Variant human breast tumor estrogen receptor with constitutive transcriptional activity
Since progesterone receptor (PgR) is normally induced by estrogen, breast cancer lacking estrogen receptor (ER) would also be expected to lack PgR. However, a small percentage of breast cancers are ER- yet PgR+. These tumors might possess an ER which is defective in estrogen binding but is still fun...
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| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 1991, Vol.51 (1), p.105-109 |
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| container_title | Cancer research (Chicago, Ill.) |
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| creator | FUQUA, S. A. W FITZGERALD, S. D CHAMNESS, G. C TANDON, A. K MCDONNELL, D. P NAWAZ, Z O'MALLEY, B. W MCGUIRE, W. L |
| description | Since progesterone receptor (PgR) is normally induced by estrogen, breast cancer lacking estrogen receptor (ER) would also be expected to lack PgR. However, a small percentage of breast cancers are ER- yet PgR+. These tumors might possess an ER which is defective in estrogen binding but is still functional in stimulating estrogen-responsive genes such as PgR. We have now detected such a variant, lacking exon 5 of the hormone-binding domain, using complementary DNA amplified by the polymerase chain reaction. This variant was the predominate ER RNA expressed in three ER-/PgR+ tumors. Furthermore, the variant ER constitutively activates transcription of a normally estrogen-dependent gene construct in yeast cells. The variant ER could explain the expression of PgR in certain tumors and have therapeutic implications. |
| format | Article |
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A. W ; FITZGERALD, S. D ; CHAMNESS, G. C ; TANDON, A. K ; MCDONNELL, D. P ; NAWAZ, Z ; O'MALLEY, B. W ; MCGUIRE, W. L</creator><creatorcontrib>FUQUA, S. A. W ; FITZGERALD, S. D ; CHAMNESS, G. C ; TANDON, A. K ; MCDONNELL, D. P ; NAWAZ, Z ; O'MALLEY, B. W ; MCGUIRE, W. L</creatorcontrib><description>Since progesterone receptor (PgR) is normally induced by estrogen, breast cancer lacking estrogen receptor (ER) would also be expected to lack PgR. However, a small percentage of breast cancers are ER- yet PgR+. These tumors might possess an ER which is defective in estrogen binding but is still functional in stimulating estrogen-responsive genes such as PgR. We have now detected such a variant, lacking exon 5 of the hormone-binding domain, using complementary DNA amplified by the polymerase chain reaction. This variant was the predominate ER RNA expressed in three ER-/PgR+ tumors. Furthermore, the variant ER constitutively activates transcription of a normally estrogen-dependent gene construct in yeast cells. The variant ER could explain the expression of PgR in certain tumors and have therapeutic implications.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 1988075</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Base Sequence ; Biological and medical sciences ; Blotting, Western ; Breast Neoplasms - genetics ; Cloning, Molecular ; Gene Expression Regulation, Neoplastic ; Gynecology. Andrology. Obstetrics ; Humans ; Mammary gland diseases ; Medical sciences ; Molecular Sequence Data ; Polymerase Chain Reaction ; Receptors, Estrogen - genetics ; Receptors, Estrogen - immunology ; Receptors, Progesterone - genetics ; Recombinant Proteins - immunology ; RNA, Messenger - genetics ; RNA, Neoplasm - genetics ; Transcription, Genetic ; Tumors</subject><ispartof>Cancer research (Chicago, Ill.), 1991, Vol.51 (1), p.105-109</ispartof><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19529764$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1988075$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FUQUA, S. A. W</creatorcontrib><creatorcontrib>FITZGERALD, S. D</creatorcontrib><creatorcontrib>CHAMNESS, G. C</creatorcontrib><creatorcontrib>TANDON, A. K</creatorcontrib><creatorcontrib>MCDONNELL, D. P</creatorcontrib><creatorcontrib>NAWAZ, Z</creatorcontrib><creatorcontrib>O'MALLEY, B. W</creatorcontrib><creatorcontrib>MCGUIRE, W. L</creatorcontrib><title>Variant human breast tumor estrogen receptor with constitutive transcriptional activity</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>Since progesterone receptor (PgR) is normally induced by estrogen, breast cancer lacking estrogen receptor (ER) would also be expected to lack PgR. However, a small percentage of breast cancers are ER- yet PgR+. These tumors might possess an ER which is defective in estrogen binding but is still functional in stimulating estrogen-responsive genes such as PgR. We have now detected such a variant, lacking exon 5 of the hormone-binding domain, using complementary DNA amplified by the polymerase chain reaction. This variant was the predominate ER RNA expressed in three ER-/PgR+ tumors. Furthermore, the variant ER constitutively activates transcription of a normally estrogen-dependent gene construct in yeast cells. The variant ER could explain the expression of PgR in certain tumors and have therapeutic implications.</description><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Breast Neoplasms - genetics</subject><subject>Cloning, Molecular</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Molecular Sequence Data</subject><subject>Polymerase Chain Reaction</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Estrogen - immunology</subject><subject>Receptors, Progesterone - genetics</subject><subject>Recombinant Proteins - immunology</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Neoplasm - genetics</subject><subject>Transcription, Genetic</subject><subject>Tumors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1991</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtLAzEUhYMotVZ_gpCN7gbybJKlFF9QcONjOdxJb21kXiYZpf_eKc7CnavLOefjcjhHZM61tIVRSh-TOWPMFloZcUrOUvoYpeZMz8iMO2uZ0XPy9goxQJvpbmigpVVESJnmoekixZRj944tjeixz6PzHfKO-q5NOeQhhy-kOUKbfAx9Dl0LNQU_2iHvz8nJFuqEF9NdkJe72-fVQ7F-un9c3ayLnXAuFxo1eouaGV8phhbAucpIEA60EGJTKae21m6kX3IhDpW5qEAZjRy9l14uyPXv3z52n8PYuGxC8ljX0GI3pNIyJYST8l-Qa7u03BzAywkcqgY3ZR9DA3FfTpON-dWUQ_JQb8cBfEh_MC2cWSr5A5Rmd2I</recordid><startdate>1991</startdate><enddate>1991</enddate><creator>FUQUA, S. A. W</creator><creator>FITZGERALD, S. D</creator><creator>CHAMNESS, G. C</creator><creator>TANDON, A. K</creator><creator>MCDONNELL, D. P</creator><creator>NAWAZ, Z</creator><creator>O'MALLEY, B. W</creator><creator>MCGUIRE, W. L</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7TM</scope><scope>7X8</scope></search><sort><creationdate>1991</creationdate><title>Variant human breast tumor estrogen receptor with constitutive transcriptional activity</title><author>FUQUA, S. A. W ; FITZGERALD, S. D ; CHAMNESS, G. C ; TANDON, A. K ; MCDONNELL, D. P ; NAWAZ, Z ; O'MALLEY, B. W ; MCGUIRE, W. L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h299t-5e5ec8e507cb40e8aa99b73a29a5222db494f88d3c6122807512ba475e1ecc3c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1991</creationdate><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Breast Neoplasms - genetics</topic><topic>Cloning, Molecular</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Molecular Sequence Data</topic><topic>Polymerase Chain Reaction</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, Estrogen - immunology</topic><topic>Receptors, Progesterone - genetics</topic><topic>Recombinant Proteins - immunology</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Neoplasm - genetics</topic><topic>Transcription, Genetic</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FUQUA, S. A. W</creatorcontrib><creatorcontrib>FITZGERALD, S. D</creatorcontrib><creatorcontrib>CHAMNESS, G. C</creatorcontrib><creatorcontrib>TANDON, A. K</creatorcontrib><creatorcontrib>MCDONNELL, D. P</creatorcontrib><creatorcontrib>NAWAZ, Z</creatorcontrib><creatorcontrib>O'MALLEY, B. W</creatorcontrib><creatorcontrib>MCGUIRE, W. L</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>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FUQUA, S. A. W</au><au>FITZGERALD, S. D</au><au>CHAMNESS, G. C</au><au>TANDON, A. K</au><au>MCDONNELL, D. P</au><au>NAWAZ, Z</au><au>O'MALLEY, B. W</au><au>MCGUIRE, W. L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Variant human breast tumor estrogen receptor with constitutive transcriptional activity</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1991</date><risdate>1991</risdate><volume>51</volume><issue>1</issue><spage>105</spage><epage>109</epage><pages>105-109</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>Since progesterone receptor (PgR) is normally induced by estrogen, breast cancer lacking estrogen receptor (ER) would also be expected to lack PgR. However, a small percentage of breast cancers are ER- yet PgR+. These tumors might possess an ER which is defective in estrogen binding but is still functional in stimulating estrogen-responsive genes such as PgR. We have now detected such a variant, lacking exon 5 of the hormone-binding domain, using complementary DNA amplified by the polymerase chain reaction. This variant was the predominate ER RNA expressed in three ER-/PgR+ tumors. Furthermore, the variant ER constitutively activates transcription of a normally estrogen-dependent gene construct in yeast cells. The variant ER could explain the expression of PgR in certain tumors and have therapeutic implications.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>1988075</pmid><tpages>5</tpages></addata></record> |
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| ispartof | Cancer research (Chicago, Ill.), 1991, Vol.51 (1), p.105-109 |
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| language | eng |
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| source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals |
| subjects | Base Sequence Biological and medical sciences Blotting, Western Breast Neoplasms - genetics Cloning, Molecular Gene Expression Regulation, Neoplastic Gynecology. Andrology. Obstetrics Humans Mammary gland diseases Medical sciences Molecular Sequence Data Polymerase Chain Reaction Receptors, Estrogen - genetics Receptors, Estrogen - immunology Receptors, Progesterone - genetics Recombinant Proteins - immunology RNA, Messenger - genetics RNA, Neoplasm - genetics Transcription, Genetic Tumors |
| title | Variant human breast tumor estrogen receptor with constitutive transcriptional activity |
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