Expression of the epidermal growth factor receptor family in prostate carcinoma before and during androgen-independence
Novel palliative strategies for patients with androgen-independent prostate cancer (AIPC) include targeting the epidermal growth factor receptor (EGFR) family. The aim of the present study was to investigate intrapatient changes of EGFRs during the development of AIPC. In total, 106 symptomatic AIPC...
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| Veröffentlicht in: | British journal of cancer 2004-01, Vol.90 (2), p.449-454 |
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| creator | Hernes, E Fosså, S D Berner, Aa Otnes, B Nesland, J M |
| description | Novel palliative strategies for patients with androgen-independent prostate cancer (AIPC) include targeting the epidermal growth factor receptor (EGFR) family. The aim of the present study was to investigate intrapatient changes of EGFRs during the development of AIPC. In total, 106 symptomatic AIPC patients were identified in whom prostatic biopsies (adenocarcinoma) were available both before the start of androgen deprivation (PRTR biopsy) and after the development of AIPC (AIPC biopsy). All four known subgroups of the EGFR family were determined by immunohistochemistry (IHC): c-erbB-1 (EGFR), c-erbB-2 (HER2/neu), c-erbB-3 (HER3) and c-erbB-4 (HER4). Moderate to strong membrane-specific staining was recorded semiquantitatively ( |
| doi_str_mv | 10.1038/sj.bjc.6601536 |
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vs
⩾10%=IHC stained tumour cells: ‘negative’
vs
‘positive’ staining). The medical records were reviewed for clinical variables. During the development of AIPC, intrapatient changes occurred in two opposite directions for each of the four EGFRs: negativity changed to positivity, and vice versa, statistically significant only for the increase of c-erbB-1 expression (
P
=0.001). The c-erbB-2 expression in the AIPC biopsy was associated with a significantly shorter survival from the time of the AIPC biopsy (
P
=0.029). Our results support ongoing therapeutic attempts of EGFR inhibition in subgroups of patients with prostate cancer. Further research is needed to understand the function of EGFRs in this malignancy.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/sj.bjc.6601536</identifier><identifier>PMID: 14735192</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adenocarcinoma - drug therapy ; Adenocarcinoma - genetics ; Adenocarcinoma - pathology ; Aged ; Aged, 80 and over ; Androgen Antagonists - pharmacology ; Androgens ; Biological and medical sciences ; Biomarkers, Tumor - analysis ; Biomedical and Life Sciences ; Biomedicine ; Biopsy ; Cancer Research ; Drug Resistance ; Drug Resistance, Neoplasm ; Epidemiology ; Epidermal growth factor ; Hospitals ; Humans ; Immunohistochemistry ; Male ; Medical research ; Medical sciences ; Middle Aged ; Molecular and Cellular Pathology ; Molecular Medicine ; Oncology ; Prostate cancer ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - pathology ; Receptor, Epidermal Growth Factor - analysis ; Receptor, Epidermal Growth Factor - biosynthesis ; Receptor, Epidermal Growth Factor - genetics ; Retrospective Studies ; Survival Analysis ; Tumors</subject><ispartof>British journal of cancer, 2004-01, Vol.90 (2), p.449-454</ispartof><rights>The Author(s) 2004</rights><rights>2004 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 26, 2004</rights><rights>Copyright © 2004 Cancer Research UK 2004 Cancer Research UK</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c580t-2d8cb5ebe1b1cfaa1ea559ed9170b55f229e306a1dc33d19d760e5705b70ae1a3</citedby><cites>FETCH-LOGICAL-c580t-2d8cb5ebe1b1cfaa1ea559ed9170b55f229e306a1dc33d19d760e5705b70ae1a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2410152/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2410152/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,41467,42536,51297,53769,53771</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15678383$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14735192$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hernes, E</creatorcontrib><creatorcontrib>Fosså, S D</creatorcontrib><creatorcontrib>Berner, Aa</creatorcontrib><creatorcontrib>Otnes, B</creatorcontrib><creatorcontrib>Nesland, J M</creatorcontrib><title>Expression of the epidermal growth factor receptor family in prostate carcinoma before and during androgen-independence</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Novel palliative strategies for patients with androgen-independent prostate cancer (AIPC) include targeting the epidermal growth factor receptor (EGFR) family. The aim of the present study was to investigate intrapatient changes of EGFRs during the development of AIPC. In total, 106 symptomatic AIPC patients were identified in whom prostatic biopsies (adenocarcinoma) were available both before the start of androgen deprivation (PRTR biopsy) and after the development of AIPC (AIPC biopsy). All four known subgroups of the EGFR family were determined by immunohistochemistry (IHC): c-erbB-1 (EGFR), c-erbB-2 (HER2/neu), c-erbB-3 (HER3) and c-erbB-4 (HER4). Moderate to strong membrane-specific staining was recorded semiquantitatively (<10%
vs
⩾10%=IHC stained tumour cells: ‘negative’
vs
‘positive’ staining). The medical records were reviewed for clinical variables. During the development of AIPC, intrapatient changes occurred in two opposite directions for each of the four EGFRs: negativity changed to positivity, and vice versa, statistically significant only for the increase of c-erbB-1 expression (
P
=0.001). The c-erbB-2 expression in the AIPC biopsy was associated with a significantly shorter survival from the time of the AIPC biopsy (
P
=0.029). Our results support ongoing therapeutic attempts of EGFR inhibition in subgroups of patients with prostate cancer. Further research is needed to understand the function of EGFRs in this malignancy.</description><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - pathology</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Androgen Antagonists - pharmacology</subject><subject>Androgens</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Biopsy</subject><subject>Cancer Research</subject><subject>Drug Resistance</subject><subject>Drug Resistance, Neoplasm</subject><subject>Epidemiology</subject><subject>Epidermal growth factor</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Molecular and Cellular Pathology</subject><subject>Molecular Medicine</subject><subject>Oncology</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Receptor, Epidermal Growth Factor - analysis</subject><subject>Receptor, Epidermal Growth Factor - biosynthesis</subject><subject>Receptor, Epidermal Growth Factor - genetics</subject><subject>Retrospective Studies</subject><subject>Survival Analysis</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkc-L1DAUx4Mo7rh69ShB0Ftnk3TStBdBlvUHLHjRc3hNXmdS2qQm7a7735thiqOCeMl7IZ98348vIS8523JW1lep37a92VYV47KsHpFNDqLgtVCPyYYxpgrWCHZBnqXU52vDavWUXPCdKiVvxIbc3_yYIqbkgqeho_MBKU7OYhxhoPsY7ucD7cDMIdKIBqdj0sHohgfqPJ1iSDPMSA1E43wYgbbYhYgUvKV2ic7vj2kMe_SF8xYnzIc3-Jw86WBI-GKNl-Tbh5uv15-K2y8fP1-_vy2MrNlcCFubVmKLvOWmA-AIUjZoG65YK2UnRIMlq4BbU5aWN1ZVDKVislUMkEN5Sd6ddKelHdEa9HOEQU_RjRAfdACn_3zx7qD34U6LHc8rFVng7SoQw_cF06xHlwwOA3gMS9I147wu6-q_IFdCVeWOZfD1X2AflujzFnQep6myNXWGtifI5BWniN2vljnTR-d16nV2Xq_O5w-vfh_0jK9WZ-DNCkAyMHQRvHHpzMlK5TnKzF2duDQd7cN4bu8fpX8CGsjKnw</recordid><startdate>20040126</startdate><enddate>20040126</enddate><creator>Hernes, E</creator><creator>Fosså, S D</creator><creator>Berner, Aa</creator><creator>Otnes, B</creator><creator>Nesland, J M</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>3V.</scope><scope>7RV</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20040126</creationdate><title>Expression of the epidermal growth factor receptor family in prostate carcinoma before and during androgen-independence</title><author>Hernes, E ; Fosså, S D ; Berner, Aa ; Otnes, B ; Nesland, J M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c580t-2d8cb5ebe1b1cfaa1ea559ed9170b55f229e306a1dc33d19d760e5705b70ae1a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - pathology</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Androgen Antagonists - pharmacology</topic><topic>Androgens</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Biopsy</topic><topic>Cancer Research</topic><topic>Drug Resistance</topic><topic>Drug Resistance, Neoplasm</topic><topic>Epidemiology</topic><topic>Epidermal growth factor</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Molecular and Cellular Pathology</topic><topic>Molecular Medicine</topic><topic>Oncology</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - 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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>Hernes, E</au><au>Fosså, S D</au><au>Berner, Aa</au><au>Otnes, B</au><au>Nesland, J M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of the epidermal growth factor receptor family in prostate carcinoma before and during androgen-independence</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2004-01-26</date><risdate>2004</risdate><volume>90</volume><issue>2</issue><spage>449</spage><epage>454</epage><pages>449-454</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Novel palliative strategies for patients with androgen-independent prostate cancer (AIPC) include targeting the epidermal growth factor receptor (EGFR) family. The aim of the present study was to investigate intrapatient changes of EGFRs during the development of AIPC. In total, 106 symptomatic AIPC patients were identified in whom prostatic biopsies (adenocarcinoma) were available both before the start of androgen deprivation (PRTR biopsy) and after the development of AIPC (AIPC biopsy). All four known subgroups of the EGFR family were determined by immunohistochemistry (IHC): c-erbB-1 (EGFR), c-erbB-2 (HER2/neu), c-erbB-3 (HER3) and c-erbB-4 (HER4). Moderate to strong membrane-specific staining was recorded semiquantitatively (<10%
vs
⩾10%=IHC stained tumour cells: ‘negative’
vs
‘positive’ staining). The medical records were reviewed for clinical variables. During the development of AIPC, intrapatient changes occurred in two opposite directions for each of the four EGFRs: negativity changed to positivity, and vice versa, statistically significant only for the increase of c-erbB-1 expression (
P
=0.001). The c-erbB-2 expression in the AIPC biopsy was associated with a significantly shorter survival from the time of the AIPC biopsy (
P
=0.029). Our results support ongoing therapeutic attempts of EGFR inhibition in subgroups of patients with prostate cancer. Further research is needed to understand the function of EGFRs in this malignancy.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>14735192</pmid><doi>10.1038/sj.bjc.6601536</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma - drug therapy Adenocarcinoma - genetics Adenocarcinoma - pathology Aged Aged, 80 and over Androgen Antagonists - pharmacology Androgens Biological and medical sciences Biomarkers, Tumor - analysis Biomedical and Life Sciences Biomedicine Biopsy Cancer Research Drug Resistance Drug Resistance, Neoplasm Epidemiology Epidermal growth factor Hospitals Humans Immunohistochemistry Male Medical research Medical sciences Middle Aged Molecular and Cellular Pathology Molecular Medicine Oncology Prostate cancer Prostatic Neoplasms - drug therapy Prostatic Neoplasms - genetics Prostatic Neoplasms - pathology Receptor, Epidermal Growth Factor - analysis Receptor, Epidermal Growth Factor - biosynthesis Receptor, Epidermal Growth Factor - genetics Retrospective Studies Survival Analysis Tumors |
| title | Expression of the epidermal growth factor receptor family in prostate carcinoma before and during androgen-independence |
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