Evaluation of feline oral squamous cell carcinomas for p16 CDKN2A protein immunoreactivity and the presence of papillomaviral DNA
Oral squamous cell carcinomas (OSCCs) develop commonly in cats. While the cause of the feline neoplasms is unknown, a quarter of human OSCCs are caused by papillomavirus (PV) infection. As PV DNA has been previously detected in a feline OSCC, it was hypothesised that PV infection could be a signific...
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| Veröffentlicht in: | Research in veterinary science 2011-04, Vol.90 (2), p.280-283 |
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| creator | Munday, John S. Knight, Cameron G. French, Adrienne F. |
| description | Oral squamous cell carcinomas (OSCCs) develop commonly in cats. While the cause of the feline neoplasms is unknown, a quarter of human OSCCs are caused by papillomavirus (PV) infection. As PV DNA has been previously detected in a feline OSCC, it was hypothesised that PV infection could be a significant cause of feline OSCCs. Human OSCCs that are caused by PVs contain increased p16
CDKN2A protein (p16), which can be detected using immunohistochemistry. In cats, increased p16 immunoreactivity has been reported within PV-associated skin lesions. This study evaluated p16 immunoreactivity within 30 feline OSCCs. Additionally, PCR was used to amplify PV DNA from the OSCCs. Increased p16 immunoreactivity was present within 2 OSCCs. However, as PV DNA was not amplified from any OSCC in this study, it cannot be confirmed that the increased p16 was caused by PV infection. Therefore, these results do not support the hypothesis that PVs are a significant cause of OSCCs in cats. Loss of p16 expression is considered an important process in the development of human non-PV-induced OSCCs. In contrast, loss of p16 immunoreactivity was only present in 2 feline OSCCs. This suggests that human and feline OSCCs develop due to different molecular mechanisms. |
| doi_str_mv | 10.1016/j.rvsc.2010.06.014 |
| format | Article |
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CDKN2A protein (p16), which can be detected using immunohistochemistry. In cats, increased p16 immunoreactivity has been reported within PV-associated skin lesions. This study evaluated p16 immunoreactivity within 30 feline OSCCs. Additionally, PCR was used to amplify PV DNA from the OSCCs. Increased p16 immunoreactivity was present within 2 OSCCs. However, as PV DNA was not amplified from any OSCC in this study, it cannot be confirmed that the increased p16 was caused by PV infection. Therefore, these results do not support the hypothesis that PVs are a significant cause of OSCCs in cats. Loss of p16 expression is considered an important process in the development of human non-PV-induced OSCCs. In contrast, loss of p16 immunoreactivity was only present in 2 feline OSCCs. This suggests that human and feline OSCCs develop due to different molecular mechanisms.</description><identifier>ISSN: 0034-5288</identifier><identifier>EISSN: 1532-2661</identifier><identifier>DOI: 10.1016/j.rvsc.2010.06.014</identifier><language>eng</language><publisher>Oxford: Elsevier India Pvt Ltd</publisher><subject>Carcinogenesis ; Cat ; Hypotheses ; Immunohistochemistry ; Oncology ; Oral squamous cell carcinoma ; P16 ; Papillomavirus ; Polymerase chain reaction ; Proteins ; Tobacco ; Veterinary medicine</subject><ispartof>Research in veterinary science, 2011-04, Vol.90 (2), p.280-283</ispartof><rights>2010 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.rvsc.2010.06.014$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids></links><search><creatorcontrib>Munday, John S.</creatorcontrib><creatorcontrib>Knight, Cameron G.</creatorcontrib><creatorcontrib>French, Adrienne F.</creatorcontrib><title>Evaluation of feline oral squamous cell carcinomas for p16 CDKN2A protein immunoreactivity and the presence of papillomaviral DNA</title><title>Research in veterinary science</title><description>Oral squamous cell carcinomas (OSCCs) develop commonly in cats. While the cause of the feline neoplasms is unknown, a quarter of human OSCCs are caused by papillomavirus (PV) infection. As PV DNA has been previously detected in a feline OSCC, it was hypothesised that PV infection could be a significant cause of feline OSCCs. Human OSCCs that are caused by PVs contain increased p16
CDKN2A protein (p16), which can be detected using immunohistochemistry. In cats, increased p16 immunoreactivity has been reported within PV-associated skin lesions. This study evaluated p16 immunoreactivity within 30 feline OSCCs. Additionally, PCR was used to amplify PV DNA from the OSCCs. Increased p16 immunoreactivity was present within 2 OSCCs. However, as PV DNA was not amplified from any OSCC in this study, it cannot be confirmed that the increased p16 was caused by PV infection. Therefore, these results do not support the hypothesis that PVs are a significant cause of OSCCs in cats. Loss of p16 expression is considered an important process in the development of human non-PV-induced OSCCs. In contrast, loss of p16 immunoreactivity was only present in 2 feline OSCCs. This suggests that human and feline OSCCs develop due to different molecular mechanisms.</description><subject>Carcinogenesis</subject><subject>Cat</subject><subject>Hypotheses</subject><subject>Immunohistochemistry</subject><subject>Oncology</subject><subject>Oral squamous cell carcinoma</subject><subject>P16</subject><subject>Papillomavirus</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Tobacco</subject><subject>Veterinary medicine</subject><issn>0034-5288</issn><issn>1532-2661</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNpdkU1L7DAUhoMoOH78AVcBF65m7knSplNwM4yj96LoRtchTU4xQ5uMSVtw6T83RVd3deDw8H7wEnLFYMWAyT_7VZySWXHID5ArYMURWbBS8CWXkh2TBYAoliVfr0_JWUp7ACgYqxbkazfpbtSDC56GlrbYOY80RN3R9DHqPoyJGuw6anQ0zodeJ9qGSA9M0u3d4zPf0EMMAzpPXd-PPkTUZnCTGz6p9pYO75gBTOgNzgYHfXBdl2UmN3vcPW8uyEmru4SXv_ecvN3vXrd_l08vD_-2m6clMpZ7VKIUTW2lBcSGg9YlmNZaDlIarCqupZCsqAu7tlY3pqoaZusGSi0bzhsjxTm5-dHNeT9GTIPqXZqraY-5paqBC1kVa57J6__IfRijz-EUA1FCAaIWmbr9oTCHnhxGlYyba1oX0QzKBpdxNc-j9mqeR83zKJAqzyO-AfvRhh8</recordid><startdate>20110401</startdate><enddate>20110401</enddate><creator>Munday, John S.</creator><creator>Knight, Cameron G.</creator><creator>French, Adrienne F.</creator><general>Elsevier India Pvt Ltd</general><general>Elsevier Limited</general><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope></search><sort><creationdate>20110401</creationdate><title>Evaluation of feline oral squamous cell carcinomas for p16 CDKN2A protein immunoreactivity and the presence of papillomaviral DNA</title><author>Munday, John S. ; Knight, Cameron G. ; French, Adrienne F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e1132-7353b9d6d0eeb20aa50cfdd2066ce772a6361494d8ddabc77b1d9b05a6b22bc63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Carcinogenesis</topic><topic>Cat</topic><topic>Hypotheses</topic><topic>Immunohistochemistry</topic><topic>Oncology</topic><topic>Oral squamous cell carcinoma</topic><topic>P16</topic><topic>Papillomavirus</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Tobacco</topic><topic>Veterinary medicine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Munday, John S.</creatorcontrib><creatorcontrib>Knight, Cameron G.</creatorcontrib><creatorcontrib>French, Adrienne F.</creatorcontrib><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Research in veterinary science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Munday, John S.</au><au>Knight, Cameron G.</au><au>French, Adrienne F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evaluation of feline oral squamous cell carcinomas for p16 CDKN2A protein immunoreactivity and the presence of papillomaviral DNA</atitle><jtitle>Research in veterinary science</jtitle><date>2011-04-01</date><risdate>2011</risdate><volume>90</volume><issue>2</issue><spage>280</spage><epage>283</epage><pages>280-283</pages><issn>0034-5288</issn><eissn>1532-2661</eissn><abstract>Oral squamous cell carcinomas (OSCCs) develop commonly in cats. 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CDKN2A protein (p16), which can be detected using immunohistochemistry. In cats, increased p16 immunoreactivity has been reported within PV-associated skin lesions. This study evaluated p16 immunoreactivity within 30 feline OSCCs. Additionally, PCR was used to amplify PV DNA from the OSCCs. Increased p16 immunoreactivity was present within 2 OSCCs. However, as PV DNA was not amplified from any OSCC in this study, it cannot be confirmed that the increased p16 was caused by PV infection. Therefore, these results do not support the hypothesis that PVs are a significant cause of OSCCs in cats. Loss of p16 expression is considered an important process in the development of human non-PV-induced OSCCs. In contrast, loss of p16 immunoreactivity was only present in 2 feline OSCCs. This suggests that human and feline OSCCs develop due to different molecular mechanisms.</abstract><cop>Oxford</cop><pub>Elsevier India Pvt Ltd</pub><doi>10.1016/j.rvsc.2010.06.014</doi><tpages>4</tpages></addata></record> |
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| ispartof | Research in veterinary science, 2011-04, Vol.90 (2), p.280-283 |
| issn | 0034-5288 1532-2661 |
| language | eng |
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| source | ScienceDirect Journals (5 years ago - present) |
| subjects | Carcinogenesis Cat Hypotheses Immunohistochemistry Oncology Oral squamous cell carcinoma P16 Papillomavirus Polymerase chain reaction Proteins Tobacco Veterinary medicine |
| title | Evaluation of feline oral squamous cell carcinomas for p16 CDKN2A protein immunoreactivity and the presence of papillomaviral DNA |
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