Expression patterns of protein kinase C isoenzymes are characteristically modulated in chronic pancreatitis and pancreatic cancer
We immunohistochemically identified protein kinase C (PKC) isoenzymes and the receptor for activated C-kinase (RACK-1) in normal, chronically inflamed, and malignant pancreas specimens. Expression patterns were specific and consistent for each microanatomic structure. In chronic pancreatitis, the ex...
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| Veröffentlicht in: | American journal of clinical pathology 2003-03, Vol.119 (3), p.392-402 |
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| container_title | American journal of clinical pathology |
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| creator | EVANS, James D CORNFORD, Philip A DUDSON, Andrew NEOPTOLEMOS, John P FOSTER, Christopher S |
| description | We immunohistochemically identified protein kinase C (PKC) isoenzymes and the receptor for activated C-kinase (RACK-1) in normal, chronically inflamed, and malignant pancreas specimens. Expression patterns were specific and consistent for each microanatomic structure. In chronic pancreatitis, the expression patterns by epithelial cells were indistinguishable from those in normal pancreas. In the stroma, there was a gain of PKC-delta (P < .05) and loss of PKC-mu (P < .0001). Expression in pancreatic duct carcinomas, compared with control normal minor ductular epithelial cells, revealed relative loss of PKC-epsilon (P < .0001), PKC-iota (P = .005), and PKC-theta (P < .0001) but no gain in any isoenzyme. Compared with control normal major duct epithelial cells, the principal differences were a relative loss in PKC-gamma (P < .05) and a relative gain in PKC-beta (P < .05), PKC-iota (P < .05), and PKC-zeta (P < .005). The stroma adjacent to ductal carcinomas was characterized by prominent expression of PKC-mu and a gain in PKC-delta (P < .0001) and PKC-zeta (P > .005). Ampullary carcinomas revealed a relative gain of PKC-iota (P < .05) and RACK-1 (P < .05). In the adjacent stroma was enhanced expression of PKC-delta (P < .005) and PKC-gamma (P < .001) and loss of PKC-mu (P < .05). Specific changes in isoenzyme expression in stroma of chronic pancreatitis and in epithelial cells and stroma of ductal and ampullary pancreatic adenocarcinomas reflect specific modulation of intracellular signaling pathways that control critical homeostatic mechanisms. |
| doi_str_mv | 10.1309/BKPC9DX98R781B87 |
| format | Article |
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Expression patterns were specific and consistent for each microanatomic structure. In chronic pancreatitis, the expression patterns by epithelial cells were indistinguishable from those in normal pancreas. In the stroma, there was a gain of PKC-delta (P < .05) and loss of PKC-mu (P < .0001). Expression in pancreatic duct carcinomas, compared with control normal minor ductular epithelial cells, revealed relative loss of PKC-epsilon (P < .0001), PKC-iota (P = .005), and PKC-theta (P < .0001) but no gain in any isoenzyme. Compared with control normal major duct epithelial cells, the principal differences were a relative loss in PKC-gamma (P < .05) and a relative gain in PKC-beta (P < .05), PKC-iota (P < .05), and PKC-zeta (P < .005). The stroma adjacent to ductal carcinomas was characterized by prominent expression of PKC-mu and a gain in PKC-delta (P < .0001) and PKC-zeta (P > .005). Ampullary carcinomas revealed a relative gain of PKC-iota (P < .05) and RACK-1 (P < .05). In the adjacent stroma was enhanced expression of PKC-delta (P < .005) and PKC-gamma (P < .001) and loss of PKC-mu (P < .05). Specific changes in isoenzyme expression in stroma of chronic pancreatitis and in epithelial cells and stroma of ductal and ampullary pancreatic adenocarcinomas reflect specific modulation of intracellular signaling pathways that control critical homeostatic mechanisms.]]></description><identifier>ISSN: 0002-9173</identifier><identifier>EISSN: 1943-7722</identifier><identifier>DOI: 10.1309/BKPC9DX98R781B87</identifier><identifier>PMID: 12645342</identifier><identifier>CODEN: AJCPAI</identifier><language>eng</language><publisher>Chicago, IL: American Society of Clinical Pathologists</publisher><subject>Biological and medical sciences ; Carcinoma, Pancreatic Ductal - enzymology ; Carcinoma, Pancreatic Ductal - pathology ; Chronic Disease ; Gastroenterology. Liver. Pancreas. Abdomen ; Humans ; Immunoenzyme Techniques ; Isoenzymes - metabolism ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Medical sciences ; Other diseases. Semiology ; Pancreas - anatomy & histology ; Pancreas - enzymology ; Pancreas - pathology ; Pancreatic Neoplasms - enzymology ; Pancreatic Neoplasms - pathology ; Pancreatitis - enzymology ; Pancreatitis - pathology ; Protein Kinase C - classification ; Protein Kinase C - metabolism ; Receptors for Activated C Kinase ; Receptors, Cell Surface - metabolism ; Tumors</subject><ispartof>American journal of clinical pathology, 2003-03, Vol.119 (3), p.392-402</ispartof><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c367t-61d002980f37356cc26adf31a0c91140e0527004fbedd0671483f1514967f6ce3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27915,27916</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14598598$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12645342$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>EVANS, James D</creatorcontrib><creatorcontrib>CORNFORD, Philip A</creatorcontrib><creatorcontrib>DUDSON, Andrew</creatorcontrib><creatorcontrib>NEOPTOLEMOS, John P</creatorcontrib><creatorcontrib>FOSTER, Christopher S</creatorcontrib><title>Expression patterns of protein kinase C isoenzymes are characteristically modulated in chronic pancreatitis and pancreatic cancer</title><title>American journal of clinical pathology</title><addtitle>Am J Clin Pathol</addtitle><description><![CDATA[We immunohistochemically identified protein kinase C (PKC) isoenzymes and the receptor for activated C-kinase (RACK-1) in normal, chronically inflamed, and malignant pancreas specimens. Expression patterns were specific and consistent for each microanatomic structure. In chronic pancreatitis, the expression patterns by epithelial cells were indistinguishable from those in normal pancreas. In the stroma, there was a gain of PKC-delta (P < .05) and loss of PKC-mu (P < .0001). Expression in pancreatic duct carcinomas, compared with control normal minor ductular epithelial cells, revealed relative loss of PKC-epsilon (P < .0001), PKC-iota (P = .005), and PKC-theta (P < .0001) but no gain in any isoenzyme. Compared with control normal major duct epithelial cells, the principal differences were a relative loss in PKC-gamma (P < .05) and a relative gain in PKC-beta (P < .05), PKC-iota (P < .05), and PKC-zeta (P < .005). The stroma adjacent to ductal carcinomas was characterized by prominent expression of PKC-mu and a gain in PKC-delta (P < .0001) and PKC-zeta (P > .005). Ampullary carcinomas revealed a relative gain of PKC-iota (P < .05) and RACK-1 (P < .05). In the adjacent stroma was enhanced expression of PKC-delta (P < .005) and PKC-gamma (P < .001) and loss of PKC-mu (P < .05). Specific changes in isoenzyme expression in stroma of chronic pancreatitis and in epithelial cells and stroma of ductal and ampullary pancreatic adenocarcinomas reflect specific modulation of intracellular signaling pathways that control critical homeostatic mechanisms.]]></description><subject>Biological and medical sciences</subject><subject>Carcinoma, Pancreatic Ductal - enzymology</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Chronic Disease</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>Isoenzymes - metabolism</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Medical sciences</subject><subject>Other diseases. Semiology</subject><subject>Pancreas - anatomy & histology</subject><subject>Pancreas - enzymology</subject><subject>Pancreas - pathology</subject><subject>Pancreatic Neoplasms - enzymology</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Pancreatitis - enzymology</subject><subject>Pancreatitis - pathology</subject><subject>Protein Kinase C - classification</subject><subject>Protein Kinase C - metabolism</subject><subject>Receptors for Activated C Kinase</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Tumors</subject><issn>0002-9173</issn><issn>1943-7722</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkM9rFDEYhoNY7LZ69yS56G3aL5PMZHK021_ShZai4G3IZr7Q6ExmzZcF11v_cyNdWBACCeF5X3gfxt4LOBMSzPnF3cPSXH433aPuxEWnX7GFMEpWWtf1a7YAgLoyQstjdkL0A0DUHag37FjUrWqkqhfs-er3JiFRmCPf2JwxReKz55s0ZwyR_wzREvIlDzRj_LObkLhNyN2TTdYVPFAOzo7jjk_zsB1txoGXnHtKcwyudEaX0OaQQwnG4fDhuCtPTG_Zkbcj4bv9fcq-XV99Xd5Wq_ubL8vPq8rJVueqFUNZYzrwUsumda5u7eClsOCMEAoQmloDKL_GYYBWC9VJLxqhTKt961Cesk8vvWXary1S7qdADsfRRpy31Osi1BS4gPACujQTJfT9JoXJpl0voP-nvf9fe4l82Hdv1xMOh8DecwE-7gFLxZZPZXqgA6ca05Uj_wIwlo1v</recordid><startdate>20030301</startdate><enddate>20030301</enddate><creator>EVANS, James D</creator><creator>CORNFORD, Philip A</creator><creator>DUDSON, Andrew</creator><creator>NEOPTOLEMOS, John P</creator><creator>FOSTER, Christopher S</creator><general>American Society of Clinical Pathologists</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>20030301</creationdate><title>Expression patterns of protein kinase C isoenzymes are characteristically modulated in chronic pancreatitis and pancreatic cancer</title><author>EVANS, James D ; CORNFORD, Philip A ; DUDSON, Andrew ; NEOPTOLEMOS, John P ; FOSTER, Christopher S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c367t-61d002980f37356cc26adf31a0c91140e0527004fbedd0671483f1514967f6ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Biological and medical sciences</topic><topic>Carcinoma, Pancreatic Ductal - enzymology</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Chronic Disease</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>Isoenzymes - metabolism</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Medical sciences</topic><topic>Other diseases. Semiology</topic><topic>Pancreas - anatomy & histology</topic><topic>Pancreas - enzymology</topic><topic>Pancreas - pathology</topic><topic>Pancreatic Neoplasms - enzymology</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Pancreatitis - enzymology</topic><topic>Pancreatitis - pathology</topic><topic>Protein Kinase C - classification</topic><topic>Protein Kinase C - metabolism</topic><topic>Receptors for Activated C Kinase</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>EVANS, James D</creatorcontrib><creatorcontrib>CORNFORD, Philip A</creatorcontrib><creatorcontrib>DUDSON, Andrew</creatorcontrib><creatorcontrib>NEOPTOLEMOS, John P</creatorcontrib><creatorcontrib>FOSTER, Christopher S</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>American journal of clinical pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>EVANS, James D</au><au>CORNFORD, Philip A</au><au>DUDSON, Andrew</au><au>NEOPTOLEMOS, John P</au><au>FOSTER, Christopher S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression patterns of protein kinase C isoenzymes are characteristically modulated in chronic pancreatitis and pancreatic cancer</atitle><jtitle>American journal of clinical pathology</jtitle><addtitle>Am J Clin Pathol</addtitle><date>2003-03-01</date><risdate>2003</risdate><volume>119</volume><issue>3</issue><spage>392</spage><epage>402</epage><pages>392-402</pages><issn>0002-9173</issn><eissn>1943-7722</eissn><coden>AJCPAI</coden><abstract><![CDATA[We immunohistochemically identified protein kinase C (PKC) isoenzymes and the receptor for activated C-kinase (RACK-1) in normal, chronically inflamed, and malignant pancreas specimens. Expression patterns were specific and consistent for each microanatomic structure. In chronic pancreatitis, the expression patterns by epithelial cells were indistinguishable from those in normal pancreas. In the stroma, there was a gain of PKC-delta (P < .05) and loss of PKC-mu (P < .0001). Expression in pancreatic duct carcinomas, compared with control normal minor ductular epithelial cells, revealed relative loss of PKC-epsilon (P < .0001), PKC-iota (P = .005), and PKC-theta (P < .0001) but no gain in any isoenzyme. Compared with control normal major duct epithelial cells, the principal differences were a relative loss in PKC-gamma (P < .05) and a relative gain in PKC-beta (P < .05), PKC-iota (P < .05), and PKC-zeta (P < .005). The stroma adjacent to ductal carcinomas was characterized by prominent expression of PKC-mu and a gain in PKC-delta (P < .0001) and PKC-zeta (P > .005). Ampullary carcinomas revealed a relative gain of PKC-iota (P < .05) and RACK-1 (P < .05). In the adjacent stroma was enhanced expression of PKC-delta (P < .005) and PKC-gamma (P < .001) and loss of PKC-mu (P < .05). Specific changes in isoenzyme expression in stroma of chronic pancreatitis and in epithelial cells and stroma of ductal and ampullary pancreatic adenocarcinomas reflect specific modulation of intracellular signaling pathways that control critical homeostatic mechanisms.]]></abstract><cop>Chicago, IL</cop><pub>American Society of Clinical Pathologists</pub><pmid>12645342</pmid><doi>10.1309/BKPC9DX98R781B87</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Biological and medical sciences Carcinoma, Pancreatic Ductal - enzymology Carcinoma, Pancreatic Ductal - pathology Chronic Disease Gastroenterology. Liver. Pancreas. Abdomen Humans Immunoenzyme Techniques Isoenzymes - metabolism Liver. Biliary tract. Portal circulation. Exocrine pancreas Medical sciences Other diseases. Semiology Pancreas - anatomy & histology Pancreas - enzymology Pancreas - pathology Pancreatic Neoplasms - enzymology Pancreatic Neoplasms - pathology Pancreatitis - enzymology Pancreatitis - pathology Protein Kinase C - classification Protein Kinase C - metabolism Receptors for Activated C Kinase Receptors, Cell Surface - metabolism Tumors |
| title | Expression patterns of protein kinase C isoenzymes are characteristically modulated in chronic pancreatitis and pancreatic cancer |
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