Is p16(INK4a) protein expression in oral ST lesions a reliable precancerous marker?
This study correlates the expression of p16(INK4a) and p53 with the detection of high risk human papillomavirus (HPV) in three clinical grades of smokeless tobacco keratosis (STK) as compared with patients without a history of smokeless tobacco use. Tissue samples, including squamous cell carcinoma...
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| Veröffentlicht in: | International journal of oral and maxillofacial surgery 2008-09, Vol.37 (9), p.840-846 |
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| container_title | International journal of oral and maxillofacial surgery |
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| creator | Greer, Jr, R O Meyers, A Said, S M Shroyer, K R |
| description | This study correlates the expression of p16(INK4a) and p53 with the detection of high risk human papillomavirus (HPV) in three clinical grades of smokeless tobacco keratosis (STK) as compared with patients without a history of smokeless tobacco use. Tissue samples, including squamous cell carcinoma (SCC) were evaluated for the expression of p16(INK4a) and p53 by indirect immunohistochemical methods using commercially obtained antibodies. HPV DNA analysis was performed using consensus sequence polymerase chain reaction (PCR). At least focal p16(INK4a) expression was detected in Grade I, II and III STK, SCC and control samples of alveolar ridge keratoses (ARK). p16(INK4a) expression in STK and in ARK was typically weak but was relatively strong in all SCC. Strong p53 nuclear staining was detected in STK, SCC and ARK. HPV DNA was detected in Grade I, II and III STK, SCC and ARK, but did not correlate with p16(INK4a) expression. p16(INK4a) distribution did not correlate with STK grade and does not appear to be related to the detection of HPV DNA by PCR in either STK or in SCC. There is an apparent relationship between the grade of STK and the presence of HPV. HPV was rarely detected in high-grade lesions. |
| doi_str_mv | 10.1016/j.ijom.2008.05.015 |
| format | Article |
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Tissue samples, including squamous cell carcinoma (SCC) were evaluated for the expression of p16(INK4a) and p53 by indirect immunohistochemical methods using commercially obtained antibodies. HPV DNA analysis was performed using consensus sequence polymerase chain reaction (PCR). At least focal p16(INK4a) expression was detected in Grade I, II and III STK, SCC and control samples of alveolar ridge keratoses (ARK). p16(INK4a) expression in STK and in ARK was typically weak but was relatively strong in all SCC. Strong p53 nuclear staining was detected in STK, SCC and ARK. HPV DNA was detected in Grade I, II and III STK, SCC and ARK, but did not correlate with p16(INK4a) expression. p16(INK4a) distribution did not correlate with STK grade and does not appear to be related to the detection of HPV DNA by PCR in either STK or in SCC. There is an apparent relationship between the grade of STK and the presence of HPV. HPV was rarely detected in high-grade lesions.</description><identifier>ISSN: 0901-5027</identifier><identifier>DOI: 10.1016/j.ijom.2008.05.015</identifier><identifier>PMID: 18606525</identifier><language>eng</language><publisher>Denmark</publisher><subject>Biomarkers, Tumor - metabolism ; Carcinoma, Squamous Cell - metabolism ; Carcinoma, Squamous Cell - virology ; Cyclin-Dependent Kinase Inhibitor p16 - metabolism ; Dentistry ; DNA, Viral - isolation & purification ; Humans ; Immunohistochemistry ; Keratosis - metabolism ; Leukoplakia, Oral - etiology ; Leukoplakia, Oral - metabolism ; Leukoplakia, Oral - pathology ; Leukoplakia, Oral - virology ; Mouth Neoplasms - etiology ; Mouth Neoplasms - metabolism ; Mouth Neoplasms - pathology ; Mouth Neoplasms - virology ; Papillomaviridae - genetics ; Papillomavirus Infections - diagnosis ; Precancerous Conditions - etiology ; Precancerous Conditions - metabolism ; Precancerous Conditions - pathology ; Precancerous Conditions - virology ; Severity of Illness Index ; Tobacco, Smokeless - adverse effects ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>International journal of oral and maxillofacial surgery, 2008-09, Vol.37 (9), p.840-846</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18606525$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Greer, Jr, R O</creatorcontrib><creatorcontrib>Meyers, A</creatorcontrib><creatorcontrib>Said, S M</creatorcontrib><creatorcontrib>Shroyer, K R</creatorcontrib><title>Is p16(INK4a) protein expression in oral ST lesions a reliable precancerous marker?</title><title>International journal of oral and maxillofacial surgery</title><addtitle>Int J Oral Maxillofac Surg</addtitle><description>This study correlates the expression of p16(INK4a) and p53 with the detection of high risk human papillomavirus (HPV) in three clinical grades of smokeless tobacco keratosis (STK) as compared with patients without a history of smokeless tobacco use. Tissue samples, including squamous cell carcinoma (SCC) were evaluated for the expression of p16(INK4a) and p53 by indirect immunohistochemical methods using commercially obtained antibodies. HPV DNA analysis was performed using consensus sequence polymerase chain reaction (PCR). At least focal p16(INK4a) expression was detected in Grade I, II and III STK, SCC and control samples of alveolar ridge keratoses (ARK). p16(INK4a) expression in STK and in ARK was typically weak but was relatively strong in all SCC. Strong p53 nuclear staining was detected in STK, SCC and ARK. HPV DNA was detected in Grade I, II and III STK, SCC and ARK, but did not correlate with p16(INK4a) expression. p16(INK4a) distribution did not correlate with STK grade and does not appear to be related to the detection of HPV DNA by PCR in either STK or in SCC. There is an apparent relationship between the grade of STK and the presence of HPV. HPV was rarely detected in high-grade lesions.</description><subject>Biomarkers, Tumor - metabolism</subject><subject>Carcinoma, Squamous Cell - metabolism</subject><subject>Carcinoma, Squamous Cell - virology</subject><subject>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</subject><subject>Dentistry</subject><subject>DNA, Viral - isolation & purification</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Keratosis - metabolism</subject><subject>Leukoplakia, Oral - etiology</subject><subject>Leukoplakia, Oral - metabolism</subject><subject>Leukoplakia, Oral - pathology</subject><subject>Leukoplakia, Oral - virology</subject><subject>Mouth Neoplasms - etiology</subject><subject>Mouth Neoplasms - metabolism</subject><subject>Mouth Neoplasms - pathology</subject><subject>Mouth Neoplasms - virology</subject><subject>Papillomaviridae - genetics</subject><subject>Papillomavirus Infections - diagnosis</subject><subject>Precancerous Conditions - etiology</subject><subject>Precancerous Conditions - metabolism</subject><subject>Precancerous Conditions - pathology</subject><subject>Precancerous Conditions - virology</subject><subject>Severity of Illness Index</subject><subject>Tobacco, Smokeless - adverse effects</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0901-5027</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kEtPwzAQhH0A0VL4AxyQTwgOCes4fp0QqnhEVHBoOUdOvJFSnAd2K8G_J4hyWs1qZvXtEHLBIGXA5O02bbdDl2YAOgWRAhNHZA4GWCIgUzNyGuMWAAzX6oTMmJYgRSbmZF1EOjJ5Xby-5PaGjmHYYdtT_BoDxtgOPZ3UEKyn6w31-LuJ1NKAvrWVxymAte1rDMM-0s6GDwx3Z-S4sT7i-WEuyPvjw2b5nKzenorl_SoZMzC7xFSmajg4qWpuOCotuXZ147ixUGUOHdjGOtWg5kLzzHHGcuWmBy3TKq8dX5Crv7sT9ece467s2lij97bHCaeURmjIFUzGy4NxX3XoyjG0E-p3-V8D_wF3fl3R</recordid><startdate>200809</startdate><enddate>200809</enddate><creator>Greer, Jr, R O</creator><creator>Meyers, A</creator><creator>Said, S M</creator><creator>Shroyer, K R</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200809</creationdate><title>Is p16(INK4a) protein expression in oral ST lesions a reliable precancerous marker?</title><author>Greer, Jr, R O ; Meyers, A ; Said, S M ; Shroyer, K R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p209t-9b9bf30d67c393e78638dcfd39a0b2ded0afad7fe835832d31147d008a1874cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Biomarkers, Tumor - metabolism</topic><topic>Carcinoma, Squamous Cell - metabolism</topic><topic>Carcinoma, Squamous Cell - virology</topic><topic>Cyclin-Dependent Kinase Inhibitor p16 - metabolism</topic><topic>Dentistry</topic><topic>DNA, Viral - isolation & purification</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Keratosis - metabolism</topic><topic>Leukoplakia, Oral - etiology</topic><topic>Leukoplakia, Oral - metabolism</topic><topic>Leukoplakia, Oral - pathology</topic><topic>Leukoplakia, Oral - virology</topic><topic>Mouth Neoplasms - etiology</topic><topic>Mouth Neoplasms - metabolism</topic><topic>Mouth Neoplasms - pathology</topic><topic>Mouth Neoplasms - virology</topic><topic>Papillomaviridae - genetics</topic><topic>Papillomavirus Infections - diagnosis</topic><topic>Precancerous Conditions - etiology</topic><topic>Precancerous Conditions - metabolism</topic><topic>Precancerous Conditions - pathology</topic><topic>Precancerous Conditions - virology</topic><topic>Severity of Illness Index</topic><topic>Tobacco, Smokeless - adverse effects</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Greer, Jr, R O</creatorcontrib><creatorcontrib>Meyers, A</creatorcontrib><creatorcontrib>Said, S M</creatorcontrib><creatorcontrib>Shroyer, K R</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of oral and maxillofacial surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Greer, Jr, R O</au><au>Meyers, A</au><au>Said, S M</au><au>Shroyer, K R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Is p16(INK4a) protein expression in oral ST lesions a reliable precancerous marker?</atitle><jtitle>International journal of oral and maxillofacial surgery</jtitle><addtitle>Int J Oral Maxillofac Surg</addtitle><date>2008-09</date><risdate>2008</risdate><volume>37</volume><issue>9</issue><spage>840</spage><epage>846</epage><pages>840-846</pages><issn>0901-5027</issn><abstract>This study correlates the expression of p16(INK4a) and p53 with the detection of high risk human papillomavirus (HPV) in three clinical grades of smokeless tobacco keratosis (STK) as compared with patients without a history of smokeless tobacco use. Tissue samples, including squamous cell carcinoma (SCC) were evaluated for the expression of p16(INK4a) and p53 by indirect immunohistochemical methods using commercially obtained antibodies. HPV DNA analysis was performed using consensus sequence polymerase chain reaction (PCR). At least focal p16(INK4a) expression was detected in Grade I, II and III STK, SCC and control samples of alveolar ridge keratoses (ARK). p16(INK4a) expression in STK and in ARK was typically weak but was relatively strong in all SCC. Strong p53 nuclear staining was detected in STK, SCC and ARK. HPV DNA was detected in Grade I, II and III STK, SCC and ARK, but did not correlate with p16(INK4a) expression. p16(INK4a) distribution did not correlate with STK grade and does not appear to be related to the detection of HPV DNA by PCR in either STK or in SCC. There is an apparent relationship between the grade of STK and the presence of HPV. 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| subjects | Biomarkers, Tumor - metabolism Carcinoma, Squamous Cell - metabolism Carcinoma, Squamous Cell - virology Cyclin-Dependent Kinase Inhibitor p16 - metabolism Dentistry DNA, Viral - isolation & purification Humans Immunohistochemistry Keratosis - metabolism Leukoplakia, Oral - etiology Leukoplakia, Oral - metabolism Leukoplakia, Oral - pathology Leukoplakia, Oral - virology Mouth Neoplasms - etiology Mouth Neoplasms - metabolism Mouth Neoplasms - pathology Mouth Neoplasms - virology Papillomaviridae - genetics Papillomavirus Infections - diagnosis Precancerous Conditions - etiology Precancerous Conditions - metabolism Precancerous Conditions - pathology Precancerous Conditions - virology Severity of Illness Index Tobacco, Smokeless - adverse effects Tumor Suppressor Protein p53 - metabolism |
| title | Is p16(INK4a) protein expression in oral ST lesions a reliable precancerous marker? |
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