Analysis of the TGF β functional pathway in epithelial ovarian carcinoma
Epithelial ovarian carcinoma is often diagnosed at an advanced stage of disease and is the leading cause of death from gynaecological neoplasia. The genetic changes that occur during the development of this carcinoma are poorly understood. It has been proposed that IGFIIR, TGFβ1 and TGFβRII act as a...
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Veröffentlicht in: | British journal of cancer 2001-09, Vol.85 (5), p.687-691 |
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description | Epithelial ovarian carcinoma is often diagnosed at an advanced stage of disease and is the leading cause of death from gynaecological neoplasia. The genetic changes that occur during the development of this carcinoma are poorly understood. It has been proposed that IGFIIR, TGFβ1 and TGFβRII act as a functional unit in the TGFβ growth inhibitory pathway, and that somatic loss-of-function mutations in any one of these genes could lead to disruption of the pathway and subsequent loss of cell cycle control. We have examined these 3 genes in 25 epithelial ovarian carcinomas using single-stranded conformational polymorphism analysis and DNA sequence analysis. A total of 3 somatic missense mutations were found in the TGFβRII gene, but none in IGFRII or TGFβ1. An association was found between TGFβRII mutations and histology, with 2 out of 3 clear cell carcinomas having TGFβRII mutations. This data supports other evidence from mutational analysis of the PTEN and β-catenin genes that there are distinct developmental pathways responsible for the progression of different epithelial ovarian cancer histologic subtypes. © 2001 Cancer Research Campaign
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www.bjcancer.com</description><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Carcinoma - genetics</subject><subject>Carcinoma - pathology</subject><subject>DNA Mutational Analysis</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Female genital diseases</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Molecular Medicine</subject><subject>Mutation, Missense - genetics</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Staging</subject><subject>Oncology</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Ovarian Neoplasms - pathology</subject><subject>Polymorphism, Single-Stranded Conformational</subject><subject>Protein-Serine-Threonine Kinases</subject><subject>Receptor, IGF Type 2 - genetics</subject><subject>Receptors, Transforming Growth Factor beta - genetics</subject><subject>Regular</subject><subject>regular-article</subject><subject>Sequence Analysis, DNA</subject><subject>Transforming Growth Factor beta - genetics</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><recordid>eNp1kc1qWzEQhUVJaRy32y6LNsnuOvq1pE0hmPxBoItmL-bKurHMteRK9yb4tfogfabI2DTpoisxOt-cGc4g9JWSGSVSXLbr5GaMEDqjRpIPaEIlZw3VTJ2gCSFENcQwcorOSlnX0hCtPqFTWinKJJ-g-6sI_a6EglOHh5XHj7c3-M9v3I3RDSFVEW9hWL3ADoeI_TZUpg_1Nz1DDhCxg-xCTBv4jD520Bf_5fhO0c-b68fFXfPw4_Z-cfXQOCHnQ9OZdqmkrhswozohlGtBK8p1J5lm3GjtifNegGLAOOdzqQ341hktlxr4FH0_uG7HduOXzschQ2-3OWwg72yCYP9VYljZp_RsGZ8LWg2n6OJokNOv0ZfBbkJxvu8h-jQWqygVxHBWwdkBdDmVkn33dwgldp-93Wdv99nbffa14dv71d7wY9gVOD8CUBz0XYboQnnjBCWaS1G5ywNXqhSffLbrNOZ6ivK_0a-2tZ12</recordid><startdate>20010901</startdate><enddate>20010901</enddate><creator>Francis-Thickpenny, K M</creator><creator>Richardson, D M</creator><creator>Ee, C C van</creator><creator>Love, D R</creator><creator>Winship, I M</creator><creator>Baguley, B C</creator><creator>Chenevix-Trench, G</creator><creator>Shelling, A N</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20010901</creationdate><title>Analysis of the TGF β functional pathway in epithelial ovarian carcinoma</title><author>Francis-Thickpenny, K M ; Richardson, D M ; Ee, C C van ; Love, D R ; Winship, I M ; Baguley, B C ; Chenevix-Trench, G ; Shelling, A N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-f9bd758115297f447cba87138f52823988e0cee4a72a23336589aebc985d8a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Carcinoma - genetics</topic><topic>Carcinoma - pathology</topic><topic>DNA Mutational Analysis</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>Female</topic><topic>Female genital diseases</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Molecular Medicine</topic><topic>Mutation, Missense - genetics</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Staging</topic><topic>Oncology</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Ovarian Neoplasms - pathology</topic><topic>Polymorphism, Single-Stranded Conformational</topic><topic>Protein-Serine-Threonine Kinases</topic><topic>Receptor, IGF Type 2 - genetics</topic><topic>Receptors, Transforming Growth Factor beta - genetics</topic><topic>Regular</topic><topic>regular-article</topic><topic>Sequence Analysis, DNA</topic><topic>Transforming Growth Factor beta - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Francis-Thickpenny, K M</creatorcontrib><creatorcontrib>Richardson, D M</creatorcontrib><creatorcontrib>Ee, C C van</creatorcontrib><creatorcontrib>Love, D R</creatorcontrib><creatorcontrib>Winship, I M</creatorcontrib><creatorcontrib>Baguley, B C</creatorcontrib><creatorcontrib>Chenevix-Trench, G</creatorcontrib><creatorcontrib>Shelling, A N</creatorcontrib><collection>Springer Nature OA Free Journals</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>MEDLINE - Academic</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>Francis-Thickpenny, K M</au><au>Richardson, D M</au><au>Ee, C C van</au><au>Love, D R</au><au>Winship, I M</au><au>Baguley, B C</au><au>Chenevix-Trench, G</au><au>Shelling, A N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of the TGF β functional pathway in epithelial ovarian carcinoma</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2001-09-01</date><risdate>2001</risdate><volume>85</volume><issue>5</issue><spage>687</spage><epage>691</epage><pages>687-691</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Epithelial ovarian carcinoma is often diagnosed at an advanced stage of disease and is the leading cause of death from gynaecological neoplasia. The genetic changes that occur during the development of this carcinoma are poorly understood. It has been proposed that IGFIIR, TGFβ1 and TGFβRII act as a functional unit in the TGFβ growth inhibitory pathway, and that somatic loss-of-function mutations in any one of these genes could lead to disruption of the pathway and subsequent loss of cell cycle control. We have examined these 3 genes in 25 epithelial ovarian carcinomas using single-stranded conformational polymorphism analysis and DNA sequence analysis. A total of 3 somatic missense mutations were found in the TGFβRII gene, but none in IGFRII or TGFβ1. An association was found between TGFβRII mutations and histology, with 2 out of 3 clear cell carcinomas having TGFβRII mutations. This data supports other evidence from mutational analysis of the PTEN and β-catenin genes that there are distinct developmental pathways responsible for the progression of different epithelial ovarian cancer histologic subtypes. © 2001 Cancer Research Campaign
www.bjcancer.com</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>11531253</pmid><doi>10.1054/bjoc.2001.1950</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Biological and medical sciences Biomedical and Life Sciences Biomedicine Cancer Research Carcinoma - genetics Carcinoma - pathology DNA Mutational Analysis Drug Resistance Epidemiology Female Female genital diseases Gynecology. Andrology. Obstetrics Humans Medical sciences Molecular Medicine Mutation, Missense - genetics Neoplasm Proteins - genetics Neoplasm Staging Oncology Ovarian Neoplasms - genetics Ovarian Neoplasms - pathology Polymorphism, Single-Stranded Conformational Protein-Serine-Threonine Kinases Receptor, IGF Type 2 - genetics Receptors, Transforming Growth Factor beta - genetics Regular regular-article Sequence Analysis, DNA Transforming Growth Factor beta - genetics Tumors |
title | Analysis of the TGF β functional pathway in epithelial ovarian carcinoma |
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