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Human glandular kallikrein 2 expression in prostate adenocarcinoma and lymph node metastases
Objectives. To describe the expression of a potential new tumor marker, human glandular kallikrein 2 (hK2), in primary adenocarcinoma and lymph node metastases that may be useful as an adjunct to prostate-specific antigen (PSA) in the diagnosis and monitoring of prostate cancer. Methods. We evaluate...
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Published in: | Urology (Ridgewood, N.J.) N.J.), 1999-05, Vol.53 (5), p.939-944 |
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container_title | Urology (Ridgewood, N.J.) |
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creator | Darson, Micheal F Pacelli, Anna Roche, Patrick Rittenhouse, Harry G Wolfert, Robert L Saeid, Mohammad S Young, Charles Y.F Klee, George G Tindall, Donald J Bostwick, David G |
description | Objectives. To describe the expression of a potential new tumor marker, human glandular kallikrein 2 (hK2), in primary adenocarcinoma and lymph node metastases that may be useful as an adjunct to prostate-specific antigen (PSA) in the diagnosis and monitoring of prostate cancer.
Methods. We evaluated 151 radical prostatectomy specimens removed at Mayo Clinic with node-positive adenocarcinoma to compare cytoplasmic expression of hK2, pro-hK2, and PSA in benign tissue, prostate adenocarcinoma, and lymph node metastases. Monoclonal antibodies for mature hK2 (hK2-G586), pro-hK2 (pro-hK2-G464), and PSA (PSA-773) were used. A polyclonal antibody for PSA was also used. Immunoreactivity in each case was tested to determine whether cancer recurrence could be predicted.
Results. Intense epithelial cytoplasmic immunoreactivity was observed in every case for hK2-G586, pro-hK2-G464, PSA-773, and polyclonal PSA (100% of cases, respectively). The intensity and extent of hK2 expression was greater in lymph node metastases than in primary cancer; furthermore, the expression in primary cancer was greater than in benign epithelium. Pro-hK2 was expressed in a greater percentage of cells in primary cancer than in benign tissue; furthermore, pro-hK2 was expressed to a greater extent in primary cancer than in lymph node metastases. In marked contrast to mature hK2, monoclonal PSA immunoreactivity was expressed to a higher extent in primary cancer than in lymph node metastases. Polyclonal PSA showed an incremental increase in expression from benign tissue to primary cancer and a further increase in expression in lymph node metastases.
Conclusions. hK2 was expressed in every cancer, and the expression incrementally increased from benign epithelium to primary cancer and lymph node metastases. Pro-hK2 was expressed to the greatest extent in primary cancer. Monoclonal PSA displayed inverse immunoreactivity compared with hK2. Polyclonal PSA showed incremental increases, suggesting that both hK2 and PSA were being detected. Tissue expression of hK2 appears to be regulated independently of PSA in benign epithelium, adenocarcinoma, and lymph node metastases. |
doi_str_mv | 10.1016/S0090-4295(98)00637-2 |
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Methods. We evaluated 151 radical prostatectomy specimens removed at Mayo Clinic with node-positive adenocarcinoma to compare cytoplasmic expression of hK2, pro-hK2, and PSA in benign tissue, prostate adenocarcinoma, and lymph node metastases. Monoclonal antibodies for mature hK2 (hK2-G586), pro-hK2 (pro-hK2-G464), and PSA (PSA-773) were used. A polyclonal antibody for PSA was also used. Immunoreactivity in each case was tested to determine whether cancer recurrence could be predicted.
Results. Intense epithelial cytoplasmic immunoreactivity was observed in every case for hK2-G586, pro-hK2-G464, PSA-773, and polyclonal PSA (100% of cases, respectively). The intensity and extent of hK2 expression was greater in lymph node metastases than in primary cancer; furthermore, the expression in primary cancer was greater than in benign epithelium. Pro-hK2 was expressed in a greater percentage of cells in primary cancer than in benign tissue; furthermore, pro-hK2 was expressed to a greater extent in primary cancer than in lymph node metastases. In marked contrast to mature hK2, monoclonal PSA immunoreactivity was expressed to a higher extent in primary cancer than in lymph node metastases. Polyclonal PSA showed an incremental increase in expression from benign tissue to primary cancer and a further increase in expression in lymph node metastases.
Conclusions. hK2 was expressed in every cancer, and the expression incrementally increased from benign epithelium to primary cancer and lymph node metastases. Pro-hK2 was expressed to the greatest extent in primary cancer. Monoclonal PSA displayed inverse immunoreactivity compared with hK2. Polyclonal PSA showed incremental increases, suggesting that both hK2 and PSA were being detected. Tissue expression of hK2 appears to be regulated independently of PSA in benign epithelium, adenocarcinoma, and lymph node metastases.</description><identifier>ISSN: 0090-4295</identifier><identifier>EISSN: 1527-9995</identifier><identifier>DOI: 10.1016/S0090-4295(98)00637-2</identifier><identifier>PMID: 10223487</identifier><identifier>CODEN: URGYAZ</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adenocarcinoma - chemistry ; Adenocarcinoma - metabolism ; Adenocarcinoma - secondary ; Aged ; Biological and medical sciences ; Biomarkers, Tumor - analysis ; Biomarkers, Tumor - biosynthesis ; Humans ; Kallikreins - analysis ; Kallikreins - biosynthesis ; Lymphatic Metastasis ; Male ; Medical sciences ; Middle Aged ; Nephrology. Urinary tract diseases ; Prostate-Specific Antigen - biosynthesis ; Prostatic Neoplasms - chemistry ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Tissue Kallikreins ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>Urology (Ridgewood, N.J.), 1999-05, Vol.53 (5), p.939-944</ispartof><rights>1999 Elsevier Science Inc.</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-e855bb1a33af1374bce45339fdc9fe39aa6e4b86810411e63393f2f48a405ddf3</citedby><cites>FETCH-LOGICAL-c419t-e855bb1a33af1374bce45339fdc9fe39aa6e4b86810411e63393f2f48a405ddf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1773417$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10223487$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Darson, Micheal F</creatorcontrib><creatorcontrib>Pacelli, Anna</creatorcontrib><creatorcontrib>Roche, Patrick</creatorcontrib><creatorcontrib>Rittenhouse, Harry G</creatorcontrib><creatorcontrib>Wolfert, Robert L</creatorcontrib><creatorcontrib>Saeid, Mohammad S</creatorcontrib><creatorcontrib>Young, Charles Y.F</creatorcontrib><creatorcontrib>Klee, George G</creatorcontrib><creatorcontrib>Tindall, Donald J</creatorcontrib><creatorcontrib>Bostwick, David G</creatorcontrib><title>Human glandular kallikrein 2 expression in prostate adenocarcinoma and lymph node metastases</title><title>Urology (Ridgewood, N.J.)</title><addtitle>Urology</addtitle><description>Objectives. To describe the expression of a potential new tumor marker, human glandular kallikrein 2 (hK2), in primary adenocarcinoma and lymph node metastases that may be useful as an adjunct to prostate-specific antigen (PSA) in the diagnosis and monitoring of prostate cancer.
Methods. We evaluated 151 radical prostatectomy specimens removed at Mayo Clinic with node-positive adenocarcinoma to compare cytoplasmic expression of hK2, pro-hK2, and PSA in benign tissue, prostate adenocarcinoma, and lymph node metastases. Monoclonal antibodies for mature hK2 (hK2-G586), pro-hK2 (pro-hK2-G464), and PSA (PSA-773) were used. A polyclonal antibody for PSA was also used. Immunoreactivity in each case was tested to determine whether cancer recurrence could be predicted.
Results. Intense epithelial cytoplasmic immunoreactivity was observed in every case for hK2-G586, pro-hK2-G464, PSA-773, and polyclonal PSA (100% of cases, respectively). The intensity and extent of hK2 expression was greater in lymph node metastases than in primary cancer; furthermore, the expression in primary cancer was greater than in benign epithelium. Pro-hK2 was expressed in a greater percentage of cells in primary cancer than in benign tissue; furthermore, pro-hK2 was expressed to a greater extent in primary cancer than in lymph node metastases. In marked contrast to mature hK2, monoclonal PSA immunoreactivity was expressed to a higher extent in primary cancer than in lymph node metastases. Polyclonal PSA showed an incremental increase in expression from benign tissue to primary cancer and a further increase in expression in lymph node metastases.
Conclusions. hK2 was expressed in every cancer, and the expression incrementally increased from benign epithelium to primary cancer and lymph node metastases. Pro-hK2 was expressed to the greatest extent in primary cancer. Monoclonal PSA displayed inverse immunoreactivity compared with hK2. Polyclonal PSA showed incremental increases, suggesting that both hK2 and PSA were being detected. Tissue expression of hK2 appears to be regulated independently of PSA in benign epithelium, adenocarcinoma, and lymph node metastases.</description><subject>Adenocarcinoma - chemistry</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - secondary</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Biomarkers, Tumor - biosynthesis</subject><subject>Humans</subject><subject>Kallikreins - analysis</subject><subject>Kallikreins - biosynthesis</subject><subject>Lymphatic Metastasis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Prostate-Specific Antigen - biosynthesis</subject><subject>Prostatic Neoplasms - chemistry</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Tissue Kallikreins</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><issn>0090-4295</issn><issn>1527-9995</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNqFkEtv1DAURq0K1A4DP6HIC4RgEbBjJ45XFar6kiqxAHZI1o19XUwTZ7CTqv33eDoj2h0r68rnu49DyDFnnzjj7edvjGlWyVo3H3T3kbFWqKo-ICve1KrSWjcvyOofckRe5fybFapt1SE54qyuhezUivy8XEaI9GaA6JYBEr2FYQi3CUOkNcX7TcKcwxRpqTdpyjPMSMFhnCwkG-I0Ai1ROjyMm180Tg7piDMULmN-TV56GDK-2b9r8uP87PvpZXX99eLq9Mt1ZSXXc4Vd0_Q9ByHAc6Fkb1E2QmjvrPYoNECLsu_ajjPJObblS_jayw4ka5zzYk3e7_qWDf8smGczhmxxKEfhtGTTasVVV3Jr0uxAW07JCb3ZpDBCejCcma1W86jVbJ0Z3ZlHraYuubf7AUs_onuW2nkswLs9ANnC4BNEG_ITp5SQfIud7DAsNu4CJpNtwGjRhYR2Nm4K_9nkLwuLlUI</recordid><startdate>19990501</startdate><enddate>19990501</enddate><creator>Darson, Micheal F</creator><creator>Pacelli, Anna</creator><creator>Roche, Patrick</creator><creator>Rittenhouse, Harry G</creator><creator>Wolfert, Robert L</creator><creator>Saeid, Mohammad S</creator><creator>Young, Charles Y.F</creator><creator>Klee, George G</creator><creator>Tindall, Donald J</creator><creator>Bostwick, David G</creator><general>Elsevier Inc</general><general>Elsevier Science</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>19990501</creationdate><title>Human glandular kallikrein 2 expression in prostate adenocarcinoma and lymph node metastases</title><author>Darson, Micheal F ; Pacelli, Anna ; Roche, Patrick ; Rittenhouse, Harry G ; Wolfert, Robert L ; Saeid, Mohammad S ; Young, Charles Y.F ; Klee, George G ; Tindall, Donald J ; Bostwick, David G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-e855bb1a33af1374bce45339fdc9fe39aa6e4b86810411e63393f2f48a405ddf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adenocarcinoma - chemistry</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - secondary</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Biomarkers, Tumor - biosynthesis</topic><topic>Humans</topic><topic>Kallikreins - analysis</topic><topic>Kallikreins - biosynthesis</topic><topic>Lymphatic Metastasis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Prostate-Specific Antigen - biosynthesis</topic><topic>Prostatic Neoplasms - chemistry</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Tissue Kallikreins</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Darson, Micheal F</creatorcontrib><creatorcontrib>Pacelli, Anna</creatorcontrib><creatorcontrib>Roche, Patrick</creatorcontrib><creatorcontrib>Rittenhouse, Harry G</creatorcontrib><creatorcontrib>Wolfert, Robert L</creatorcontrib><creatorcontrib>Saeid, Mohammad S</creatorcontrib><creatorcontrib>Young, Charles Y.F</creatorcontrib><creatorcontrib>Klee, George G</creatorcontrib><creatorcontrib>Tindall, Donald J</creatorcontrib><creatorcontrib>Bostwick, David G</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>Urology (Ridgewood, N.J.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Darson, Micheal F</au><au>Pacelli, Anna</au><au>Roche, Patrick</au><au>Rittenhouse, Harry G</au><au>Wolfert, Robert L</au><au>Saeid, Mohammad S</au><au>Young, Charles Y.F</au><au>Klee, George G</au><au>Tindall, Donald J</au><au>Bostwick, David G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human glandular kallikrein 2 expression in prostate adenocarcinoma and lymph node metastases</atitle><jtitle>Urology (Ridgewood, N.J.)</jtitle><addtitle>Urology</addtitle><date>1999-05-01</date><risdate>1999</risdate><volume>53</volume><issue>5</issue><spage>939</spage><epage>944</epage><pages>939-944</pages><issn>0090-4295</issn><eissn>1527-9995</eissn><coden>URGYAZ</coden><abstract>Objectives. To describe the expression of a potential new tumor marker, human glandular kallikrein 2 (hK2), in primary adenocarcinoma and lymph node metastases that may be useful as an adjunct to prostate-specific antigen (PSA) in the diagnosis and monitoring of prostate cancer.
Methods. We evaluated 151 radical prostatectomy specimens removed at Mayo Clinic with node-positive adenocarcinoma to compare cytoplasmic expression of hK2, pro-hK2, and PSA in benign tissue, prostate adenocarcinoma, and lymph node metastases. Monoclonal antibodies for mature hK2 (hK2-G586), pro-hK2 (pro-hK2-G464), and PSA (PSA-773) were used. A polyclonal antibody for PSA was also used. Immunoreactivity in each case was tested to determine whether cancer recurrence could be predicted.
Results. Intense epithelial cytoplasmic immunoreactivity was observed in every case for hK2-G586, pro-hK2-G464, PSA-773, and polyclonal PSA (100% of cases, respectively). The intensity and extent of hK2 expression was greater in lymph node metastases than in primary cancer; furthermore, the expression in primary cancer was greater than in benign epithelium. Pro-hK2 was expressed in a greater percentage of cells in primary cancer than in benign tissue; furthermore, pro-hK2 was expressed to a greater extent in primary cancer than in lymph node metastases. In marked contrast to mature hK2, monoclonal PSA immunoreactivity was expressed to a higher extent in primary cancer than in lymph node metastases. Polyclonal PSA showed an incremental increase in expression from benign tissue to primary cancer and a further increase in expression in lymph node metastases.
Conclusions. hK2 was expressed in every cancer, and the expression incrementally increased from benign epithelium to primary cancer and lymph node metastases. Pro-hK2 was expressed to the greatest extent in primary cancer. Monoclonal PSA displayed inverse immunoreactivity compared with hK2. Polyclonal PSA showed incremental increases, suggesting that both hK2 and PSA were being detected. Tissue expression of hK2 appears to be regulated independently of PSA in benign epithelium, adenocarcinoma, and lymph node metastases.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>10223487</pmid><doi>10.1016/S0090-4295(98)00637-2</doi><tpages>6</tpages></addata></record> |
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subjects | Adenocarcinoma - chemistry Adenocarcinoma - metabolism Adenocarcinoma - secondary Aged Biological and medical sciences Biomarkers, Tumor - analysis Biomarkers, Tumor - biosynthesis Humans Kallikreins - analysis Kallikreins - biosynthesis Lymphatic Metastasis Male Medical sciences Middle Aged Nephrology. Urinary tract diseases Prostate-Specific Antigen - biosynthesis Prostatic Neoplasms - chemistry Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Tissue Kallikreins Tumors of the urinary system Urinary tract. Prostate gland |
title | Human glandular kallikrein 2 expression in prostate adenocarcinoma and lymph node metastases |
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