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p16 Immunostaining of Canine Squamous Cell Carcinomas Is Not Associated with Papillomaviral DNA

Identifieur interne : 000030 ( Pmc/Curation ); précédent : 000029; suivant : 000031

p16 Immunostaining of Canine Squamous Cell Carcinomas Is Not Associated with Papillomaviral DNA

Auteurs : Silvia Sabattini [Italie] ; Federica Savini [Italie] ; Laura Gallina [Italie] ; Alessandra Scagliarini [Italie] ; Patrizia Bassi [Italie] ; Giuliano Bettini [Italie]

Source :

RBID : PMC:4956233

Abstract

While papillomavirus (PVs) are an established cause of human cancer, few reports have supported a relationship between PV and canine squamous cell carcinomas (SCCs). Human oncogenic PVs lead to an increased expression of the p16 tumor suppressor protein, and the latter can be demonstrated immunohistochemically to support a likely causal relationship between tumor and PV infection. In the present study, archive samples of canine SCC from different anatomical locations were tested by polymerase chain reaction for the presence of PV DNA and by p16 immunohistochemistry. The aims were to investigate the relationship between p16 expression and presence of PV DNA, in order to assess the utility of p16 overexpression as a biomarker of PV infection in canine SCC. A total of 52 SCCs were included. Nine cases (17.3%) showed moderate p16 immunoreactivity, with no association with tumor degree of differentiation, histotype or mitotic activity. The canPVf/FAP64 primers amplified Canis familiaris PV-1 DNA from 3 out of 52 tumors (5.8%), one cutaneous, one oral and one tonsillar SCC. There was no association between PV presence and p16 immunostaining. These results do not support a significant role of PVs in the development of canine SCCs. Additionally, PV infection was apparently not the cause of the p16 immunostaining observed in a subset of canine SCCs. A better awareness of p16 level of expression and cellular function in canine cancer may help to define its diagnostic and prognostic role.


Url:
DOI: 10.1371/journal.pone.0159687
PubMed: 27441555
PubMed Central: 4956233

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PMC:4956233

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<p>While papillomavirus (PVs) are an established cause of human cancer, few reports have supported a relationship between PV and canine squamous cell carcinomas (SCCs). Human oncogenic PVs lead to an increased expression of the p16 tumor suppressor protein, and the latter can be demonstrated immunohistochemically to support a likely causal relationship between tumor and PV infection. In the present study, archive samples of canine SCC from different anatomical locations were tested by polymerase chain reaction for the presence of PV DNA and by p16 immunohistochemistry. The aims were to investigate the relationship between p16 expression and presence of PV DNA, in order to assess the utility of p16 overexpression as a biomarker of PV infection in canine SCC. A total of 52 SCCs were included. Nine cases (17.3%) showed moderate p16 immunoreactivity, with no association with tumor degree of differentiation, histotype or mitotic activity. The canPVf/FAP64 primers amplified
<italic>Canis familiaris</italic>
PV-1 DNA from 3 out of 52 tumors (5.8%), one cutaneous, one oral and one tonsillar SCC. There was no association between PV presence and p16 immunostaining. These results do not support a significant role of PVs in the development of canine SCCs. Additionally, PV infection was apparently not the cause of the p16 immunostaining observed in a subset of canine SCCs. A better awareness of p16 level of expression and cellular function in canine cancer may help to define its diagnostic and prognostic role.</p>
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<article-id pub-id-type="pmc">4956233</article-id>
<article-id pub-id-type="doi">10.1371/journal.pone.0159687</article-id>
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<article-title>p16 Immunostaining of Canine Squamous Cell Carcinomas Is Not Associated with Papillomaviral DNA</article-title>
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<contrib contrib-type="author">
<name>
<surname>Sabattini</surname>
<given-names>Silvia</given-names>
</name>
<xref ref-type="aff" rid="aff001">
<sup>1</sup>
</xref>
</contrib>
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<name>
<surname>Savini</surname>
<given-names>Federica</given-names>
</name>
<xref ref-type="aff" rid="aff002">
<sup>2</sup>
</xref>
</contrib>
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<name>
<surname>Gallina</surname>
<given-names>Laura</given-names>
</name>
<xref ref-type="aff" rid="aff002">
<sup>2</sup>
</xref>
</contrib>
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<name>
<surname>Scagliarini</surname>
<given-names>Alessandra</given-names>
</name>
<xref ref-type="aff" rid="aff002">
<sup>2</sup>
</xref>
</contrib>
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<name>
<surname>Bassi</surname>
<given-names>Patrizia</given-names>
</name>
<xref ref-type="aff" rid="aff001">
<sup>1</sup>
</xref>
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<contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0003-1857-7329</contrib-id>
<name>
<surname>Bettini</surname>
<given-names>Giuliano</given-names>
</name>
<xref ref-type="aff" rid="aff001">
<sup>1</sup>
</xref>
<xref ref-type="corresp" rid="cor001">*</xref>
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<aff id="aff001">
<label>1</label>
<addr-line>Pathology Division, Department of Veterinary Medical Sciences, University of Bologna, Ozzano Emilia (BO), Italy</addr-line>
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<aff id="aff002">
<label>2</label>
<addr-line>Virology Division, Department of Veterinary Medical Sciences, University of Bologna, Ozzano dell’Emilia (BO), Italy</addr-line>
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<name>
<surname>McLaughlin-Drubin</surname>
<given-names>Margaret</given-names>
</name>
<role>Editor</role>
<xref ref-type="aff" rid="edit1"></xref>
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</contrib-group>
<aff id="edit1">
<addr-line>Brigham and Women's Hospital/Harvard Medical School, UNITED STATES</addr-line>
</aff>
<author-notes>
<fn fn-type="conflict" id="coi001">
<p>
<bold>Competing Interests: </bold>
The authors have declared that no competing interests exist.</p>
</fn>
<fn fn-type="con" id="contrib001">
<p>Conceived and designed the experiments: SS GB. Performed the experiments: SS FS LG AS PB. Analyzed the data: SS. Contributed reagents/materials/analysis tools: AS. Wrote the paper: SS LG GB.</p>
</fn>
<corresp id="cor001">* E-mail:
<email>giuliano.bettini@unibo.it</email>
</corresp>
</author-notes>
<pub-date pub-type="epub">
<day>21</day>
<month>7</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="collection">
<year>2016</year>
</pub-date>
<volume>11</volume>
<issue>7</issue>
<elocation-id>e0159687</elocation-id>
<history>
<date date-type="received">
<day>12</day>
<month>3</month>
<year>2016</year>
</date>
<date date-type="accepted">
<day>5</day>
<month>7</month>
<year>2016</year>
</date>
</history>
<permissions>
<copyright-statement>© 2016 Sabattini et al</copyright-statement>
<copyright-year>2016</copyright-year>
<copyright-holder>Sabattini et al</copyright-holder>
<license xlink:href="http://creativecommons.org/licenses/by/4.0/">
<license-p>This is an open access article distributed under the terms of the
<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">Creative Commons Attribution License</ext-link>
, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</license-p>
</license>
</permissions>
<self-uri content-type="pdf" xlink:href="pone.0159687.pdf"></self-uri>
<abstract>
<p>While papillomavirus (PVs) are an established cause of human cancer, few reports have supported a relationship between PV and canine squamous cell carcinomas (SCCs). Human oncogenic PVs lead to an increased expression of the p16 tumor suppressor protein, and the latter can be demonstrated immunohistochemically to support a likely causal relationship between tumor and PV infection. In the present study, archive samples of canine SCC from different anatomical locations were tested by polymerase chain reaction for the presence of PV DNA and by p16 immunohistochemistry. The aims were to investigate the relationship between p16 expression and presence of PV DNA, in order to assess the utility of p16 overexpression as a biomarker of PV infection in canine SCC. A total of 52 SCCs were included. Nine cases (17.3%) showed moderate p16 immunoreactivity, with no association with tumor degree of differentiation, histotype or mitotic activity. The canPVf/FAP64 primers amplified
<italic>Canis familiaris</italic>
PV-1 DNA from 3 out of 52 tumors (5.8%), one cutaneous, one oral and one tonsillar SCC. There was no association between PV presence and p16 immunostaining. These results do not support a significant role of PVs in the development of canine SCCs. Additionally, PV infection was apparently not the cause of the p16 immunostaining observed in a subset of canine SCCs. A better awareness of p16 level of expression and cellular function in canine cancer may help to define its diagnostic and prognostic role.</p>
</abstract>
<funding-group>
<award-group id="award001">
<funding-source>
<institution>FARB—Finanziamenti di Ateneo alla ricerca di base, University of Bologna</institution>
</funding-source>
<principal-award-recipient>
<contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0003-1857-7329</contrib-id>
<name>
<surname>Bettini</surname>
<given-names>Giuliano</given-names>
</name>
</principal-award-recipient>
</award-group>
<funding-statement>This work was supported by grants from the University of Bologna (FARB—Finanziamenti di Ateneo alla ricerca di base). The funding source had no involvement in the study design or in the writing of the report.</funding-statement>
</funding-group>
<counts>
<fig-count count="2"></fig-count>
<table-count count="0"></table-count>
<page-count count="11"></page-count>
</counts>
<custom-meta-group>
<custom-meta id="data-availability">
<meta-name>Data Availability</meta-name>
<meta-value>All relevant data are within the paper and its Supporting Information files.</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
<notes>
<title>Data Availability</title>
<p>All relevant data are within the paper and its Supporting Information files.</p>
</notes>
</front>
</pmc>
</record>

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