DCC promoter hypermethylation in esophageal squamous cell carcinoma
Deleted in Colorectal Cancer (DCC) is a putative tumor suppressor gene, whose loss has been implicated in colorectal tumorigenesis. Decreased or loss of DCC expression has been demonstrated in a number of human cancers, including esophageal cancer. In this study, we analyzed esophageal squamous cell...
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| Veröffentlicht in: | International journal of cancer 2008-06, Vol.122 (11), p.2498-2502 |
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| creator | Lui Park, Hannah Sook Kim, Myoung Yamashita, Keishi Westra, William Lopes Carvalho, Andre Lee, Juna Jiang, Wei‐Wen Hyen Baek, Jin Liu, Junwei Osada, Motonobu Moon, Chul‐So Califano, Joseph A. Mori, Masaki Sidransky, David |
| description | Deleted in Colorectal Cancer (DCC) is a putative tumor suppressor gene, whose loss has been implicated in colorectal tumorigenesis. Decreased or loss of DCC expression has been demonstrated in a number of human cancers, including esophageal cancer. In this study, we analyzed esophageal squamous cell carcinoma (ESCC) cell lines and primary ESCCs as well as normal esophageal tissues for DCC methylation by bisulfite sequencing, methylation‐specific PCR (MSP) and/or quantitative methylation‐specific PCR (qMSP). When a qMSP cut‐off value for positivity was set to 1.0, DCC methylation was detected in 10 of 12 ESCC cell lines tested, 74% of primary ESCCs (n = 70), 0% of corresponding normal esophageal tissues (n = 20) and 0% of normal esophagus from healthy individuals (n = 19). DCC expression was undetectable in the majority of ESCC cell lines, and treatment with the DNA methyltransferase inhibitor 5‐aza‐2′‐deoxycytidine reactivated gene expression. DCC overexpression suppressed colony formation in ESCC cell lines, suggesting that DCC may function as a tumor suppressor gene in the esophagus. However, DCC methylation was not associated with any clinical or pathologic parameters measured. We have demonstrated that DCC methylation is a frequent and cancer‐specific event in primary ESCCs, suggesting that DCC and associated pathways may represent a new diagnostical therapeutic target. © 2008 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/ijc.23434 |
| format | Article |
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Decreased or loss of DCC expression has been demonstrated in a number of human cancers, including esophageal cancer. In this study, we analyzed esophageal squamous cell carcinoma (ESCC) cell lines and primary ESCCs as well as normal esophageal tissues for DCC methylation by bisulfite sequencing, methylation‐specific PCR (MSP) and/or quantitative methylation‐specific PCR (qMSP). When a qMSP cut‐off value for positivity was set to 1.0, DCC methylation was detected in 10 of 12 ESCC cell lines tested, 74% of primary ESCCs (n = 70), 0% of corresponding normal esophageal tissues (n = 20) and 0% of normal esophagus from healthy individuals (n = 19). DCC expression was undetectable in the majority of ESCC cell lines, and treatment with the DNA methyltransferase inhibitor 5‐aza‐2′‐deoxycytidine reactivated gene expression. DCC overexpression suppressed colony formation in ESCC cell lines, suggesting that DCC may function as a tumor suppressor gene in the esophagus. However, DCC methylation was not associated with any clinical or pathologic parameters measured. We have demonstrated that DCC methylation is a frequent and cancer‐specific event in primary ESCCs, suggesting that DCC and associated pathways may represent a new diagnostical therapeutic target. © 2008 Wiley‐Liss, Inc.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.23434</identifier><identifier>PMID: 18302152</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Aged ; Biological and medical sciences ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - pathology ; Cell Line, Tumor ; DCC ; DNA Methylation ; Early Diagnosis ; epigenetic ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - pathology ; esophageal squamous cell carcinoma ; Esophagus ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Genes, DCC ; Genes, Tumor Suppressor ; Humans ; hypermethylation ; Lymphatic Metastasis ; Male ; Medical sciences ; methylation ; Middle Aged ; Neoplasm Invasiveness ; Polymerase Chain Reaction ; Promoter Regions, Genetic ; Reverse Transcriptase Polymerase Chain Reaction ; Tumors</subject><ispartof>International journal of cancer, 2008-06, Vol.122 (11), p.2498-2502</ispartof><rights>Copyright © 2008 Wiley‐Liss, Inc.</rights><rights>2008 INIST-CNRS</rights><rights>(c) 2008 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4854-b136f92d0b362f57008c58bb269a4b4be3ef25dcc610e366aeb78e915d4efc483</citedby><cites>FETCH-LOGICAL-c4854-b136f92d0b362f57008c58bb269a4b4be3ef25dcc610e366aeb78e915d4efc483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fijc.23434$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fijc.23434$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20271291$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18302152$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lui Park, Hannah</creatorcontrib><creatorcontrib>Sook Kim, Myoung</creatorcontrib><creatorcontrib>Yamashita, Keishi</creatorcontrib><creatorcontrib>Westra, William</creatorcontrib><creatorcontrib>Lopes Carvalho, Andre</creatorcontrib><creatorcontrib>Lee, Juna</creatorcontrib><creatorcontrib>Jiang, Wei‐Wen</creatorcontrib><creatorcontrib>Hyen Baek, Jin</creatorcontrib><creatorcontrib>Liu, Junwei</creatorcontrib><creatorcontrib>Osada, Motonobu</creatorcontrib><creatorcontrib>Moon, Chul‐So</creatorcontrib><creatorcontrib>Califano, Joseph A.</creatorcontrib><creatorcontrib>Mori, Masaki</creatorcontrib><creatorcontrib>Sidransky, David</creatorcontrib><title>DCC promoter hypermethylation in esophageal squamous cell carcinoma</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>Deleted in Colorectal Cancer (DCC) is a putative tumor suppressor gene, whose loss has been implicated in colorectal tumorigenesis. Decreased or loss of DCC expression has been demonstrated in a number of human cancers, including esophageal cancer. In this study, we analyzed esophageal squamous cell carcinoma (ESCC) cell lines and primary ESCCs as well as normal esophageal tissues for DCC methylation by bisulfite sequencing, methylation‐specific PCR (MSP) and/or quantitative methylation‐specific PCR (qMSP). When a qMSP cut‐off value for positivity was set to 1.0, DCC methylation was detected in 10 of 12 ESCC cell lines tested, 74% of primary ESCCs (n = 70), 0% of corresponding normal esophageal tissues (n = 20) and 0% of normal esophagus from healthy individuals (n = 19). DCC expression was undetectable in the majority of ESCC cell lines, and treatment with the DNA methyltransferase inhibitor 5‐aza‐2′‐deoxycytidine reactivated gene expression. DCC overexpression suppressed colony formation in ESCC cell lines, suggesting that DCC may function as a tumor suppressor gene in the esophagus. However, DCC methylation was not associated with any clinical or pathologic parameters measured. We have demonstrated that DCC methylation is a frequent and cancer‐specific event in primary ESCCs, suggesting that DCC and associated pathways may represent a new diagnostical therapeutic target. © 2008 Wiley‐Liss, Inc.</description><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>DCC</subject><subject>DNA Methylation</subject><subject>Early Diagnosis</subject><subject>epigenetic</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - pathology</subject><subject>esophageal squamous cell carcinoma</subject><subject>Esophagus</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Genes, DCC</subject><subject>Genes, Tumor Suppressor</subject><subject>Humans</subject><subject>hypermethylation</subject><subject>Lymphatic Metastasis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>methylation</subject><subject>Middle Aged</subject><subject>Neoplasm Invasiveness</subject><subject>Polymerase Chain Reaction</subject><subject>Promoter Regions, Genetic</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Tumors</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0DtPwzAUBWALgWgpDPwBlAUkhrTXjp3HiMKrqBILzJHj3NBUedVOhPLvcUkEE2Ly4E_nHh1CLiksKQBbFTu1ZB73-BGZU4gCFxgVx2Ru_8ANqOfPyJkxOwBKBfBTMqOhdyBsTuL7OHZa3VRNh9rZDi3qCrvtUMquaGqnqB00TbuVHyhLx-x7WTW9cRSWpaOkVkXdVPKcnOSyNHgxvQvy_vjwFj-7m9endXy3cRUPBXdTWySPWAap57NcBAChEmGaMj-SPOUpepgzkSnlU0DP9yWmQYgRFRnH3EZ4C3Iz5tq--x5Nl1SFOVSRNdpWSQBchFHE_oUMbJ_IDyy8HaHSjTEa86TVRSX1kFBIDtMmdtrke1prr6bQPq0w-5XTlhZcT0AaJctcy1oV5scxYAFlEbVuNbrPosTh74vJ-iUeT38B1yiPMQ</recordid><startdate>20080601</startdate><enddate>20080601</enddate><creator>Lui Park, Hannah</creator><creator>Sook Kim, Myoung</creator><creator>Yamashita, Keishi</creator><creator>Westra, William</creator><creator>Lopes Carvalho, Andre</creator><creator>Lee, Juna</creator><creator>Jiang, Wei‐Wen</creator><creator>Hyen Baek, Jin</creator><creator>Liu, Junwei</creator><creator>Osada, Motonobu</creator><creator>Moon, Chul‐So</creator><creator>Califano, Joseph A.</creator><creator>Mori, Masaki</creator><creator>Sidransky, David</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>7TM</scope><scope>7TO</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20080601</creationdate><title>DCC promoter hypermethylation in esophageal squamous cell carcinoma</title><author>Lui Park, Hannah ; Sook Kim, Myoung ; Yamashita, Keishi ; Westra, William ; Lopes Carvalho, Andre ; Lee, Juna ; Jiang, Wei‐Wen ; Hyen Baek, Jin ; Liu, Junwei ; Osada, Motonobu ; Moon, Chul‐So ; Califano, Joseph A. ; Mori, Masaki ; Sidransky, David</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4854-b136f92d0b362f57008c58bb269a4b4be3ef25dcc610e366aeb78e915d4efc483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>DCC</topic><topic>DNA Methylation</topic><topic>Early Diagnosis</topic><topic>epigenetic</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophageal Neoplasms - pathology</topic><topic>esophageal squamous cell carcinoma</topic><topic>Esophagus</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Genes, DCC</topic><topic>Genes, Tumor Suppressor</topic><topic>Humans</topic><topic>hypermethylation</topic><topic>Lymphatic Metastasis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>methylation</topic><topic>Middle Aged</topic><topic>Neoplasm Invasiveness</topic><topic>Polymerase Chain Reaction</topic><topic>Promoter Regions, Genetic</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lui Park, Hannah</creatorcontrib><creatorcontrib>Sook Kim, Myoung</creatorcontrib><creatorcontrib>Yamashita, Keishi</creatorcontrib><creatorcontrib>Westra, William</creatorcontrib><creatorcontrib>Lopes Carvalho, Andre</creatorcontrib><creatorcontrib>Lee, Juna</creatorcontrib><creatorcontrib>Jiang, Wei‐Wen</creatorcontrib><creatorcontrib>Hyen Baek, Jin</creatorcontrib><creatorcontrib>Liu, Junwei</creatorcontrib><creatorcontrib>Osada, Motonobu</creatorcontrib><creatorcontrib>Moon, Chul‐So</creatorcontrib><creatorcontrib>Califano, Joseph A.</creatorcontrib><creatorcontrib>Mori, Masaki</creatorcontrib><creatorcontrib>Sidransky, David</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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lui Park, Hannah</au><au>Sook Kim, Myoung</au><au>Yamashita, Keishi</au><au>Westra, William</au><au>Lopes Carvalho, Andre</au><au>Lee, Juna</au><au>Jiang, Wei‐Wen</au><au>Hyen Baek, Jin</au><au>Liu, Junwei</au><au>Osada, Motonobu</au><au>Moon, Chul‐So</au><au>Califano, Joseph A.</au><au>Mori, Masaki</au><au>Sidransky, David</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>DCC promoter hypermethylation in esophageal squamous cell carcinoma</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>2008-06-01</date><risdate>2008</risdate><volume>122</volume><issue>11</issue><spage>2498</spage><epage>2502</epage><pages>2498-2502</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><coden>IJCNAW</coden><abstract>Deleted in Colorectal Cancer (DCC) is a putative tumor suppressor gene, whose loss has been implicated in colorectal tumorigenesis. Decreased or loss of DCC expression has been demonstrated in a number of human cancers, including esophageal cancer. In this study, we analyzed esophageal squamous cell carcinoma (ESCC) cell lines and primary ESCCs as well as normal esophageal tissues for DCC methylation by bisulfite sequencing, methylation‐specific PCR (MSP) and/or quantitative methylation‐specific PCR (qMSP). When a qMSP cut‐off value for positivity was set to 1.0, DCC methylation was detected in 10 of 12 ESCC cell lines tested, 74% of primary ESCCs (n = 70), 0% of corresponding normal esophageal tissues (n = 20) and 0% of normal esophagus from healthy individuals (n = 19). DCC expression was undetectable in the majority of ESCC cell lines, and treatment with the DNA methyltransferase inhibitor 5‐aza‐2′‐deoxycytidine reactivated gene expression. DCC overexpression suppressed colony formation in ESCC cell lines, suggesting that DCC may function as a tumor suppressor gene in the esophagus. However, DCC methylation was not associated with any clinical or pathologic parameters measured. We have demonstrated that DCC methylation is a frequent and cancer‐specific event in primary ESCCs, suggesting that DCC and associated pathways may represent a new diagnostical therapeutic target. © 2008 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>18302152</pmid><doi>10.1002/ijc.23434</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Biological and medical sciences Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - pathology Cell Line, Tumor DCC DNA Methylation Early Diagnosis epigenetic Esophageal Neoplasms - genetics Esophageal Neoplasms - pathology esophageal squamous cell carcinoma Esophagus Female Gastroenterology. Liver. Pancreas. Abdomen Genes, DCC Genes, Tumor Suppressor Humans hypermethylation Lymphatic Metastasis Male Medical sciences methylation Middle Aged Neoplasm Invasiveness Polymerase Chain Reaction Promoter Regions, Genetic Reverse Transcriptase Polymerase Chain Reaction Tumors |
| title | DCC promoter hypermethylation in esophageal squamous cell carcinoma |
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