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Inactivation of p16/CDKN2 and p15/MTS2 is associated with prognosis and response to chemotherapy in ovarian cancer
To define the involvement of p16/CDKN2 and p15/MTS2 tumor‐suppressor genes for response to chemotherapy in primary epithelial ovarian cancer, we analyzed alterations of the gene in 45 patients who were treated with primary cytoreductive surgery followed by 6 courses of cis‐diamminedichloroplatinum (...
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| Published in: | International journal of cancer 2002-06, Vol.99 (4), p.579-582 |
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| container_end_page | 582 |
| container_issue | 4 |
| container_start_page | 579 |
| container_title | International journal of cancer |
| container_volume | 99 |
| creator | Kudoh, Kazuya Ichikawa, Yoshihito Yoshida, Sadao Hirai, Misako Kikuchi, Yoshihiro Nagata, Ichiro Miwa, Masanao Uchida, Kazuhiko |
| description | To define the involvement of p16/CDKN2 and p15/MTS2 tumor‐suppressor genes for response to chemotherapy in primary epithelial ovarian cancer, we analyzed alterations of the gene in 45 patients who were treated with primary cytoreductive surgery followed by 6 courses of cis‐diamminedichloroplatinum (II) (cisplatin)‐based combination chemotherapy. Homozygous deletion of p16/CDKN2 and p15/MTS2 genes was found in 8 (18%) and 15 (33%) cases, respectively. Response to the chemotherapy was confirmed by finding at second surgery after the chemotherapy in 26 patients, resulting in 17 responders and 9 nonresponders. The abundance of gene deletion in nonresponders (56%) was significantly higher (p = 0.0463) when compared to that in responders (18%). Moreover, the deletion of genes was a significant poor prognostic factor (p = 0.0441) in advanced ovarian cancer. These results suggest that deletion of p16/CDKN2 and/or p15/MTS2 is a potential indicator for poor chemotherapy response and adverse prognosis in ovarian cancer patients. © 2002 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/ijc.10331 |
| format | article |
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Homozygous deletion of p16/CDKN2 and p15/MTS2 genes was found in 8 (18%) and 15 (33%) cases, respectively. Response to the chemotherapy was confirmed by finding at second surgery after the chemotherapy in 26 patients, resulting in 17 responders and 9 nonresponders. The abundance of gene deletion in nonresponders (56%) was significantly higher (p = 0.0463) when compared to that in responders (18%). Moreover, the deletion of genes was a significant poor prognostic factor (p = 0.0441) in advanced ovarian cancer. These results suggest that deletion of p16/CDKN2 and/or p15/MTS2 is a potential indicator for poor chemotherapy response and adverse prognosis in ovarian cancer patients. © 2002 Wiley‐Liss, Inc.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.10331</identifier><identifier>PMID: 11992549</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Antineoplastic agents ; Biological and medical sciences ; Cell Cycle Proteins - genetics ; Chemotherapy ; Cisplatin - therapeutic use ; Cyclin-Dependent Kinase Inhibitor p15 ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; Female ; Female genital diseases ; Gene Deletion ; Genes, p16 ; Gynecology. Andrology. Obstetrics ; Humans ; Medical sciences ; Middle Aged ; ovarian cancer ; Ovarian Neoplasms - diagnosis ; Ovarian Neoplasms - genetics ; p15/MTS2 ; p16/CDKN2 ; Pharmacology. Drug treatments ; Polymerase Chain Reaction ; Prognosis ; Time Factors ; Treatment Outcome ; Tumor Suppressor Proteins ; Tumors</subject><ispartof>International journal of cancer, 2002-06, Vol.99 (4), p.579-582</ispartof><rights>Copyright © 2002 Wiley‐Liss, Inc.</rights><rights>2002 INIST-CNRS</rights><rights>Copyright 2002 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3821-a49e8cda1f9c06627062702f82ab8f793e4142f19eafb2412443d6c063fdf34c3</citedby><cites>FETCH-LOGICAL-c3821-a49e8cda1f9c06627062702f82ab8f793e4142f19eafb2412443d6c063fdf34c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13668498$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11992549$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kudoh, Kazuya</creatorcontrib><creatorcontrib>Ichikawa, Yoshihito</creatorcontrib><creatorcontrib>Yoshida, Sadao</creatorcontrib><creatorcontrib>Hirai, Misako</creatorcontrib><creatorcontrib>Kikuchi, Yoshihiro</creatorcontrib><creatorcontrib>Nagata, Ichiro</creatorcontrib><creatorcontrib>Miwa, Masanao</creatorcontrib><creatorcontrib>Uchida, Kazuhiko</creatorcontrib><title>Inactivation of p16/CDKN2 and p15/MTS2 is associated with prognosis and response to chemotherapy in ovarian cancer</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>To define the involvement of p16/CDKN2 and p15/MTS2 tumor‐suppressor genes for response to chemotherapy in primary epithelial ovarian cancer, we analyzed alterations of the gene in 45 patients who were treated with primary cytoreductive surgery followed by 6 courses of cis‐diamminedichloroplatinum (II) (cisplatin)‐based combination chemotherapy. Homozygous deletion of p16/CDKN2 and p15/MTS2 genes was found in 8 (18%) and 15 (33%) cases, respectively. Response to the chemotherapy was confirmed by finding at second surgery after the chemotherapy in 26 patients, resulting in 17 responders and 9 nonresponders. The abundance of gene deletion in nonresponders (56%) was significantly higher (p = 0.0463) when compared to that in responders (18%). Moreover, the deletion of genes was a significant poor prognostic factor (p = 0.0441) in advanced ovarian cancer. These results suggest that deletion of p16/CDKN2 and/or p15/MTS2 is a potential indicator for poor chemotherapy response and adverse prognosis in ovarian cancer patients. © 2002 Wiley‐Liss, Inc.</description><subject>Adult</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Chemotherapy</subject><subject>Cisplatin - therapeutic use</subject><subject>Cyclin-Dependent Kinase Inhibitor p15</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - genetics</subject><subject>Female</subject><subject>Female genital diseases</subject><subject>Gene Deletion</subject><subject>Genes, p16</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>ovarian cancer</subject><subject>Ovarian Neoplasms - diagnosis</subject><subject>Ovarian Neoplasms - genetics</subject><subject>p15/MTS2</subject><subject>p16/CDKN2</subject><subject>Pharmacology. Drug treatments</subject><subject>Polymerase Chain Reaction</subject><subject>Prognosis</subject><subject>Time Factors</subject><subject>Treatment Outcome</subject><subject>Tumor Suppressor Proteins</subject><subject>Tumors</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNqF0cFOGzEQAFCrKioBeugPVL60EoclHtvZtY9VWiAQ4EB6Xk28dmO0WW_tDSh_X4dE4oR6sGxrnmZGM4R8AXYBjPGxfzL5IQR8ICNguioYh8lHMsoxVlQgymNyktITYwATJj-RYwCt-UTqEYmzDs3gn3HwoaPB0R7K8fTn7T2n2DX5NxnfLR459YliSsF4HGxDX_ywon0Mf7qQdpEso0196JKlQ6BmZddhWNmI_Zb6nPYZo8eOGuyMjWfkyGGb7OfDfUp-X_5aTK-L-cPVbPpjXhihOBQotVWmQXDasLLkFdsd7hTHpXKVFlaC5A60RbfkEriUoikzFa5xQhpxSr7v8-ZG_25sGuq1T8a2LXY2bFJdQR6N4uV_ISjJmQKd4fkemhhSitbVffRrjNsaWL3bRJ03Ub9uItuvh6Sb5do2b_Iw-gy-HQAmg62LeTg-vTlRlkpqld147158a7fvV6xnN9N96X_6v53L</recordid><startdate>20020601</startdate><enddate>20020601</enddate><creator>Kudoh, Kazuya</creator><creator>Ichikawa, Yoshihito</creator><creator>Yoshida, Sadao</creator><creator>Hirai, Misako</creator><creator>Kikuchi, Yoshihiro</creator><creator>Nagata, Ichiro</creator><creator>Miwa, Masanao</creator><creator>Uchida, Kazuhiko</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</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>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20020601</creationdate><title>Inactivation of p16/CDKN2 and p15/MTS2 is associated with prognosis and response to chemotherapy in ovarian cancer</title><author>Kudoh, Kazuya ; Ichikawa, Yoshihito ; Yoshida, Sadao ; Hirai, Misako ; Kikuchi, Yoshihiro ; Nagata, Ichiro ; Miwa, Masanao ; Uchida, Kazuhiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3821-a49e8cda1f9c06627062702f82ab8f793e4142f19eafb2412443d6c063fdf34c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adult</topic><topic>Antineoplastic agents</topic><topic>Biological and medical sciences</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Chemotherapy</topic><topic>Cisplatin - therapeutic use</topic><topic>Cyclin-Dependent Kinase Inhibitor p15</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - genetics</topic><topic>Female</topic><topic>Female genital diseases</topic><topic>Gene Deletion</topic><topic>Genes, p16</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>ovarian cancer</topic><topic>Ovarian Neoplasms - diagnosis</topic><topic>Ovarian Neoplasms - genetics</topic><topic>p15/MTS2</topic><topic>p16/CDKN2</topic><topic>Pharmacology. 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Homozygous deletion of p16/CDKN2 and p15/MTS2 genes was found in 8 (18%) and 15 (33%) cases, respectively. Response to the chemotherapy was confirmed by finding at second surgery after the chemotherapy in 26 patients, resulting in 17 responders and 9 nonresponders. The abundance of gene deletion in nonresponders (56%) was significantly higher (p = 0.0463) when compared to that in responders (18%). Moreover, the deletion of genes was a significant poor prognostic factor (p = 0.0441) in advanced ovarian cancer. These results suggest that deletion of p16/CDKN2 and/or p15/MTS2 is a potential indicator for poor chemotherapy response and adverse prognosis in ovarian cancer patients. © 2002 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>11992549</pmid><doi>10.1002/ijc.10331</doi><tpages>4</tpages></addata></record> |
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| subjects | Adult Antineoplastic agents Biological and medical sciences Cell Cycle Proteins - genetics Chemotherapy Cisplatin - therapeutic use Cyclin-Dependent Kinase Inhibitor p15 Cyclin-Dependent Kinase Inhibitor p16 - genetics Female Female genital diseases Gene Deletion Genes, p16 Gynecology. Andrology. Obstetrics Humans Medical sciences Middle Aged ovarian cancer Ovarian Neoplasms - diagnosis Ovarian Neoplasms - genetics p15/MTS2 p16/CDKN2 Pharmacology. Drug treatments Polymerase Chain Reaction Prognosis Time Factors Treatment Outcome Tumor Suppressor Proteins Tumors |
| title | Inactivation of p16/CDKN2 and p15/MTS2 is associated with prognosis and response to chemotherapy in ovarian cancer |
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