Abnormal cell-cycle expression of the proteins p27, mdm2 and cathepsin B in oral squamous-cell carcinoma infected with human papillomavirus

Since the role of human papillomavirus (HPV) infection in oral carcinogenesis is still unclear, the purpose of this study was to verify the association between the expression of p27, mdm2 and cathepsin B and by HPV-related oral lesions. Fifty-five oral biopsies were studied and HPV detection and typ...

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Published in:Acta histochemica Vol. 113; no. 2; pp. 109 - 116
Main Authors: Cristina Mazon, Renata, Rovigatti Gerbelli, Thaís, Benatti Neto, Carlos, de Oliveira, Maria Rita Brancini, Antonio Donadi, Eduardo, Guimarães Gonçalves, Maria Alice, Garcia Soares, Edson, Patrícia Klay, Carla, Tersariol, Ivarne, Aparecida Pinhal, Maria, Resende, Luis, Pienna Soares, Christiane
Format: Journal Article
Language:English
Published: Germany Elsevier GmbH 01-02-2011
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Abstract Since the role of human papillomavirus (HPV) infection in oral carcinogenesis is still unclear, the purpose of this study was to verify the association between the expression of p27, mdm2 and cathepsin B and by HPV-related oral lesions. Fifty-five oral biopsies were studied and HPV detection and typing (6/11, 16, 18, 31 and 33) were performed using polymerase chain reaction techniques. The distribution p27, mdm2 and cathepsin B was determined by immunohistochemistry. Twenty-one (38%) out of the 55 oral lesions tested positive for HPV, of which 6 (33%) were HPV 6/11, 1 (5%) was HPV 16, 14 (72%) were HPV 18 and none was HPV 33/31. Among the 55 biopsies, immunopostivity for p27, mdm2 and cathepsin B was observed in 17 (30.9%), 37 (67.2%) and 37 (67.2%), respectively. Among 21 HPV-positive oral lesions, immunopostivity of mdm2, p27 and cathepsin B was found, respectively, in 6 (33%) out of 18 benign lesions (BL), 4 (22%) out of 18 potential malignant epithelial lesions (PMEL) and 11 (57.9%) out of 19 malignant lesions (ML). High-risk HPV types may be associated with oral carcinoma, by cell-cycle control dysregulation, contributing to oral carcinogenesis and the overexpression of mdm2, p27 and cathepsin B.
AbstractList Since the role of human papillomavirus (HPV) infection in oral carcinogenesis is still unclear, the purpose of this study was to verify the association between the expression of p27, mdm2 and cathepsin B and by HPV-related oral lesions. Fifty-five oral biopsies were studied and HPV detection and typing (6/11, 16, 18, 31 and 33) were performed using polymerase chain reaction techniques. The distribution p27, mdm2 and cathepsin B was determined by immunohistochemistry. Twenty-one (38%) out of the 55 oral lesions tested positive for HPV, of which 6 (33%) were HPV 6/11, 1 (5%) was HPV 16, 14 (72%) were HPV 18 and none was HPV 33/31. Among the 55 biopsies, immunopostivity for p27, mdm2 and cathepsin B was observed in 17 (30.9%), 37 (67.2%) and 37 (67.2%), respectively. Among 21 HPV-positive oral lesions, immunopostivity of mdm2, p27 and cathepsin B was found, respectively, in 6 (33%) out of 18 benign lesions (BL), 4 (22%) out of 18 potential malignant epithelial lesions (PMEL) and 11 (57.9%) out of 19 malignant lesions (ML). High-risk HPV types may be associated with oral carcinoma, by cell-cycle control dysregulation, contributing to oral carcinogenesis and the overexpression of mdm2, p27 and cathepsin B.
Since the role of human papillomavirus (HPV) infection in oral carcinogenesis is still unclear, the purpose of this study was to verify the association between the expression of p27, mdm2 and cathepsin B and by HPV-related oral lesions. Fifty-five oral biopsies were studied and HPV detection and typing (6/11, 16, 18, 31 and 33) were performed using polymerase chain reaction techniques. The distribution p27, mdm2 and cathepsin B was determined by immunohistochemistry. Twenty-one (38%) out of the 55 oral lesions tested positive for HPV, of which 6 (33%) were HPV 6/11, 1 (5%) was HPV 16, 14 (72%) were HPV 18 and none was HPV 33/31. Among the 55 biopsies, immunopositivity for p27, mdm2 and cathepsin B was observed in 17 (30.9%), 37 (67.2%) and 37 (67.2%), respectively. Among 21 HPV-positive oral lesions, immunopositivity of mdm2, p27 and cathepsin B was found, respectively, in 6 (33%) out of 18 benign lesions (BL), 4 (22%) out of 18 potential malignant epithelial lesions (PMEL) and 11 (57.9%) out of 19 malignant lesions (ML). High-risk HPV types may be associated with oral carcinoma, by cell-cycle control dysregulation, contributing to oral carcinogenesis and the overexpression of mdm2, p27 and cathepsin B.
Author Garcia Soares, Edson
Antonio Donadi, Eduardo
Guimarães Gonçalves, Maria Alice
Patrícia Klay, Carla
Resende, Luis
Tersariol, Ivarne
Cristina Mazon, Renata
Aparecida Pinhal, Maria
Pienna Soares, Christiane
Benatti Neto, Carlos
de Oliveira, Maria Rita Brancini
Rovigatti Gerbelli, Thaís
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Issue 2
Keywords Immunohistochemistry
Cathepsin B
Oral cancer
p27
HPV
mdm2
Language English
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Snippet Since the role of human papillomavirus (HPV) infection in oral carcinogenesis is still unclear, the purpose of this study was to verify the association between...
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SubjectTerms Benign
Carcinoma, Squamous Cell - genetics
Carcinoma, Squamous Cell - virology
Cathepsin B
Cathepsin B - analysis
Cathepsin B - biosynthesis
Cathepsin B - genetics
Cell Cycle - genetics
Cyclin-Dependent Kinase Inhibitor p27 - analysis
Cyclin-Dependent Kinase Inhibitor p27 - biosynthesis
Cyclin-Dependent Kinase Inhibitor p27 - genetics
HPV
Human papillomavirus
Humans
Immunohistochemistry
mdm2
Mouth Neoplasms - genetics
Mouth Neoplasms - virology
Oral cancer
p27
Papillomavirus Infections - complications
Papillomavirus Infections - genetics
Proto-Oncogene Proteins c-mdm2 - analysis
Proto-Oncogene Proteins c-mdm2 - biosynthesis
Proto-Oncogene Proteins c-mdm2 - genetics
Reverse Transcriptase Polymerase Chain Reaction
Title Abnormal cell-cycle expression of the proteins p27, mdm2 and cathepsin B in oral squamous-cell carcinoma infected with human papillomavirus
URI https://dx.doi.org/10.1016/j.acthis.2009.08.008
https://www.ncbi.nlm.nih.gov/pubmed/19811804
https://search.proquest.com/docview/911150629
Volume 113
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