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Overexpression of cyclo-oxygenase-2 is an independent predictor of unfavourable outcome in node-negative breast cancer, but is not associated with protein kinase B (Akt) and mitogen-activated protein kinase (ERK1/2, p38) activation or with Her-2/neu signalling pathways
Background and aim: The production of prostaglandins is regulated by cyclo-oxygenases (COXs), which also have a role in tumour development and progression in various malignancies, including breast cancer. The mechanisms by which COX-2 contributes to unfavourable prognosis are still poorly understood...
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| Published in: | Journal of clinical pathology 2006-07, Vol.59 (7), p.685-691 |
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| container_title | Journal of clinical pathology |
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| creator | Schmitz, K J Callies, R Wohlschlaeger, J Kimmig, R Otterbach, F Bohr, J Lee, H-S Takeda, A Schmid, K W Baba, H A |
| description | Background and aim: The production of prostaglandins is regulated by cyclo-oxygenases (COXs), which also have a role in tumour development and progression in various malignancies, including breast cancer. The mechanisms by which COX-2 contributes to unfavourable prognosis are still poorly understood. The association between expression of COX-2 and possible linked signalling pathways—namely, Akt, extracellular regulated kinases (ERK1/2), the stress-activated kinase p38 or Her-2/neu—is assessed in a series of 113 node-negative breast cancers. Results: COX-2 was identified as an independent prognostic factor (p = 0.034) in node-negative breast cancer by survival analysis. The lack of a relationship between COX-2 expression and activated Akt, Erk1/2, p38 and Her-2/neu was indicated by statistical analysis. Conclusions: The prognostic effect of COX-2 expression on lymph node-negative breast cancer is confirmed—COX-2 is probably not regulated by HER-2, Akt, Erk1/2 or p38. Further studies are necessary for the elucidation of the signalling pathways responsible for the modification of COX-2 expression and the increased aggressiveness of breast cancers overexpressing COX-2. |
| doi_str_mv | 10.1136/jcp.2005.030650 |
| format | article |
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The mechanisms by which COX-2 contributes to unfavourable prognosis are still poorly understood. The association between expression of COX-2 and possible linked signalling pathways—namely, Akt, extracellular regulated kinases (ERK1/2), the stress-activated kinase p38 or Her-2/neu—is assessed in a series of 113 node-negative breast cancers. Results: COX-2 was identified as an independent prognostic factor (p = 0.034) in node-negative breast cancer by survival analysis. The lack of a relationship between COX-2 expression and activated Akt, Erk1/2, p38 and Her-2/neu was indicated by statistical analysis. Conclusions: The prognostic effect of COX-2 expression on lymph node-negative breast cancer is confirmed—COX-2 is probably not regulated by HER-2, Akt, Erk1/2 or p38. Further studies are necessary for the elucidation of the signalling pathways responsible for the modification of COX-2 expression and the increased aggressiveness of breast cancers overexpressing COX-2.</description><identifier>ISSN: 0021-9746</identifier><identifier>EISSN: 1472-4146</identifier><identifier>DOI: 10.1136/jcp.2005.030650</identifier><identifier>PMID: 16497869</identifier><identifier>CODEN: JCPAAK</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd and Association of Clinical Pathologists</publisher><subject>Aged ; Biomarkers, Tumor - metabolism ; Breast cancer ; Breast Neoplasms - enzymology ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; COX ; cyclo-oxygenase ; Cyclooxygenase 2 - metabolism ; ERK ; extracellular regulated kinases ; familial adenomatous polyposis ; FAP ; Female ; FISH ; fluorescent in situ hybridisation ; Follow-Up Studies ; Genotype & phenotype ; Growth factors ; Humans ; IHC ; Immunoglobulins ; immunohistochemistry ; In Situ Hybridization, Fluorescence ; Kinases ; Lymphatic system ; MAPK ; Medical prognosis ; Middle Aged ; mitogen-activated protein kinase ; Neoplasm Proteins - metabolism ; non-steroidal anti-inflammatory drug ; NSAID ; Original ; p38 Mitogen-Activated Protein Kinases - metabolism ; pAkt ; pERK ; PGE2 ; Phosphatase ; phospho-Akt ; phospho-ERK ; phospho-p38 ; Phosphorylation ; pp38 ; Prognosis ; prostaglandin E2 ; Protein expression ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Receptor, ErbB-2 - metabolism ; Signal Transduction ; sodium salt citrate ; SSC ; Statistical analysis ; Studies ; Survival Analysis ; Tumors</subject><ispartof>Journal of clinical pathology, 2006-07, Vol.59 (7), p.685-691</ispartof><rights>Copyright 2006 Journal of Clinical Pathology</rights><rights>Copyright: 2006 Copyright 2006 Journal of Clinical Pathology</rights><rights>Copyright © 2006 The BMJ Publishing Group and the Association of Clinical Pathologists</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b4380-3401de8e37295491a66888b876f07328fabeb142d818e6157929a03fe8267cd53</citedby><cites>FETCH-LOGICAL-b4380-3401de8e37295491a66888b876f07328fabeb142d818e6157929a03fe8267cd53</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/PMC1860412/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1860412/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,733,786,790,891,27957,27958,53827,53829</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16497869$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schmitz, K J</creatorcontrib><creatorcontrib>Callies, R</creatorcontrib><creatorcontrib>Wohlschlaeger, J</creatorcontrib><creatorcontrib>Kimmig, R</creatorcontrib><creatorcontrib>Otterbach, F</creatorcontrib><creatorcontrib>Bohr, J</creatorcontrib><creatorcontrib>Lee, H-S</creatorcontrib><creatorcontrib>Takeda, A</creatorcontrib><creatorcontrib>Schmid, K W</creatorcontrib><creatorcontrib>Baba, H A</creatorcontrib><title>Overexpression of cyclo-oxygenase-2 is an independent predictor of unfavourable outcome in node-negative breast cancer, but is not associated with protein kinase B (Akt) and mitogen-activated protein kinase (ERK1/2, p38) activation or with Her-2/neu signalling pathways</title><title>Journal of clinical pathology</title><addtitle>J Clin Pathol</addtitle><description>Background and aim: The production of prostaglandins is regulated by cyclo-oxygenases (COXs), which also have a role in tumour development and progression in various malignancies, including breast cancer. The mechanisms by which COX-2 contributes to unfavourable prognosis are still poorly understood. The association between expression of COX-2 and possible linked signalling pathways—namely, Akt, extracellular regulated kinases (ERK1/2), the stress-activated kinase p38 or Her-2/neu—is assessed in a series of 113 node-negative breast cancers. Results: COX-2 was identified as an independent prognostic factor (p = 0.034) in node-negative breast cancer by survival analysis. The lack of a relationship between COX-2 expression and activated Akt, Erk1/2, p38 and Her-2/neu was indicated by statistical analysis. Conclusions: The prognostic effect of COX-2 expression on lymph node-negative breast cancer is confirmed—COX-2 is probably not regulated by HER-2, Akt, Erk1/2 or p38. Further studies are necessary for the elucidation of the signalling pathways responsible for the modification of COX-2 expression and the increased aggressiveness of breast cancers overexpressing COX-2.</description><subject>Aged</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - enzymology</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>COX</subject><subject>cyclo-oxygenase</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>ERK</subject><subject>extracellular regulated kinases</subject><subject>familial adenomatous polyposis</subject><subject>FAP</subject><subject>Female</subject><subject>FISH</subject><subject>fluorescent in situ hybridisation</subject><subject>Follow-Up Studies</subject><subject>Genotype & phenotype</subject><subject>Growth factors</subject><subject>Humans</subject><subject>IHC</subject><subject>Immunoglobulins</subject><subject>immunohistochemistry</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Kinases</subject><subject>Lymphatic system</subject><subject>MAPK</subject><subject>Medical prognosis</subject><subject>Middle Aged</subject><subject>mitogen-activated protein kinase</subject><subject>Neoplasm Proteins - metabolism</subject><subject>non-steroidal anti-inflammatory drug</subject><subject>NSAID</subject><subject>Original</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>pAkt</subject><subject>pERK</subject><subject>PGE2</subject><subject>Phosphatase</subject><subject>phospho-Akt</subject><subject>phospho-ERK</subject><subject>phospho-p38</subject><subject>Phosphorylation</subject><subject>pp38</subject><subject>Prognosis</subject><subject>prostaglandin E2</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Signal Transduction</subject><subject>sodium salt citrate</subject><subject>SSC</subject><subject>Statistical analysis</subject><subject>Studies</subject><subject>Survival Analysis</subject><subject>Tumors</subject><issn>0021-9746</issn><issn>1472-4146</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNqFkktv1DAUhQMC0aF0zQ5ZqoQKajp-JI6zQSpVSxEVlUbA1nKSm6mnGTvYzrTz73GaqkA33dgLf-fch0-SvCX4iBDG56u6P6IY50eYYZ7j58mMZAVNM5LxF8kMY0rSssj4TvLa-xXGhBWEvUp2CM_KQvBy9mzvcgMObnsH3mtrkG1Rva07m9rb7RKM8pBSpD1SBmnTQA_xMAFFvtF1sG4UDKZVGzs4VXWA7BBqu4ZII2MbSA0sVdAbQJUD5QOqlanBHaJqCKOvsQEp722tVYAG3ehwFc1tgKi_1mN99BkdHF-HD7GFBq11sLGtVNXR807xCD44XXwjc3qIeiaiZMLuBnOT-Tm4lM4NDMjrpVFdp80S9Spc3aitf5O8bFXnYe_-3k1-np3-ODlPLy6_fD05vkirjAmcsgyTBgSwgpZ5VhLFuRCiEgVvccGoaFUFFcloI4gATvKipKXCrAVBeVE3OdtNPk2-_VCtoanjSp3qZO_0WrmttErL_1-MvpJLu5FEcJwRGg3e3xs4-3sAH-Ra-xq6Thmwg5dc5IKzgj8JkoJygcUI7j8CV_FL44JGRhBMOS5FpOYTVTvrvYP2oWeC5ZhIGRMpx0TKKZFR8e7fUf_y9xGMQDoB2ge4fXhX7lryghW5_P7rRC7Y4owv8IUcG_048dV69WT1Pwkx--Y</recordid><startdate>200607</startdate><enddate>200607</enddate><creator>Schmitz, K J</creator><creator>Callies, R</creator><creator>Wohlschlaeger, J</creator><creator>Kimmig, R</creator><creator>Otterbach, F</creator><creator>Bohr, J</creator><creator>Lee, H-S</creator><creator>Takeda, A</creator><creator>Schmid, K W</creator><creator>Baba, H A</creator><general>BMJ Publishing Group Ltd and Association of Clinical Pathologists</general><general>BMJ Publishing Group LTD</general><general>BMJ Group</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7TO</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>200607</creationdate><title>Overexpression of cyclo-oxygenase-2 is an independent predictor of unfavourable outcome in node-negative breast cancer, but is not associated with protein kinase B (Akt) and mitogen-activated protein kinase (ERK1/2, p38) activation or with Her-2/neu signalling pathways</title><author>Schmitz, K J ; Callies, R ; Wohlschlaeger, J ; Kimmig, R ; Otterbach, F ; Bohr, J ; Lee, H-S ; Takeda, A ; Schmid, K W ; Baba, H A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b4380-3401de8e37295491a66888b876f07328fabeb142d818e6157929a03fe8267cd53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Aged</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - enzymology</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>COX</topic><topic>cyclo-oxygenase</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>ERK</topic><topic>extracellular regulated kinases</topic><topic>familial adenomatous polyposis</topic><topic>FAP</topic><topic>Female</topic><topic>FISH</topic><topic>fluorescent in situ hybridisation</topic><topic>Follow-Up Studies</topic><topic>Genotype & phenotype</topic><topic>Growth factors</topic><topic>Humans</topic><topic>IHC</topic><topic>Immunoglobulins</topic><topic>immunohistochemistry</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Kinases</topic><topic>Lymphatic system</topic><topic>MAPK</topic><topic>Medical prognosis</topic><topic>Middle Aged</topic><topic>mitogen-activated protein kinase</topic><topic>Neoplasm Proteins - metabolism</topic><topic>non-steroidal anti-inflammatory drug</topic><topic>NSAID</topic><topic>Original</topic><topic>p38 Mitogen-Activated Protein Kinases - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of clinical pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schmitz, K J</au><au>Callies, R</au><au>Wohlschlaeger, J</au><au>Kimmig, R</au><au>Otterbach, F</au><au>Bohr, J</au><au>Lee, H-S</au><au>Takeda, A</au><au>Schmid, K W</au><au>Baba, H A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of cyclo-oxygenase-2 is an independent predictor of unfavourable outcome in node-negative breast cancer, but is not associated with protein kinase B (Akt) and mitogen-activated protein kinase (ERK1/2, p38) activation or with Her-2/neu signalling pathways</atitle><jtitle>Journal of clinical pathology</jtitle><addtitle>J Clin Pathol</addtitle><date>2006-07</date><risdate>2006</risdate><volume>59</volume><issue>7</issue><spage>685</spage><epage>691</epage><pages>685-691</pages><issn>0021-9746</issn><eissn>1472-4146</eissn><coden>JCPAAK</coden><notes>istex:6CD3C917F8A39A6C0751ACE4545F5DFBC948C8D4</notes><notes>Correspondence to:
H A Baba
Institute of Pathology, University Hospital of Essen, D-45147 Essen, Hufelandstr 55, Germany; hideo.baba@medizin.uni-essen.de</notes><notes>local:0590685</notes><notes>ark:/67375/NVC-R3RF6R0L-6</notes><notes>PMID:16497869</notes><notes>href:jclinpath-59-685.pdf</notes><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Background and aim: The production of prostaglandins is regulated by cyclo-oxygenases (COXs), which also have a role in tumour development and progression in various malignancies, including breast cancer. The mechanisms by which COX-2 contributes to unfavourable prognosis are still poorly understood. The association between expression of COX-2 and possible linked signalling pathways—namely, Akt, extracellular regulated kinases (ERK1/2), the stress-activated kinase p38 or Her-2/neu—is assessed in a series of 113 node-negative breast cancers. Results: COX-2 was identified as an independent prognostic factor (p = 0.034) in node-negative breast cancer by survival analysis. The lack of a relationship between COX-2 expression and activated Akt, Erk1/2, p38 and Her-2/neu was indicated by statistical analysis. Conclusions: The prognostic effect of COX-2 expression on lymph node-negative breast cancer is confirmed—COX-2 is probably not regulated by HER-2, Akt, Erk1/2 or p38. Further studies are necessary for the elucidation of the signalling pathways responsible for the modification of COX-2 expression and the increased aggressiveness of breast cancers overexpressing COX-2.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd and Association of Clinical Pathologists</pub><pmid>16497869</pmid><doi>10.1136/jcp.2005.030650</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Biomarkers, Tumor - metabolism Breast cancer Breast Neoplasms - enzymology Breast Neoplasms - metabolism Breast Neoplasms - pathology COX cyclo-oxygenase Cyclooxygenase 2 - metabolism ERK extracellular regulated kinases familial adenomatous polyposis FAP Female FISH fluorescent in situ hybridisation Follow-Up Studies Genotype & phenotype Growth factors Humans IHC Immunoglobulins immunohistochemistry In Situ Hybridization, Fluorescence Kinases Lymphatic system MAPK Medical prognosis Middle Aged mitogen-activated protein kinase Neoplasm Proteins - metabolism non-steroidal anti-inflammatory drug NSAID Original p38 Mitogen-Activated Protein Kinases - metabolism pAkt pERK PGE2 Phosphatase phospho-Akt phospho-ERK phospho-p38 Phosphorylation pp38 Prognosis prostaglandin E2 Protein expression Proteins Proto-Oncogene Proteins c-akt - metabolism Receptor, ErbB-2 - metabolism Signal Transduction sodium salt citrate SSC Statistical analysis Studies Survival Analysis Tumors |
| title | Overexpression of cyclo-oxygenase-2 is an independent predictor of unfavourable outcome in node-negative breast cancer, but is not associated with protein kinase B (Akt) and mitogen-activated protein kinase (ERK1/2, p38) activation or with Her-2/neu signalling pathways |
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