.13.990</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma, Clear Cell - genetics Adenocarcinoma, Clear Cell - metabolism Adenocarcinoma, Mucinous - genetics Adenocarcinoma, Mucinous - metabolism Aged Biological and medical sciences BRCA1 Protein - genetics BRCA2 Protein - genetics Carcinoma, Endometrioid - genetics Carcinoma, Endometrioid - metabolism Cystadenocarcinoma, Serous - genetics Cystadenocarcinoma, Serous - metabolism DNA Primers - chemistry Female Female genital diseases Gene Expression Profiling Gene Expression Regulation, Neoplastic Genotype Germ-Line Mutation Gynecology. Andrology. Obstetrics Humans Medical sciences Middle Aged Oligonucleotide Array Sequence Analysis Ovarian Neoplasms - genetics Ovarian Neoplasms - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - analysis RNA, Messenger - genetics RNA, Neoplasm - analysis Tumors |
| title | Gene Expression Profiles of BRCA1-Linked, BRCA2-Linked, and Sporadic Ovarian Cancers |
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