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p53 polymorphism and association of human papillomavirus in oral submucous fibrosis and oral squamous cell carcinoma: A case-control study
The tumor-suppressor p53 protein is inactivated by the human papillomavirus (HPV) E6 oncoprotein, causing polymorphism of the p53 at codon 72 of exon either proline (Pro) or arginine (Arg). Specific allele predisposition has been reported in the literature. The association between the p53 allele and...
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Published in: | Journal of oral and maxillofacial pathology : JOMFP 2019-01, Vol.23 (1), p.97-103 |
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creator | Hallikeri, Kaveri Burde, Krishna Anehosur, Venktesh Kulkarni, Bhushan B Hiremath, Shivaprakash V |
description | The tumor-suppressor p53 protein is inactivated by the human papillomavirus (HPV) E6 oncoprotein, causing polymorphism of the p53 at codon 72 of exon either proline (Pro) or arginine (Arg). Specific allele predisposition has been reported in the literature. The association between the p53 allele and HPV types has been reported. We analyzed the association between p53 polymorphism at codon 72 and HPV 16 and 18 genotypes in control, oral submucous fibrosis (OSF) and oral squamous cell carcinoma (OSCC).
Of the total 90 cases, biopsy tissues of all groups (30 cases of OSF, OSCC and control each) were collected to extract DNA. Polymerase chain reaction was used to detect HPV 16 and 18 and alleles of codon 72 in p53 were evaluated in all the samples.
In control, OSF and OSCC samples showed the presence HPV 63.3%, 33.3% and 60%, respectively. In OSF, HPV 16 and 18 was detected in four and four cases, respectively, whereas in OSCC, HPV 16 and 18 was detected in ten and nine cases, respectively. In all three groups, predominantly, Arg/Arg protein was present followed by Pro/Pro and Arg/Pro. Among the control, Arg/Arg type protein was frequently seen followed by Arg/Pro, Pro/Pro in the presence of HPV. OSF and OSCC were associated homologous genes in the presence of HPV.
The definite association between p53 codon 72, polymorphism and HPV 16 and 18 was seen in OSCC with low frequency in OSF. Frequency of homozygous genotype is at high risk in the presence of HPV 16 and 18 in developing OSCC. |
doi_str_mv | 10.4103/jomfp.JOMFP_180_18 |
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Of the total 90 cases, biopsy tissues of all groups (30 cases of OSF, OSCC and control each) were collected to extract DNA. Polymerase chain reaction was used to detect HPV 16 and 18 and alleles of codon 72 in p53 were evaluated in all the samples.
In control, OSF and OSCC samples showed the presence HPV 63.3%, 33.3% and 60%, respectively. In OSF, HPV 16 and 18 was detected in four and four cases, respectively, whereas in OSCC, HPV 16 and 18 was detected in ten and nine cases, respectively. In all three groups, predominantly, Arg/Arg protein was present followed by Pro/Pro and Arg/Pro. Among the control, Arg/Arg type protein was frequently seen followed by Arg/Pro, Pro/Pro in the presence of HPV. OSF and OSCC were associated homologous genes in the presence of HPV.
The definite association between p53 codon 72, polymorphism and HPV 16 and 18 was seen in OSCC with low frequency in OSF. Frequency of homozygous genotype is at high risk in the presence of HPV 16 and 18 in developing OSCC.</description><identifier>ISSN: 0973-029X</identifier><identifier>EISSN: 1998-393X</identifier><identifier>DOI: 10.4103/jomfp.JOMFP_180_18</identifier><identifier>PMID: 31110424</identifier><language>eng</language><publisher>India: Medknow Publications and Media Pvt. Ltd</publisher><subject>Age ; Alleles ; Analysis ; ARG protein ; Arginine ; Biopsy ; Cancer ; Carcinoma ; Cell cycle ; Cervical cancer ; Codons ; Deoxyribonucleic acid ; DNA ; Fibrosis ; Gene polymorphism ; Genetic aspects ; Genotype & phenotype ; Genotypes ; Human papillomavirus ; Infections ; Oral cancer ; Oral squamous cell carcinoma ; p53 Protein ; Papillomavirus ; Papillomavirus infections ; Polymerase chain reaction ; Polymorphism ; Proline ; Squamous cell carcinoma ; Tumor proteins ; Tumors</subject><ispartof>Journal of oral and maxillofacial pathology : JOMFP, 2019-01, Vol.23 (1), p.97-103</ispartof><rights>COPYRIGHT 2019 Medknow Publications and Media Pvt. Ltd.</rights><rights>2019. This work is published under https://creativecommons.org/licenses/by-nc-sa/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c313t-f7889cd3fa094c2a00523480ee9c0a45af7f09ca80ea6b0cecb665ed7a7edd413</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/2213065351?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,4024,25753,27923,27924,27925,37012,37013,44590</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31110424$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hallikeri, Kaveri</creatorcontrib><creatorcontrib>Burde, Krishna</creatorcontrib><creatorcontrib>Anehosur, Venktesh</creatorcontrib><creatorcontrib>Kulkarni, Bhushan B</creatorcontrib><creatorcontrib>Hiremath, Shivaprakash V</creatorcontrib><title>p53 polymorphism and association of human papillomavirus in oral submucous fibrosis and oral squamous cell carcinoma: A case-control study</title><title>Journal of oral and maxillofacial pathology : JOMFP</title><addtitle>J Oral Maxillofac Pathol</addtitle><description>The tumor-suppressor p53 protein is inactivated by the human papillomavirus (HPV) E6 oncoprotein, causing polymorphism of the p53 at codon 72 of exon either proline (Pro) or arginine (Arg). Specific allele predisposition has been reported in the literature. The association between the p53 allele and HPV types has been reported. We analyzed the association between p53 polymorphism at codon 72 and HPV 16 and 18 genotypes in control, oral submucous fibrosis (OSF) and oral squamous cell carcinoma (OSCC).
Of the total 90 cases, biopsy tissues of all groups (30 cases of OSF, OSCC and control each) were collected to extract DNA. Polymerase chain reaction was used to detect HPV 16 and 18 and alleles of codon 72 in p53 were evaluated in all the samples.
In control, OSF and OSCC samples showed the presence HPV 63.3%, 33.3% and 60%, respectively. In OSF, HPV 16 and 18 was detected in four and four cases, respectively, whereas in OSCC, HPV 16 and 18 was detected in ten and nine cases, respectively. In all three groups, predominantly, Arg/Arg protein was present followed by Pro/Pro and Arg/Pro. Among the control, Arg/Arg type protein was frequently seen followed by Arg/Pro, Pro/Pro in the presence of HPV. OSF and OSCC were associated homologous genes in the presence of HPV.
The definite association between p53 codon 72, polymorphism and HPV 16 and 18 was seen in OSCC with low frequency in OSF. Frequency of homozygous genotype is at high risk in the presence of HPV 16 and 18 in developing OSCC.</description><subject>Age</subject><subject>Alleles</subject><subject>Analysis</subject><subject>ARG protein</subject><subject>Arginine</subject><subject>Biopsy</subject><subject>Cancer</subject><subject>Carcinoma</subject><subject>Cell cycle</subject><subject>Cervical cancer</subject><subject>Codons</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Fibrosis</subject><subject>Gene polymorphism</subject><subject>Genetic aspects</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Human papillomavirus</subject><subject>Infections</subject><subject>Oral cancer</subject><subject>Oral squamous cell carcinoma</subject><subject>p53 Protein</subject><subject>Papillomavirus</subject><subject>Papillomavirus infections</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism</subject><subject>Proline</subject><subject>Squamous cell carcinoma</subject><subject>Tumor proteins</subject><subject>Tumors</subject><issn>0973-029X</issn><issn>1998-393X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNptUtuKFDEQDaK44-gP-CABX3zpMbee7vg2LK4XVtYHhX0LNenEzdDp9CbdC_MLfrU1M-sVKUJI1TmHk6oi5DlnK8WZfL1L0Y-rj1efLj4b3jI8D8iCa91WUsvrh2TBdCMrJvT1GXlSyo6xulW1eEzOJOecKaEW5PtYSzqmfh9THm9CiRSGjkIpyQaYQhpo8vRmjjDQEcbQ9ynCXchzoQFLGXpa5m2cbcKMD9ucSihHiVPtdoZ4KFnX99RCtmFAgTd0g4_iKpuGKSfETXO3f0oeeeiLe3Z_L8nXi7dfzt9Xl1fvPpxvLisruZwq37Sttp30wLSyAvBXQqqWOactA1WDbzzTFjAD6y2zzm7X69p1DTSu6xSXS_LqpDvmdDu7MpkYysEgDA69GiGkQGnNBUJf_gPdpTkP6A5RXLJ1LWv-G_UNemfC4NOUwR5EzaZupVTHWJLVf1AYnYsBG-F8wPxfBHEiWOxqyc6bMYcIeW84M4cFMMcFMH8uAJJe3DvGsbjuF-XnxOUPbuuv1g</recordid><startdate>201901</startdate><enddate>201901</enddate><creator>Hallikeri, Kaveri</creator><creator>Burde, Krishna</creator><creator>Anehosur, Venktesh</creator><creator>Kulkarni, Bhushan B</creator><creator>Hiremath, Shivaprakash V</creator><general>Medknow Publications and Media Pvt. 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Kulkarni, Bhushan B ; Hiremath, Shivaprakash V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c313t-f7889cd3fa094c2a00523480ee9c0a45af7f09ca80ea6b0cecb665ed7a7edd413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Age</topic><topic>Alleles</topic><topic>Analysis</topic><topic>ARG protein</topic><topic>Arginine</topic><topic>Biopsy</topic><topic>Cancer</topic><topic>Carcinoma</topic><topic>Cell cycle</topic><topic>Cervical cancer</topic><topic>Codons</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Fibrosis</topic><topic>Gene polymorphism</topic><topic>Genetic aspects</topic><topic>Genotype & phenotype</topic><topic>Genotypes</topic><topic>Human papillomavirus</topic><topic>Infections</topic><topic>Oral cancer</topic><topic>Oral squamous cell carcinoma</topic><topic>p53 Protein</topic><topic>Papillomavirus</topic><topic>Papillomavirus infections</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism</topic><topic>Proline</topic><topic>Squamous cell carcinoma</topic><topic>Tumor proteins</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hallikeri, Kaveri</creatorcontrib><creatorcontrib>Burde, Krishna</creatorcontrib><creatorcontrib>Anehosur, Venktesh</creatorcontrib><creatorcontrib>Kulkarni, Bhushan B</creatorcontrib><creatorcontrib>Hiremath, Shivaprakash V</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest research library</collection><collection>ProQuest Biological Science Journals</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of oral and maxillofacial pathology : JOMFP</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hallikeri, Kaveri</au><au>Burde, Krishna</au><au>Anehosur, Venktesh</au><au>Kulkarni, Bhushan B</au><au>Hiremath, Shivaprakash V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>p53 polymorphism and association of human papillomavirus in oral submucous fibrosis and oral squamous cell carcinoma: A case-control study</atitle><jtitle>Journal of oral and maxillofacial pathology : JOMFP</jtitle><addtitle>J Oral Maxillofac Pathol</addtitle><date>2019-01</date><risdate>2019</risdate><volume>23</volume><issue>1</issue><spage>97</spage><epage>103</epage><pages>97-103</pages><issn>0973-029X</issn><eissn>1998-393X</eissn><abstract>The tumor-suppressor p53 protein is inactivated by the human papillomavirus (HPV) E6 oncoprotein, causing polymorphism of the p53 at codon 72 of exon either proline (Pro) or arginine (Arg). Specific allele predisposition has been reported in the literature. The association between the p53 allele and HPV types has been reported. We analyzed the association between p53 polymorphism at codon 72 and HPV 16 and 18 genotypes in control, oral submucous fibrosis (OSF) and oral squamous cell carcinoma (OSCC).
Of the total 90 cases, biopsy tissues of all groups (30 cases of OSF, OSCC and control each) were collected to extract DNA. Polymerase chain reaction was used to detect HPV 16 and 18 and alleles of codon 72 in p53 were evaluated in all the samples.
In control, OSF and OSCC samples showed the presence HPV 63.3%, 33.3% and 60%, respectively. In OSF, HPV 16 and 18 was detected in four and four cases, respectively, whereas in OSCC, HPV 16 and 18 was detected in ten and nine cases, respectively. In all three groups, predominantly, Arg/Arg protein was present followed by Pro/Pro and Arg/Pro. Among the control, Arg/Arg type protein was frequently seen followed by Arg/Pro, Pro/Pro in the presence of HPV. OSF and OSCC were associated homologous genes in the presence of HPV.
The definite association between p53 codon 72, polymorphism and HPV 16 and 18 was seen in OSCC with low frequency in OSF. Frequency of homozygous genotype is at high risk in the presence of HPV 16 and 18 in developing OSCC.</abstract><cop>India</cop><pub>Medknow Publications and Media Pvt. Ltd</pub><pmid>31110424</pmid><doi>10.4103/jomfp.JOMFP_180_18</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Age Alleles Analysis ARG protein Arginine Biopsy Cancer Carcinoma Cell cycle Cervical cancer Codons Deoxyribonucleic acid DNA Fibrosis Gene polymorphism Genetic aspects Genotype & phenotype Genotypes Human papillomavirus Infections Oral cancer Oral squamous cell carcinoma p53 Protein Papillomavirus Papillomavirus infections Polymerase chain reaction Polymorphism Proline Squamous cell carcinoma Tumor proteins Tumors |
title | p53 polymorphism and association of human papillomavirus in oral submucous fibrosis and oral squamous cell carcinoma: A case-control study |
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