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Fibroblast growth factor receptor 1 gene amplification in pancreatic ductal adenocarcinoma
Aims Pancreatic ductal adenocarcinomas (PDACs) are chemoresistant, resulting in extremely poor survival of patients; therefore, novel molecular targets, even in small subsets of genetically characterized tumours, are urgently needed. Tyrosine kinase receptor inhibitors (TKIs) are already in clinical...
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| Published in: | Histopathology 2013-08, Vol.63 (2), p.157-166 |
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| container_end_page | 166 |
| container_issue | 2 |
| container_start_page | 157 |
| container_title | Histopathology |
| container_volume | 63 |
| creator | Lehnen, Nils C von Mässenhausen, Anne Kalthoff, Holger Zhou, Hui Glowka, Tim Schütte, Ute Höller, Tobias Riesner, Katarina Boehm, Diana Merkelbach-Bruse, Sabine Kirfel, Jutta Perner, Sven Gütgemann, Ines |
| description | Aims
Pancreatic ductal adenocarcinomas (PDACs) are chemoresistant, resulting in extremely poor survival of patients; therefore, novel molecular targets, even in small subsets of genetically characterized tumours, are urgently needed. Tyrosine kinase receptor inhibitors (TKIs) are already in clinical use. The aims of this study were to examine the gene copy number and expression of fibroblast growth factor receptor 1 (FGFR1) in 155 patients with PDAC, and investigate the effects of the FGFR‐specific inhibitor BGJ398 on FGFR1‐amplified pancreatic tumour cells in vitro.
Methods and results
Fluorescence in‐situ hybridization (FISH) and immunohistochemical analysis of 155 PDACs were performed using tissue microarrays. Amplification of FGFR1 was found in 2.6% (4/155) of cases. Four per cent of tumours (5/125) were shown to express FGFR1 by immunohistochemistry. Sequence analysis demonstrated an activating KRAS mutation (exon 2) in all FGFR1‐amplified cases. The FGFR1‐amplified pancreatic carcinoma cell line PT45P1 showed high levels of FGFR1 mRNA and protein expression. Proliferation of this cell line can be inhibited using the FGFR1 inhibitor BGJ398.
Conclusions
FGFR1 represents a potential new therapeutic target in a subset of patients harbouring FGFR1‐amplified tumours. Identification of pancreatic cancers harbouring FGFR1 amplification may be important in preselecting patients and/or interpreting clinical studies using TKIs. |
| doi_str_mv | 10.1111/his.12115 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1430861129</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1412503330</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4905-c1a382e14dcc06daf4862d76d5470bfd34ac6ce8d00814981c2528699fec67e73</originalsourceid><addsrcrecordid>eNqN0cFu1DAQBmALgejScuAFUCQucEjrsWPHOaKK7hYt5dAiEBfLO3ZalyRO7USlb4-XbXtAqsRcbEvf_BprCHkD9BByHV35dAgMQDwjC-BSlEyI5jlZUE6bkoKs98irlK4phZoz9pLsMa6oUowtyM8Tv4lh05k0FZcx3E5XRWtwCrGIDt24vUBx6QZXmH7sfOvRTD4MhR-K0QwYXX5iYWecTFcY64aAJqIfQm8OyIvWdMm9vj_3ybeTTxfHq3L9dXl6_HFdYtVQUSIYrpiDyiJSaU1bKclsLa2oarppLa8MSnTKUqqgahQgE0zJpmkdytrVfJ-83-WOMdzMLk269wld15nBhTlpqDhVEoA1_0GBCco5p5m--4dehzkO-SNblUvmGbL6sFMYQ0rRtXqMvjfxTgPVW6XzbvTf3WT79j5x3vTOPsqHZWRwtAO3vnN3Tyfp1en5Q2S56_Bpcr8fO0z8pWXNa6G_ny31D7o-h9WXpf7M_wDqoaZu</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1411116869</pqid></control><display><type>article</type><title>Fibroblast growth factor receptor 1 gene amplification in pancreatic ductal adenocarcinoma</title><source>Wiley-Blackwell Read & Publish Collection</source><creator>Lehnen, Nils C ; von Mässenhausen, Anne ; Kalthoff, Holger ; Zhou, Hui ; Glowka, Tim ; Schütte, Ute ; Höller, Tobias ; Riesner, Katarina ; Boehm, Diana ; Merkelbach-Bruse, Sabine ; Kirfel, Jutta ; Perner, Sven ; Gütgemann, Ines</creator><creatorcontrib>Lehnen, Nils C ; von Mässenhausen, Anne ; Kalthoff, Holger ; Zhou, Hui ; Glowka, Tim ; Schütte, Ute ; Höller, Tobias ; Riesner, Katarina ; Boehm, Diana ; Merkelbach-Bruse, Sabine ; Kirfel, Jutta ; Perner, Sven ; Gütgemann, Ines</creatorcontrib><description>Aims
Pancreatic ductal adenocarcinomas (PDACs) are chemoresistant, resulting in extremely poor survival of patients; therefore, novel molecular targets, even in small subsets of genetically characterized tumours, are urgently needed. Tyrosine kinase receptor inhibitors (TKIs) are already in clinical use. The aims of this study were to examine the gene copy number and expression of fibroblast growth factor receptor 1 (FGFR1) in 155 patients with PDAC, and investigate the effects of the FGFR‐specific inhibitor BGJ398 on FGFR1‐amplified pancreatic tumour cells in vitro.
Methods and results
Fluorescence in‐situ hybridization (FISH) and immunohistochemical analysis of 155 PDACs were performed using tissue microarrays. Amplification of FGFR1 was found in 2.6% (4/155) of cases. Four per cent of tumours (5/125) were shown to express FGFR1 by immunohistochemistry. Sequence analysis demonstrated an activating KRAS mutation (exon 2) in all FGFR1‐amplified cases. The FGFR1‐amplified pancreatic carcinoma cell line PT45P1 showed high levels of FGFR1 mRNA and protein expression. Proliferation of this cell line can be inhibited using the FGFR1 inhibitor BGJ398.
Conclusions
FGFR1 represents a potential new therapeutic target in a subset of patients harbouring FGFR1‐amplified tumours. Identification of pancreatic cancers harbouring FGFR1 amplification may be important in preselecting patients and/or interpreting clinical studies using TKIs.</description><identifier>ISSN: 0309-0167</identifier><identifier>EISSN: 1365-2559</identifier><identifier>DOI: 10.1111/his.12115</identifier><identifier>PMID: 23808822</identifier><identifier>CODEN: HISTDD</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Adenocarcinoma ; Adult ; Aged ; Aged, 80 and over ; amplification ; Carcinoma, Pancreatic Ductal - genetics ; Carcinoma, Pancreatic Ductal - metabolism ; Carcinoma, Pancreatic Ductal - pathology ; Cell Line, Tumor ; Cells ; DNA, Neoplasm - genetics ; Female ; fibroblast growth factor receptor 1 ; fluorescence in-situ hybridization ; Gene Amplification ; Humans ; Immunohistochemistry ; In Situ Hybridization, Fluorescence ; Male ; Middle Aged ; Mutation ; Pancreas ; pancreatic ductal adenocarcinoma ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; Prognosis ; Proteins ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins p21(ras) ; ras Proteins - genetics ; Receptor, Fibroblast Growth Factor, Type 1 - antagonists & inhibitors ; Receptor, Fibroblast Growth Factor, Type 1 - genetics ; Receptor, Fibroblast Growth Factor, Type 1 - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; RNA, Neoplasm - genetics ; RNA, Neoplasm - metabolism ; Tissue Array Analysis</subject><ispartof>Histopathology, 2013-08, Vol.63 (2), p.157-166</ispartof><rights>2013 John Wiley & Sons Ltd</rights><rights>2013 John Wiley & Sons Ltd.</rights><rights>Copyright © 2013 John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4905-c1a382e14dcc06daf4862d76d5470bfd34ac6ce8d00814981c2528699fec67e73</citedby><cites>FETCH-LOGICAL-c4905-c1a382e14dcc06daf4862d76d5470bfd34ac6ce8d00814981c2528699fec67e73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23808822$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lehnen, Nils C</creatorcontrib><creatorcontrib>von Mässenhausen, Anne</creatorcontrib><creatorcontrib>Kalthoff, Holger</creatorcontrib><creatorcontrib>Zhou, Hui</creatorcontrib><creatorcontrib>Glowka, Tim</creatorcontrib><creatorcontrib>Schütte, Ute</creatorcontrib><creatorcontrib>Höller, Tobias</creatorcontrib><creatorcontrib>Riesner, Katarina</creatorcontrib><creatorcontrib>Boehm, Diana</creatorcontrib><creatorcontrib>Merkelbach-Bruse, Sabine</creatorcontrib><creatorcontrib>Kirfel, Jutta</creatorcontrib><creatorcontrib>Perner, Sven</creatorcontrib><creatorcontrib>Gütgemann, Ines</creatorcontrib><title>Fibroblast growth factor receptor 1 gene amplification in pancreatic ductal adenocarcinoma</title><title>Histopathology</title><addtitle>Histopathology</addtitle><description>Aims
Pancreatic ductal adenocarcinomas (PDACs) are chemoresistant, resulting in extremely poor survival of patients; therefore, novel molecular targets, even in small subsets of genetically characterized tumours, are urgently needed. Tyrosine kinase receptor inhibitors (TKIs) are already in clinical use. The aims of this study were to examine the gene copy number and expression of fibroblast growth factor receptor 1 (FGFR1) in 155 patients with PDAC, and investigate the effects of the FGFR‐specific inhibitor BGJ398 on FGFR1‐amplified pancreatic tumour cells in vitro.
Methods and results
Fluorescence in‐situ hybridization (FISH) and immunohistochemical analysis of 155 PDACs were performed using tissue microarrays. Amplification of FGFR1 was found in 2.6% (4/155) of cases. Four per cent of tumours (5/125) were shown to express FGFR1 by immunohistochemistry. Sequence analysis demonstrated an activating KRAS mutation (exon 2) in all FGFR1‐amplified cases. The FGFR1‐amplified pancreatic carcinoma cell line PT45P1 showed high levels of FGFR1 mRNA and protein expression. Proliferation of this cell line can be inhibited using the FGFR1 inhibitor BGJ398.
Conclusions
FGFR1 represents a potential new therapeutic target in a subset of patients harbouring FGFR1‐amplified tumours. Identification of pancreatic cancers harbouring FGFR1 amplification may be important in preselecting patients and/or interpreting clinical studies using TKIs.</description><subject>Adenocarcinoma</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>amplification</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Carcinoma, Pancreatic Ductal - metabolism</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cells</subject><subject>DNA, Neoplasm - genetics</subject><subject>Female</subject><subject>fibroblast growth factor receptor 1</subject><subject>fluorescence in-situ hybridization</subject><subject>Gene Amplification</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Pancreas</subject><subject>pancreatic ductal adenocarcinoma</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins p21(ras)</subject><subject>ras Proteins - genetics</subject><subject>Receptor, Fibroblast Growth Factor, Type 1 - antagonists & inhibitors</subject><subject>Receptor, Fibroblast Growth Factor, Type 1 - genetics</subject><subject>Receptor, Fibroblast Growth Factor, Type 1 - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Neoplasm - genetics</subject><subject>RNA, Neoplasm - metabolism</subject><subject>Tissue Array Analysis</subject><issn>0309-0167</issn><issn>1365-2559</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNqN0cFu1DAQBmALgejScuAFUCQucEjrsWPHOaKK7hYt5dAiEBfLO3ZalyRO7USlb4-XbXtAqsRcbEvf_BprCHkD9BByHV35dAgMQDwjC-BSlEyI5jlZUE6bkoKs98irlK4phZoz9pLsMa6oUowtyM8Tv4lh05k0FZcx3E5XRWtwCrGIDt24vUBx6QZXmH7sfOvRTD4MhR-K0QwYXX5iYWecTFcY64aAJqIfQm8OyIvWdMm9vj_3ybeTTxfHq3L9dXl6_HFdYtVQUSIYrpiDyiJSaU1bKclsLa2oarppLa8MSnTKUqqgahQgE0zJpmkdytrVfJ-83-WOMdzMLk269wld15nBhTlpqDhVEoA1_0GBCco5p5m--4dehzkO-SNblUvmGbL6sFMYQ0rRtXqMvjfxTgPVW6XzbvTf3WT79j5x3vTOPsqHZWRwtAO3vnN3Tyfp1en5Q2S56_Bpcr8fO0z8pWXNa6G_ny31D7o-h9WXpf7M_wDqoaZu</recordid><startdate>201308</startdate><enddate>201308</enddate><creator>Lehnen, Nils C</creator><creator>von Mässenhausen, Anne</creator><creator>Kalthoff, Holger</creator><creator>Zhou, Hui</creator><creator>Glowka, Tim</creator><creator>Schütte, Ute</creator><creator>Höller, Tobias</creator><creator>Riesner, Katarina</creator><creator>Boehm, Diana</creator><creator>Merkelbach-Bruse, Sabine</creator><creator>Kirfel, Jutta</creator><creator>Perner, Sven</creator><creator>Gütgemann, Ines</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>201308</creationdate><title>Fibroblast growth factor receptor 1 gene amplification in pancreatic ductal adenocarcinoma</title><author>Lehnen, Nils C ; von Mässenhausen, Anne ; Kalthoff, Holger ; Zhou, Hui ; Glowka, Tim ; Schütte, Ute ; Höller, Tobias ; Riesner, Katarina ; Boehm, Diana ; Merkelbach-Bruse, Sabine ; Kirfel, Jutta ; Perner, Sven ; Gütgemann, Ines</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4905-c1a382e14dcc06daf4862d76d5470bfd34ac6ce8d00814981c2528699fec67e73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adenocarcinoma</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>amplification</topic><topic>Carcinoma, Pancreatic Ductal - genetics</topic><topic>Carcinoma, Pancreatic Ductal - metabolism</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cells</topic><topic>DNA, Neoplasm - genetics</topic><topic>Female</topic><topic>fibroblast growth factor receptor 1</topic><topic>fluorescence in-situ hybridization</topic><topic>Gene Amplification</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Pancreas</topic><topic>pancreatic ductal adenocarcinoma</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins p21(ras)</topic><topic>ras Proteins - genetics</topic><topic>Receptor, Fibroblast Growth Factor, Type 1 - antagonists & inhibitors</topic><topic>Receptor, Fibroblast Growth Factor, Type 1 - genetics</topic><topic>Receptor, Fibroblast Growth Factor, Type 1 - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA, Neoplasm - genetics</topic><topic>RNA, Neoplasm - metabolism</topic><topic>Tissue Array Analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lehnen, Nils C</creatorcontrib><creatorcontrib>von Mässenhausen, Anne</creatorcontrib><creatorcontrib>Kalthoff, Holger</creatorcontrib><creatorcontrib>Zhou, Hui</creatorcontrib><creatorcontrib>Glowka, Tim</creatorcontrib><creatorcontrib>Schütte, Ute</creatorcontrib><creatorcontrib>Höller, Tobias</creatorcontrib><creatorcontrib>Riesner, Katarina</creatorcontrib><creatorcontrib>Boehm, Diana</creatorcontrib><creatorcontrib>Merkelbach-Bruse, Sabine</creatorcontrib><creatorcontrib>Kirfel, Jutta</creatorcontrib><creatorcontrib>Perner, Sven</creatorcontrib><creatorcontrib>Gütgemann, Ines</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Histopathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lehnen, Nils C</au><au>von Mässenhausen, Anne</au><au>Kalthoff, Holger</au><au>Zhou, Hui</au><au>Glowka, Tim</au><au>Schütte, Ute</au><au>Höller, Tobias</au><au>Riesner, Katarina</au><au>Boehm, Diana</au><au>Merkelbach-Bruse, Sabine</au><au>Kirfel, Jutta</au><au>Perner, Sven</au><au>Gütgemann, Ines</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fibroblast growth factor receptor 1 gene amplification in pancreatic ductal adenocarcinoma</atitle><jtitle>Histopathology</jtitle><addtitle>Histopathology</addtitle><date>2013-08</date><risdate>2013</risdate><volume>63</volume><issue>2</issue><spage>157</spage><epage>166</epage><pages>157-166</pages><issn>0309-0167</issn><eissn>1365-2559</eissn><coden>HISTDD</coden><abstract>Aims
Pancreatic ductal adenocarcinomas (PDACs) are chemoresistant, resulting in extremely poor survival of patients; therefore, novel molecular targets, even in small subsets of genetically characterized tumours, are urgently needed. Tyrosine kinase receptor inhibitors (TKIs) are already in clinical use. The aims of this study were to examine the gene copy number and expression of fibroblast growth factor receptor 1 (FGFR1) in 155 patients with PDAC, and investigate the effects of the FGFR‐specific inhibitor BGJ398 on FGFR1‐amplified pancreatic tumour cells in vitro.
Methods and results
Fluorescence in‐situ hybridization (FISH) and immunohistochemical analysis of 155 PDACs were performed using tissue microarrays. Amplification of FGFR1 was found in 2.6% (4/155) of cases. Four per cent of tumours (5/125) were shown to express FGFR1 by immunohistochemistry. Sequence analysis demonstrated an activating KRAS mutation (exon 2) in all FGFR1‐amplified cases. The FGFR1‐amplified pancreatic carcinoma cell line PT45P1 showed high levels of FGFR1 mRNA and protein expression. Proliferation of this cell line can be inhibited using the FGFR1 inhibitor BGJ398.
Conclusions
FGFR1 represents a potential new therapeutic target in a subset of patients harbouring FGFR1‐amplified tumours. Identification of pancreatic cancers harbouring FGFR1 amplification may be important in preselecting patients and/or interpreting clinical studies using TKIs.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>23808822</pmid><doi>10.1111/his.12115</doi><tpages>10</tpages></addata></record> |
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| subjects | Adenocarcinoma Adult Aged Aged, 80 and over amplification Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - metabolism Carcinoma, Pancreatic Ductal - pathology Cell Line, Tumor Cells DNA, Neoplasm - genetics Female fibroblast growth factor receptor 1 fluorescence in-situ hybridization Gene Amplification Humans Immunohistochemistry In Situ Hybridization, Fluorescence Male Middle Aged Mutation Pancreas pancreatic ductal adenocarcinoma Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Prognosis Proteins Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins p21(ras) ras Proteins - genetics Receptor, Fibroblast Growth Factor, Type 1 - antagonists & inhibitors Receptor, Fibroblast Growth Factor, Type 1 - genetics Receptor, Fibroblast Growth Factor, Type 1 - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism RNA, Neoplasm - genetics RNA, Neoplasm - metabolism Tissue Array Analysis |
| title | Fibroblast growth factor receptor 1 gene amplification in pancreatic ductal adenocarcinoma |
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