Copy Number of Chromosome 17 but Not HER2 Amplification Predicts Clinical Outcome of Patients With Pancreatic Ductal Adenocarcinoma
To determine the frequency and the potential clinical use of HER2 (17q21) gene amplification and chromosome 17 aneuploidy in pancreatic ductal adenocarcinoma (PDAC). Serial tissue sections of 50 resected PDACs were analyzed with chromogenic in situ hybridization using locus-specific HER2 probes and...
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| Veröffentlicht in: | Journal of clinical oncology 2004-12, Vol.22 (23), p.4737-4693 |
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| creator | STOECKLEIN, Nikolas H LUEBKE, Andreas M IZBICKI, Jakob R KLEIN, Christoph A HOSCH, Stefan B ERBERSDOBLER, Andreas KNOEFEL, Wolfram T SCHRAUT, Winfried VERDE, Pablo E STERN, Franziska SCHEUNEMANN, Peter PEIPER, Matthias EISENBERGER, Claus F |
| description | To determine the frequency and the potential clinical use of HER2 (17q21) gene amplification and chromosome 17 aneuploidy in pancreatic ductal adenocarcinoma (PDAC).
Serial tissue sections of 50 resected PDACs were analyzed with chromogenic in situ hybridization using locus-specific HER2 probes and centromeric probes for chromosome 17. Centromeric probes for chromosome 7 and 8 were hybridized to confirm ploidy levels. Expression of HER2 protein was assessed by immunohistochemistry. Correlations of experimental findings with clinical and follow-up data were tested.
The HER2 gene locus was frequently (24%) amplified in PDAC and the rate of overexpression (2+ and 3+) was 10%, but no prognostic significance was found. Copy number analysis of chromosomes 7, 8, and 17 revealed disomic (40%), trisomic (36%), and hypertetrasomic (24%) tumors. Compared with patients with disomic tumors, patients with hypertetrasomic tumors exhibited a significantly decreased relapse-free and overall survival (5.0 v 13.0 months, P = .0144 and 7.0 v 20.0 months, P = .0099, respectively). Multivariate analysis confirmed the independent prognostic significance of hypertetrasomy.
Tumor ploidy levels correlate with prognosis of PDAC patients, indicating characteristic biologic properties of PDAC with high chromosomal instability. In contrast, no prognostic influence on patient outcome was found for the amplification of the HER2 oncogene or p185(HER2) overexpression. Therefore, evaluation of ploidy levels offers new opportunities for patient stratification in clinical trials and enables novel approaches to study the well-known aggressiveness of PDAC. |
| doi_str_mv | 10.1200/JCO.2004.05.142 |
| format | Article |
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Serial tissue sections of 50 resected PDACs were analyzed with chromogenic in situ hybridization using locus-specific HER2 probes and centromeric probes for chromosome 17. Centromeric probes for chromosome 7 and 8 were hybridized to confirm ploidy levels. Expression of HER2 protein was assessed by immunohistochemistry. Correlations of experimental findings with clinical and follow-up data were tested.
The HER2 gene locus was frequently (24%) amplified in PDAC and the rate of overexpression (2+ and 3+) was 10%, but no prognostic significance was found. Copy number analysis of chromosomes 7, 8, and 17 revealed disomic (40%), trisomic (36%), and hypertetrasomic (24%) tumors. Compared with patients with disomic tumors, patients with hypertetrasomic tumors exhibited a significantly decreased relapse-free and overall survival (5.0 v 13.0 months, P = .0144 and 7.0 v 20.0 months, P = .0099, respectively). Multivariate analysis confirmed the independent prognostic significance of hypertetrasomy.
Tumor ploidy levels correlate with prognosis of PDAC patients, indicating characteristic biologic properties of PDAC with high chromosomal instability. In contrast, no prognostic influence on patient outcome was found for the amplification of the HER2 oncogene or p185(HER2) overexpression. Therefore, evaluation of ploidy levels offers new opportunities for patient stratification in clinical trials and enables novel approaches to study the well-known aggressiveness of PDAC.</description><identifier>ISSN: 0732-183X</identifier><identifier>EISSN: 1527-7755</identifier><identifier>DOI: 10.1200/JCO.2004.05.142</identifier><identifier>PMID: 15570074</identifier><language>eng</language><publisher>Baltimore, MD: American Society of Clinical Oncology</publisher><subject>Aneuploidy ; Biological and medical sciences ; Biomarkers, Tumor - analysis ; Biopsy, Needle ; Carcinoma, Pancreatic Ductal - genetics ; Carcinoma, Pancreatic Ductal - mortality ; Carcinoma, Pancreatic Ductal - pathology ; Carcinoma, Pancreatic Ductal - therapy ; Chromosomes, Human, Pair 17 ; Cohort Studies ; Female ; Gene Amplification ; Gene Expression Regulation, Neoplastic ; Genes, erbB-2 - genetics ; Humans ; Immunohistochemistry ; In Situ Hybridization, Fluorescence ; Male ; Medical sciences ; Multivariate Analysis ; Pancreatic Ducts - pathology ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - mortality ; Pancreatic Neoplasms - pathology ; Pancreatic Neoplasms - therapy ; Predictive Value of Tests ; Probability ; Prognosis ; Risk Assessment ; Sampling Studies ; Survival Rate ; Tissue Culture Techniques ; Tumors</subject><ispartof>Journal of clinical oncology, 2004-12, Vol.22 (23), p.4737-4693</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c398t-468e4f09211bf032fb8e39300745e8b8f265bf65796acd8b0678f65c363a795d3</citedby><cites>FETCH-LOGICAL-c398t-468e4f09211bf032fb8e39300745e8b8f265bf65796acd8b0678f65c363a795d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3716,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16316502$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15570074$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>STOECKLEIN, Nikolas H</creatorcontrib><creatorcontrib>LUEBKE, Andreas M</creatorcontrib><creatorcontrib>IZBICKI, Jakob R</creatorcontrib><creatorcontrib>KLEIN, Christoph A</creatorcontrib><creatorcontrib>HOSCH, Stefan B</creatorcontrib><creatorcontrib>ERBERSDOBLER, Andreas</creatorcontrib><creatorcontrib>KNOEFEL, Wolfram T</creatorcontrib><creatorcontrib>SCHRAUT, Winfried</creatorcontrib><creatorcontrib>VERDE, Pablo E</creatorcontrib><creatorcontrib>STERN, Franziska</creatorcontrib><creatorcontrib>SCHEUNEMANN, Peter</creatorcontrib><creatorcontrib>PEIPER, Matthias</creatorcontrib><creatorcontrib>EISENBERGER, Claus F</creatorcontrib><title>Copy Number of Chromosome 17 but Not HER2 Amplification Predicts Clinical Outcome of Patients With Pancreatic Ductal Adenocarcinoma</title><title>Journal of clinical oncology</title><addtitle>J Clin Oncol</addtitle><description>To determine the frequency and the potential clinical use of HER2 (17q21) gene amplification and chromosome 17 aneuploidy in pancreatic ductal adenocarcinoma (PDAC).
Serial tissue sections of 50 resected PDACs were analyzed with chromogenic in situ hybridization using locus-specific HER2 probes and centromeric probes for chromosome 17. Centromeric probes for chromosome 7 and 8 were hybridized to confirm ploidy levels. Expression of HER2 protein was assessed by immunohistochemistry. Correlations of experimental findings with clinical and follow-up data were tested.
The HER2 gene locus was frequently (24%) amplified in PDAC and the rate of overexpression (2+ and 3+) was 10%, but no prognostic significance was found. Copy number analysis of chromosomes 7, 8, and 17 revealed disomic (40%), trisomic (36%), and hypertetrasomic (24%) tumors. Compared with patients with disomic tumors, patients with hypertetrasomic tumors exhibited a significantly decreased relapse-free and overall survival (5.0 v 13.0 months, P = .0144 and 7.0 v 20.0 months, P = .0099, respectively). Multivariate analysis confirmed the independent prognostic significance of hypertetrasomy.
Tumor ploidy levels correlate with prognosis of PDAC patients, indicating characteristic biologic properties of PDAC with high chromosomal instability. In contrast, no prognostic influence on patient outcome was found for the amplification of the HER2 oncogene or p185(HER2) overexpression. Therefore, evaluation of ploidy levels offers new opportunities for patient stratification in clinical trials and enables novel approaches to study the well-known aggressiveness of PDAC.</description><subject>Aneuploidy</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Biopsy, Needle</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Carcinoma, Pancreatic Ductal - mortality</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Carcinoma, Pancreatic Ductal - therapy</subject><subject>Chromosomes, Human, Pair 17</subject><subject>Cohort Studies</subject><subject>Female</subject><subject>Gene Amplification</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, erbB-2 - genetics</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Multivariate Analysis</subject><subject>Pancreatic Ducts - pathology</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - mortality</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Pancreatic Neoplasms - therapy</subject><subject>Predictive Value of Tests</subject><subject>Probability</subject><subject>Prognosis</subject><subject>Risk Assessment</subject><subject>Sampling Studies</subject><subject>Survival Rate</subject><subject>Tissue Culture Techniques</subject><subject>Tumors</subject><issn>0732-183X</issn><issn>1527-7755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1v1DAQhi1ERbctZ27IF-CUrT9iOzmuQqFUVbdCILhZjmOzruJ4azuqeuaP19Gu1NNoZp55pXkA-IDRGhOELm-67brUeo3YGtfkDVhhRkQlBGNvwQoJSirc0L-n4CylB4Rw3VD2DpxixgRCol6B_13YP8O72fcmwmBht4vBhxS8gVjAfs7wLmR4ffWTwI3fj846rbILE7yPZnA6J9iNbirDEW7nrJe7knJfGDOV5R-Xd6WbdDRlpOHXWeeCbgYzBa2idlPw6gKcWDUm8_5Yz8Hvb1e_uuvqdvv9R7e5rTRtm1zVvDG1RS3BuLeIEts3hrZ0-YOZpm8s4ay3nImWKz00PeKiKa2mnCrRsoGeg8-H3H0Mj7NJWXqXtBlHNZkwJ8kFJi1qcQEvD6COIaVorNxH51V8lhjJxbss3uXiXSImi_dy8fEYPffeDK_8UXQBPh0BlYosG4sTl145TjFnaAn6cuB27t_uyUUjk1fjWGKJfNCBEEmorAUV9AWXIJer</recordid><startdate>20041201</startdate><enddate>20041201</enddate><creator>STOECKLEIN, Nikolas H</creator><creator>LUEBKE, Andreas M</creator><creator>IZBICKI, Jakob R</creator><creator>KLEIN, Christoph A</creator><creator>HOSCH, Stefan B</creator><creator>ERBERSDOBLER, Andreas</creator><creator>KNOEFEL, Wolfram T</creator><creator>SCHRAUT, Winfried</creator><creator>VERDE, Pablo E</creator><creator>STERN, Franziska</creator><creator>SCHEUNEMANN, Peter</creator><creator>PEIPER, Matthias</creator><creator>EISENBERGER, Claus F</creator><general>American Society of Clinical Oncology</general><general>Lippincott Williams & Wilkins</general><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></search><sort><creationdate>20041201</creationdate><title>Copy Number of Chromosome 17 but Not HER2 Amplification Predicts Clinical Outcome of Patients With Pancreatic Ductal Adenocarcinoma</title><author>STOECKLEIN, Nikolas H ; LUEBKE, Andreas M ; IZBICKI, Jakob R ; KLEIN, Christoph A ; HOSCH, Stefan B ; ERBERSDOBLER, Andreas ; KNOEFEL, Wolfram T ; SCHRAUT, Winfried ; VERDE, Pablo E ; STERN, Franziska ; SCHEUNEMANN, Peter ; PEIPER, Matthias ; EISENBERGER, Claus F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c398t-468e4f09211bf032fb8e39300745e8b8f265bf65796acd8b0678f65c363a795d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Aneuploidy</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Biopsy, Needle</topic><topic>Carcinoma, Pancreatic Ductal - genetics</topic><topic>Carcinoma, Pancreatic Ductal - mortality</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Carcinoma, Pancreatic Ductal - therapy</topic><topic>Chromosomes, Human, Pair 17</topic><topic>Cohort Studies</topic><topic>Female</topic><topic>Gene Amplification</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, erbB-2 - genetics</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Multivariate Analysis</topic><topic>Pancreatic Ducts - pathology</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - mortality</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Pancreatic Neoplasms - therapy</topic><topic>Predictive Value of Tests</topic><topic>Probability</topic><topic>Prognosis</topic><topic>Risk Assessment</topic><topic>Sampling Studies</topic><topic>Survival Rate</topic><topic>Tissue Culture Techniques</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>STOECKLEIN, Nikolas H</creatorcontrib><creatorcontrib>LUEBKE, Andreas M</creatorcontrib><creatorcontrib>IZBICKI, Jakob R</creatorcontrib><creatorcontrib>KLEIN, Christoph A</creatorcontrib><creatorcontrib>HOSCH, Stefan B</creatorcontrib><creatorcontrib>ERBERSDOBLER, Andreas</creatorcontrib><creatorcontrib>KNOEFEL, Wolfram T</creatorcontrib><creatorcontrib>SCHRAUT, Winfried</creatorcontrib><creatorcontrib>VERDE, Pablo E</creatorcontrib><creatorcontrib>STERN, Franziska</creatorcontrib><creatorcontrib>SCHEUNEMANN, Peter</creatorcontrib><creatorcontrib>PEIPER, Matthias</creatorcontrib><creatorcontrib>EISENBERGER, Claus F</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>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>STOECKLEIN, Nikolas H</au><au>LUEBKE, Andreas M</au><au>IZBICKI, Jakob R</au><au>KLEIN, Christoph A</au><au>HOSCH, Stefan B</au><au>ERBERSDOBLER, Andreas</au><au>KNOEFEL, Wolfram T</au><au>SCHRAUT, Winfried</au><au>VERDE, Pablo E</au><au>STERN, Franziska</au><au>SCHEUNEMANN, Peter</au><au>PEIPER, Matthias</au><au>EISENBERGER, Claus F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Copy Number of Chromosome 17 but Not HER2 Amplification Predicts Clinical Outcome of Patients With Pancreatic Ductal Adenocarcinoma</atitle><jtitle>Journal of clinical oncology</jtitle><addtitle>J Clin Oncol</addtitle><date>2004-12-01</date><risdate>2004</risdate><volume>22</volume><issue>23</issue><spage>4737</spage><epage>4693</epage><pages>4737-4693</pages><issn>0732-183X</issn><eissn>1527-7755</eissn><abstract>To determine the frequency and the potential clinical use of HER2 (17q21) gene amplification and chromosome 17 aneuploidy in pancreatic ductal adenocarcinoma (PDAC).
Serial tissue sections of 50 resected PDACs were analyzed with chromogenic in situ hybridization using locus-specific HER2 probes and centromeric probes for chromosome 17. Centromeric probes for chromosome 7 and 8 were hybridized to confirm ploidy levels. Expression of HER2 protein was assessed by immunohistochemistry. Correlations of experimental findings with clinical and follow-up data were tested.
The HER2 gene locus was frequently (24%) amplified in PDAC and the rate of overexpression (2+ and 3+) was 10%, but no prognostic significance was found. Copy number analysis of chromosomes 7, 8, and 17 revealed disomic (40%), trisomic (36%), and hypertetrasomic (24%) tumors. Compared with patients with disomic tumors, patients with hypertetrasomic tumors exhibited a significantly decreased relapse-free and overall survival (5.0 v 13.0 months, P = .0144 and 7.0 v 20.0 months, P = .0099, respectively). Multivariate analysis confirmed the independent prognostic significance of hypertetrasomy.
Tumor ploidy levels correlate with prognosis of PDAC patients, indicating characteristic biologic properties of PDAC with high chromosomal instability. In contrast, no prognostic influence on patient outcome was found for the amplification of the HER2 oncogene or p185(HER2) overexpression. Therefore, evaluation of ploidy levels offers new opportunities for patient stratification in clinical trials and enables novel approaches to study the well-known aggressiveness of PDAC.</abstract><cop>Baltimore, MD</cop><pub>American Society of Clinical Oncology</pub><pmid>15570074</pmid><doi>10.1200/JCO.2004.05.142</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aneuploidy Biological and medical sciences Biomarkers, Tumor - analysis Biopsy, Needle Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - mortality Carcinoma, Pancreatic Ductal - pathology Carcinoma, Pancreatic Ductal - therapy Chromosomes, Human, Pair 17 Cohort Studies Female Gene Amplification Gene Expression Regulation, Neoplastic Genes, erbB-2 - genetics Humans Immunohistochemistry In Situ Hybridization, Fluorescence Male Medical sciences Multivariate Analysis Pancreatic Ducts - pathology Pancreatic Neoplasms - genetics Pancreatic Neoplasms - mortality Pancreatic Neoplasms - pathology Pancreatic Neoplasms - therapy Predictive Value of Tests Probability Prognosis Risk Assessment Sampling Studies Survival Rate Tissue Culture Techniques Tumors |
| title | Copy Number of Chromosome 17 but Not HER2 Amplification Predicts Clinical Outcome of Patients With Pancreatic Ductal Adenocarcinoma |
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