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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Bibliographic Details
Published in:Journal of oral and maxillofacial pathology : JOMFP 2019-01, Vol.23 (1), p.97-103
Main Authors: Hallikeri, Kaveri, Burde, Krishna, Anehosur, Venktesh, Kulkarni, Bhushan B, Hiremath, Shivaprakash V
Format: Article
Language:English
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
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Summary: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.
ISSN:0973-029X
1998-393X
DOI:10.4103/jomfp.JOMFP_180_18