Promoter hypermethylation profile of tumor‐associated genes p16, p15, hMLH1, MGMT and E‐cadherin in oral squamous cell carcinoma
Aberrant promoter hypermethylation of tumor‐associated genes leading to their inactivation is a common event in many cancer types. Using a sensitive restriction‐multiplex PCR method, we studied the promoter hypermethylation profile of the p16, p15, hMLH1, MGMT and E‐cad genes in oral squamous cell c...
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| Veröffentlicht in: | International journal of cancer 2003-05, Vol.105 (1), p.41-46 |
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| description | Aberrant promoter hypermethylation of tumor‐associated genes leading to their inactivation is a common event in many cancer types. Using a sensitive restriction‐multiplex PCR method, we studied the promoter hypermethylation profile of the p16, p15, hMLH1, MGMT and E‐cad genes in oral squamous cell carcinoma (OSCC) of Indians. We analyzed a total of 51 samples for the p15 tumor‐suppressor gene and 99 samples for each of the remaining genes. Our studies indicate an incidence of promoter hypermethylation of 23% each for p16 and p15, 8% for hMLH1, 41% for MGMT and 35% for E‐cad. We observed aberrant hypermethylation of the promoter region of at least 1 of these genes in 74.5% of cases (n = 51) for which all the 5 genes were studied. Abnormal methylation was detected in tumors irrespective of stage and location in the oral cavity, whereas no abnormal methylation was detectable in normal oral squamous tissues obtained from 25 OSCC patients. Detection of aberrant hypermethylation patterns of cancer‐associated genes listed above is therefore suitable for diagnosis of OSCC in individuals at high risk for this disease. © 2003 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/ijc.11028 |
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Using a sensitive restriction‐multiplex PCR method, we studied the promoter hypermethylation profile of the p16, p15, hMLH1, MGMT and E‐cad genes in oral squamous cell carcinoma (OSCC) of Indians. We analyzed a total of 51 samples for the p15 tumor‐suppressor gene and 99 samples for each of the remaining genes. Our studies indicate an incidence of promoter hypermethylation of 23% each for p16 and p15, 8% for hMLH1, 41% for MGMT and 35% for E‐cad. We observed aberrant hypermethylation of the promoter region of at least 1 of these genes in 74.5% of cases (n = 51) for which all the 5 genes were studied. Abnormal methylation was detected in tumors irrespective of stage and location in the oral cavity, whereas no abnormal methylation was detectable in normal oral squamous tissues obtained from 25 OSCC patients. Detection of aberrant hypermethylation patterns of cancer‐associated genes listed above is therefore suitable for diagnosis of OSCC in individuals at high risk for this disease. © 2003 Wiley‐Liss, Inc.</description><identifier>ISSN: 0020-7136</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.11028</identifier><identifier>PMID: 12672028</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adaptor Proteins, Signal Transducing ; Biological and medical sciences ; Cadherins - biosynthesis ; Cadherins - genetics ; Carcinoma, Squamous Cell - genetics ; Carcinoma, Squamous Cell - metabolism ; Carrier Proteins ; Cell Cycle Proteins - biosynthesis ; Cell Cycle Proteins - genetics ; CpG Islands ; Cyclin-Dependent Kinase Inhibitor p15 ; Cyclin-Dependent Kinase Inhibitor p16 - biosynthesis ; Cyclin-Dependent Kinase Inhibitor p16 - genetics ; DNA - metabolism ; DNA Methylation ; Ent. Stomatology ; E‐cadherin ; hMLH1 ; Humans ; Investigative techniques, diagnostic techniques (general aspects) ; Medical sciences ; MGMT ; Models, Genetic ; Mouth Neoplasms - genetics ; Mouth Neoplasms - metabolism ; MutL Protein Homolog 1 ; Neoplasm Proteins - biosynthesis ; Neoplasm Proteins - genetics ; Nuclear Proteins ; O-Methylguanine-DNA Methyltransferase - biosynthesis ; O-Methylguanine-DNA Methyltransferase - genetics ; oral squamous cell carcinoma ; p15 ; p16 ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Polymerase Chain Reaction ; promoter hypermethylation ; Promoter Regions, Genetic ; Risk Factors ; Tumor Cells, Cultured ; Tumor Suppressor Proteins</subject><ispartof>International journal of cancer, 2003-05, Vol.105 (1), p.41-46</ispartof><rights>Copyright © 2003 Wiley‐Liss, Inc.</rights><rights>2003 INIST-CNRS</rights><rights>Copyright 2003 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4838-68ab45e68988c89b26939c58dba1fa168813a2cf84f79094add91211ae30b32e3</citedby><cites>FETCH-LOGICAL-c4838-68ab45e68988c89b26939c58dba1fa168813a2cf84f79094add91211ae30b32e3</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.11028$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fijc.11028$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14751739$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12672028$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Viswanathan, Muthusamy</creatorcontrib><creatorcontrib>Tsuchida, Nobuo</creatorcontrib><creatorcontrib>Shanmugam, Govindaswamy</creatorcontrib><title>Promoter hypermethylation profile of tumor‐associated genes p16, p15, hMLH1, MGMT and E‐cadherin in oral squamous cell carcinoma</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>Aberrant promoter hypermethylation of tumor‐associated genes leading to their inactivation is a common event in many cancer types. Using a sensitive restriction‐multiplex PCR method, we studied the promoter hypermethylation profile of the p16, p15, hMLH1, MGMT and E‐cad genes in oral squamous cell carcinoma (OSCC) of Indians. We analyzed a total of 51 samples for the p15 tumor‐suppressor gene and 99 samples for each of the remaining genes. Our studies indicate an incidence of promoter hypermethylation of 23% each for p16 and p15, 8% for hMLH1, 41% for MGMT and 35% for E‐cad. We observed aberrant hypermethylation of the promoter region of at least 1 of these genes in 74.5% of cases (n = 51) for which all the 5 genes were studied. Abnormal methylation was detected in tumors irrespective of stage and location in the oral cavity, whereas no abnormal methylation was detectable in normal oral squamous tissues obtained from 25 OSCC patients. Detection of aberrant hypermethylation patterns of cancer‐associated genes listed above is therefore suitable for diagnosis of OSCC in individuals at high risk for this disease. © 2003 Wiley‐Liss, Inc.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>Biological and medical sciences</subject><subject>Cadherins - biosynthesis</subject><subject>Cadherins - genetics</subject><subject>Carcinoma, Squamous Cell - genetics</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carrier Proteins</subject><subject>Cell Cycle Proteins - biosynthesis</subject><subject>Cell Cycle Proteins - genetics</subject><subject>CpG Islands</subject><subject>Cyclin-Dependent Kinase Inhibitor p15</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - biosynthesis</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - genetics</subject><subject>DNA - metabolism</subject><subject>DNA Methylation</subject><subject>Ent. Stomatology</subject><subject>E‐cadherin</subject><subject>hMLH1</subject><subject>Humans</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Medical sciences</subject><subject>MGMT</subject><subject>Models, Genetic</subject><subject>Mouth Neoplasms - genetics</subject><subject>Mouth Neoplasms - metabolism</subject><subject>MutL Protein Homolog 1</subject><subject>Neoplasm Proteins - biosynthesis</subject><subject>Neoplasm Proteins - genetics</subject><subject>Nuclear Proteins</subject><subject>O-Methylguanine-DNA Methyltransferase - biosynthesis</subject><subject>O-Methylguanine-DNA Methyltransferase - genetics</subject><subject>oral squamous cell carcinoma</subject><subject>p15</subject><subject>p16</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>Polymerase Chain Reaction</subject><subject>promoter hypermethylation</subject><subject>Promoter Regions, Genetic</subject><subject>Risk Factors</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Suppressor Proteins</subject><issn>0020-7136</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1DAQhi0EokvhwAsgX0BC2rQeO4mdI1qVtmhXcCjnaOJMWFdJvLUTob1x4AF4Rp4EL7tSTwjJsg_-9M8_-hh7DeIChJCX7t5eAAhpnrAFiEpnQkLxlC3Sn8g0qPKMvYjxXgiAQuTP2RnIUsvEL9jPL8EPfqLAt_sdhYGm7b7HyfmR74LvXE_cd3yaBx9-__iFMXrrcKKWf6ORIt9BuUxXseTbzfoGlnxzvbnjOLb8KuEW2y0FN_J0fMCex4cZBz9HbqnvucVg3egHfMmeddhHenV6z9nXj1d3q5ts_fn6dvVhndncKJOVBpu8oNJUxlhTNbKsVGUL0zYIHUJpDCiUtjN5pytR5di2FUgAJCUaJUmds3fH3LTaw0xxqgcXD1VwpNSq1gpKqVPq_0Aw2ghVFAl8fwRt8DEG6updcAOGfQ2iPripk5v6r5vEvjmFzs1A7SN5kpGAtycAo8W-CzhaFx-5XBeg1aHd5ZH7nvTs_z2xvv20Oo7-A71Xpj4</recordid><startdate>20030520</startdate><enddate>20030520</enddate><creator>Viswanathan, Muthusamy</creator><creator>Tsuchida, Nobuo</creator><creator>Shanmugam, Govindaswamy</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>20030520</creationdate><title>Promoter hypermethylation profile of tumor‐associated genes p16, p15, hMLH1, MGMT and E‐cadherin in oral squamous cell carcinoma</title><author>Viswanathan, Muthusamy ; Tsuchida, Nobuo ; Shanmugam, Govindaswamy</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4838-68ab45e68988c89b26939c58dba1fa168813a2cf84f79094add91211ae30b32e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>Biological and medical sciences</topic><topic>Cadherins - biosynthesis</topic><topic>Cadherins - genetics</topic><topic>Carcinoma, Squamous Cell - genetics</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carrier Proteins</topic><topic>Cell Cycle Proteins - biosynthesis</topic><topic>Cell Cycle Proteins - genetics</topic><topic>CpG Islands</topic><topic>Cyclin-Dependent Kinase Inhibitor p15</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - biosynthesis</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - genetics</topic><topic>DNA - metabolism</topic><topic>DNA Methylation</topic><topic>Ent. Stomatology</topic><topic>E‐cadherin</topic><topic>hMLH1</topic><topic>Humans</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Medical sciences</topic><topic>MGMT</topic><topic>Models, Genetic</topic><topic>Mouth Neoplasms - genetics</topic><topic>Mouth Neoplasms - metabolism</topic><topic>MutL Protein Homolog 1</topic><topic>Neoplasm Proteins - biosynthesis</topic><topic>Neoplasm Proteins - genetics</topic><topic>Nuclear Proteins</topic><topic>O-Methylguanine-DNA Methyltransferase - biosynthesis</topic><topic>O-Methylguanine-DNA Methyltransferase - genetics</topic><topic>oral squamous cell carcinoma</topic><topic>p15</topic><topic>p16</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>Polymerase Chain Reaction</topic><topic>promoter hypermethylation</topic><topic>Promoter Regions, Genetic</topic><topic>Risk Factors</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Suppressor Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Viswanathan, Muthusamy</creatorcontrib><creatorcontrib>Tsuchida, Nobuo</creatorcontrib><creatorcontrib>Shanmugam, Govindaswamy</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>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>Viswanathan, Muthusamy</au><au>Tsuchida, Nobuo</au><au>Shanmugam, Govindaswamy</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Promoter hypermethylation profile of tumor‐associated genes p16, p15, hMLH1, MGMT and E‐cadherin in oral squamous cell carcinoma</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>2003-05-20</date><risdate>2003</risdate><volume>105</volume><issue>1</issue><spage>41</spage><epage>46</epage><pages>41-46</pages><issn>0020-7136</issn><eissn>1097-0215</eissn><coden>IJCNAW</coden><abstract>Aberrant promoter hypermethylation of tumor‐associated genes leading to their inactivation is a common event in many cancer types. Using a sensitive restriction‐multiplex PCR method, we studied the promoter hypermethylation profile of the p16, p15, hMLH1, MGMT and E‐cad genes in oral squamous cell carcinoma (OSCC) of Indians. We analyzed a total of 51 samples for the p15 tumor‐suppressor gene and 99 samples for each of the remaining genes. Our studies indicate an incidence of promoter hypermethylation of 23% each for p16 and p15, 8% for hMLH1, 41% for MGMT and 35% for E‐cad. We observed aberrant hypermethylation of the promoter region of at least 1 of these genes in 74.5% of cases (n = 51) for which all the 5 genes were studied. Abnormal methylation was detected in tumors irrespective of stage and location in the oral cavity, whereas no abnormal methylation was detectable in normal oral squamous tissues obtained from 25 OSCC patients. Detection of aberrant hypermethylation patterns of cancer‐associated genes listed above is therefore suitable for diagnosis of OSCC in individuals at high risk for this disease. © 2003 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>12672028</pmid><doi>10.1002/ijc.11028</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing Biological and medical sciences Cadherins - biosynthesis Cadherins - genetics Carcinoma, Squamous Cell - genetics Carcinoma, Squamous Cell - metabolism Carrier Proteins Cell Cycle Proteins - biosynthesis Cell Cycle Proteins - genetics CpG Islands Cyclin-Dependent Kinase Inhibitor p15 Cyclin-Dependent Kinase Inhibitor p16 - biosynthesis Cyclin-Dependent Kinase Inhibitor p16 - genetics DNA - metabolism DNA Methylation Ent. Stomatology E‐cadherin hMLH1 Humans Investigative techniques, diagnostic techniques (general aspects) Medical sciences MGMT Models, Genetic Mouth Neoplasms - genetics Mouth Neoplasms - metabolism MutL Protein Homolog 1 Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics Nuclear Proteins O-Methylguanine-DNA Methyltransferase - biosynthesis O-Methylguanine-DNA Methyltransferase - genetics oral squamous cell carcinoma p15 p16 Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques Polymerase Chain Reaction promoter hypermethylation Promoter Regions, Genetic Risk Factors Tumor Cells, Cultured Tumor Suppressor Proteins |
| title | Promoter hypermethylation profile of tumor‐associated genes p16, p15, hMLH1, MGMT and E‐cadherin in oral squamous cell carcinoma |
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