Frequent abnormalities of the putative tumor suppressor gene FHIT at 3p14.2 in pancreatic carcinoma cell lines
The FHIT gene is localized on chromosome 3p14, a region including a tumor cell-specific, commonly deleted region. To determine the role of the FHIT gene in pancreatic carcinogenesis, 14 pancreatic carcinoma cell lines were analyzed by reverse transcription-PCR and exon-specific PCR amplification of...
Gespeichert in:
| Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 1998-04, Vol.58 (8), p.1583-1587 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1587 |
|---|---|
| container_issue | 8 |
| container_start_page | 1583 |
| container_title | Cancer research (Chicago, Ill.) |
| container_volume | 58 |
| creator | SIMON, B BARTSCH, D BARTH, P PRASNIKAR, N MÜNCH, K BLUM, A ARNOLD, R GÖKE, B |
| description | The FHIT gene is localized on chromosome 3p14, a region including a tumor cell-specific, commonly deleted region. To determine the role of the FHIT gene in pancreatic carcinogenesis, 14 pancreatic carcinoma cell lines were analyzed by reverse transcription-PCR and exon-specific PCR amplification of genomic DNA. The full-length FHIT transcript was lost in 70% of the pancreatic carcinoma cell lines analyzed, while 66% also revealed intragenic homozygous deletions of exons 3, 4, and 5. Truncated FHIT transcripts lacking a variable number of exons most likely represented alternative splicing products. Fhit protein expression was dependent on a full-length FHIT transcript. The results suggest that the FHIT gene may be a target tumor suppressor gene involved in pancreatic carcinogenesis. |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_17213884</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>17213884</sourcerecordid><originalsourceid>FETCH-LOGICAL-h299t-a8a08db0779d994e3311f3e1b765ce10e27fd6e5c33f3eef657c73f271dce34b3</originalsourceid><addsrcrecordid>eNo9kE1LxDAQhoMo67r6E4QcxFsln017FHHdhQUv67mk6dSNtGlMUsF_b8TiaT7eZ4Z55wytqeRVoYSQ52hNCKkKKRS7RFcxfuRSUiJXaFXLkotSrJHbBvicwSWsWzeFUQ82WYh46nE6AfZz0sl-AU7zOAUcZ-8DxJjTd3CAt7v9EeuEuafigWHrsNfOBMgzBhsdjHXTqLGBYcCDdRCv0UWvhwg3S9ygt-3z8WlXHF5f9k-Ph-LE6joVutKk6lqiVN3VtQDOKe050FaV0gAlwFTflSAN57kNfSmVUbxninYGuGj5Bt3_7fVhyvZiakYbf8_QDqY5NlQxyqtKZPB2Aed2hK7xwY46fDfLg7J-t-g6Gj30Ifuz8R9jjNFaVPwH8tNwIw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17213884</pqid></control><display><type>article</type><title>Frequent abnormalities of the putative tumor suppressor gene FHIT at 3p14.2 in pancreatic carcinoma cell lines</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>American Association for Cancer Research</source><creator>SIMON, B ; BARTSCH, D ; BARTH, P ; PRASNIKAR, N ; MÜNCH, K ; BLUM, A ; ARNOLD, R ; GÖKE, B</creator><creatorcontrib>SIMON, B ; BARTSCH, D ; BARTH, P ; PRASNIKAR, N ; MÜNCH, K ; BLUM, A ; ARNOLD, R ; GÖKE, B</creatorcontrib><description>The FHIT gene is localized on chromosome 3p14, a region including a tumor cell-specific, commonly deleted region. To determine the role of the FHIT gene in pancreatic carcinogenesis, 14 pancreatic carcinoma cell lines were analyzed by reverse transcription-PCR and exon-specific PCR amplification of genomic DNA. The full-length FHIT transcript was lost in 70% of the pancreatic carcinoma cell lines analyzed, while 66% also revealed intragenic homozygous deletions of exons 3, 4, and 5. Truncated FHIT transcripts lacking a variable number of exons most likely represented alternative splicing products. Fhit protein expression was dependent on a full-length FHIT transcript. The results suggest that the FHIT gene may be a target tumor suppressor gene involved in pancreatic carcinogenesis.</description><identifier>ISSN: 0008-5472</identifier><identifier>EISSN: 1538-7445</identifier><identifier>PMID: 9563464</identifier><identifier>CODEN: CNREA8</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Acid Anhydride Hydrolases ; Alternative Splicing ; Biological and medical sciences ; Carcinoma - genetics ; Carcinoma - metabolism ; Chromosomes, Human, Pair 3 ; Colonic Neoplasms - genetics ; DNA, Neoplasm - analysis ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Deletion ; Humans ; Immunohistochemistry ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Medical sciences ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - metabolism ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; Proteins - genetics ; Proteins - metabolism ; Transcription, Genetic ; Tumor Cells, Cultured ; Tumors</subject><ispartof>Cancer research (Chicago, Ill.), 1998-04, Vol.58 (8), p.1583-1587</ispartof><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2221948$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9563464$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SIMON, B</creatorcontrib><creatorcontrib>BARTSCH, D</creatorcontrib><creatorcontrib>BARTH, P</creatorcontrib><creatorcontrib>PRASNIKAR, N</creatorcontrib><creatorcontrib>MÜNCH, K</creatorcontrib><creatorcontrib>BLUM, A</creatorcontrib><creatorcontrib>ARNOLD, R</creatorcontrib><creatorcontrib>GÖKE, B</creatorcontrib><title>Frequent abnormalities of the putative tumor suppressor gene FHIT at 3p14.2 in pancreatic carcinoma cell lines</title><title>Cancer research (Chicago, Ill.)</title><addtitle>Cancer Res</addtitle><description>The FHIT gene is localized on chromosome 3p14, a region including a tumor cell-specific, commonly deleted region. To determine the role of the FHIT gene in pancreatic carcinogenesis, 14 pancreatic carcinoma cell lines were analyzed by reverse transcription-PCR and exon-specific PCR amplification of genomic DNA. The full-length FHIT transcript was lost in 70% of the pancreatic carcinoma cell lines analyzed, while 66% also revealed intragenic homozygous deletions of exons 3, 4, and 5. Truncated FHIT transcripts lacking a variable number of exons most likely represented alternative splicing products. Fhit protein expression was dependent on a full-length FHIT transcript. The results suggest that the FHIT gene may be a target tumor suppressor gene involved in pancreatic carcinogenesis.</description><subject>Acid Anhydride Hydrolases</subject><subject>Alternative Splicing</subject><subject>Biological and medical sciences</subject><subject>Carcinoma - genetics</subject><subject>Carcinoma - metabolism</subject><subject>Chromosomes, Human, Pair 3</subject><subject>Colonic Neoplasms - genetics</subject><subject>DNA, Neoplasm - analysis</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Deletion</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Medical sciences</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Polymerase Chain Reaction</subject><subject>Polymorphism, Single-Stranded Conformational</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>Transcription, Genetic</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><issn>0008-5472</issn><issn>1538-7445</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1LxDAQhoMo67r6E4QcxFsln017FHHdhQUv67mk6dSNtGlMUsF_b8TiaT7eZ4Z55wytqeRVoYSQ52hNCKkKKRS7RFcxfuRSUiJXaFXLkotSrJHbBvicwSWsWzeFUQ82WYh46nE6AfZz0sl-AU7zOAUcZ-8DxJjTd3CAt7v9EeuEuafigWHrsNfOBMgzBhsdjHXTqLGBYcCDdRCv0UWvhwg3S9ygt-3z8WlXHF5f9k-Ph-LE6joVutKk6lqiVN3VtQDOKe050FaV0gAlwFTflSAN57kNfSmVUbxninYGuGj5Bt3_7fVhyvZiakYbf8_QDqY5NlQxyqtKZPB2Aed2hK7xwY46fDfLg7J-t-g6Gj30Ifuz8R9jjNFaVPwH8tNwIw</recordid><startdate>19980415</startdate><enddate>19980415</enddate><creator>SIMON, B</creator><creator>BARTSCH, D</creator><creator>BARTH, P</creator><creator>PRASNIKAR, N</creator><creator>MÜNCH, K</creator><creator>BLUM, A</creator><creator>ARNOLD, R</creator><creator>GÖKE, B</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>7TO</scope><scope>H94</scope></search><sort><creationdate>19980415</creationdate><title>Frequent abnormalities of the putative tumor suppressor gene FHIT at 3p14.2 in pancreatic carcinoma cell lines</title><author>SIMON, B ; BARTSCH, D ; BARTH, P ; PRASNIKAR, N ; MÜNCH, K ; BLUM, A ; ARNOLD, R ; GÖKE, B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h299t-a8a08db0779d994e3311f3e1b765ce10e27fd6e5c33f3eef657c73f271dce34b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Acid Anhydride Hydrolases</topic><topic>Alternative Splicing</topic><topic>Biological and medical sciences</topic><topic>Carcinoma - genetics</topic><topic>Carcinoma - metabolism</topic><topic>Chromosomes, Human, Pair 3</topic><topic>Colonic Neoplasms - genetics</topic><topic>DNA, Neoplasm - analysis</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Deletion</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Medical sciences</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Polymerase Chain Reaction</topic><topic>Polymorphism, Single-Stranded Conformational</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>Transcription, Genetic</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SIMON, B</creatorcontrib><creatorcontrib>BARTSCH, D</creatorcontrib><creatorcontrib>BARTH, P</creatorcontrib><creatorcontrib>PRASNIKAR, N</creatorcontrib><creatorcontrib>MÜNCH, K</creatorcontrib><creatorcontrib>BLUM, A</creatorcontrib><creatorcontrib>ARNOLD, R</creatorcontrib><creatorcontrib>GÖKE, B</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>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Cancer research (Chicago, Ill.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SIMON, B</au><au>BARTSCH, D</au><au>BARTH, P</au><au>PRASNIKAR, N</au><au>MÜNCH, K</au><au>BLUM, A</au><au>ARNOLD, R</au><au>GÖKE, B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Frequent abnormalities of the putative tumor suppressor gene FHIT at 3p14.2 in pancreatic carcinoma cell lines</atitle><jtitle>Cancer research (Chicago, Ill.)</jtitle><addtitle>Cancer Res</addtitle><date>1998-04-15</date><risdate>1998</risdate><volume>58</volume><issue>8</issue><spage>1583</spage><epage>1587</epage><pages>1583-1587</pages><issn>0008-5472</issn><eissn>1538-7445</eissn><coden>CNREA8</coden><abstract>The FHIT gene is localized on chromosome 3p14, a region including a tumor cell-specific, commonly deleted region. To determine the role of the FHIT gene in pancreatic carcinogenesis, 14 pancreatic carcinoma cell lines were analyzed by reverse transcription-PCR and exon-specific PCR amplification of genomic DNA. The full-length FHIT transcript was lost in 70% of the pancreatic carcinoma cell lines analyzed, while 66% also revealed intragenic homozygous deletions of exons 3, 4, and 5. Truncated FHIT transcripts lacking a variable number of exons most likely represented alternative splicing products. Fhit protein expression was dependent on a full-length FHIT transcript. The results suggest that the FHIT gene may be a target tumor suppressor gene involved in pancreatic carcinogenesis.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>9563464</pmid><tpages>5</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0008-5472 |
| ispartof | Cancer research (Chicago, Ill.), 1998-04, Vol.58 (8), p.1583-1587 |
| issn | 0008-5472 1538-7445 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_17213884 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; American Association for Cancer Research |
| subjects | Acid Anhydride Hydrolases Alternative Splicing Biological and medical sciences Carcinoma - genetics Carcinoma - metabolism Chromosomes, Human, Pair 3 Colonic Neoplasms - genetics DNA, Neoplasm - analysis Gastroenterology. Liver. Pancreas. Abdomen Gene Deletion Humans Immunohistochemistry Liver. Biliary tract. Portal circulation. Exocrine pancreas Medical sciences Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Polymerase Chain Reaction Polymorphism, Single-Stranded Conformational Proteins - genetics Proteins - metabolism Transcription, Genetic Tumor Cells, Cultured Tumors |
| title | Frequent abnormalities of the putative tumor suppressor gene FHIT at 3p14.2 in pancreatic carcinoma cell lines |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-08T04%3A42%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Frequent%20abnormalities%20of%20the%20putative%20tumor%20suppressor%20gene%20FHIT%20at%203p14.2%20in%20pancreatic%20carcinoma%20cell%20lines&rft.jtitle=Cancer%20research%20(Chicago,%20Ill.)&rft.au=SIMON,%20B&rft.date=1998-04-15&rft.volume=58&rft.issue=8&rft.spage=1583&rft.epage=1587&rft.pages=1583-1587&rft.issn=0008-5472&rft.eissn=1538-7445&rft.coden=CNREA8&rft_id=info:doi/&rft_dat=%3Cproquest_pubme%3E17213884%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=17213884&rft_id=info:pmid/9563464&rfr_iscdi=true |