Dataset Information

P53 polymorphism and association of human papillomavirus in oral submucous fibrosis and oral squamous cell carcinoma: A case-control study.

ABSTRACT: Introduction: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). Materials and Methods: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. Results: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. Conclusion: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.

SUBMITTER: Hallikeri K

PROVIDER: S-EPMC6503778 | biostudies-literature | 2019 Jan-Apr

REPOSITORIES: biostudies-literature

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p53 polymorphism and association of human papillomavirus in oral submucous fibrosis and oral squamous cell carcinoma: A case-control study.

Hallikeri Kaveri K Burde Krishna K Anehosur Venktesh V Kulkarni Bhushan B BB Hiremath Shivaprakash V SV

Journal of oral and maxillofacial pathology : JOMFP 20190101 1

<h4>Introduction</h4>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 squam ...[more]

PMID: 31110424

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Project description:Squamous cell carcinoma of the penis is a rare but often aggressive disease. A large proportion of penile cancers are associated with HPV infection, mainly with HPV high-risk subtypes 16 and 18. From other HPV-related malignancies a link between a functional SNP in the p53 gene (rs1042522, p.Arg72Pro) and a higher disease risk in the presence of HPV is documented. The p53 p.Arg72 variant was described as a risk factor for developing a malignancy in combination with the presence of HPV as the p.72Arg variant is more prone to HPV E6 protein-mediated degradation than the p.72Pro variant. For penile carcinoma there are only sparse data available on this topic. We therefore analyzed the distribution of this p53 codon 72 SNP in a cohort of 107 penile cancer patients and a healthy control group (n=194) using Restriction Fragment Length Polymorphism (RFLP) analysis. After DNA isolation a PCR amplicon including the variant nucleotide was generated. Based on the variant nucleotide this amplicon can be cleaved into two parts or remain unaffected by a restriction enzyme. Subsequent electrophoresis allowed the discrimination of SNP alleles in the investigated sample. Comparison of the allelic variants revealed no significant differences in the distribution of this SNP between cases and controls (p=0,622). There was also no difference in SNP distribution between cases with/without HPV infection (p=0,558) or histologic variants (p=0.339). In order to strengthen the impact of our data we performed a combined analysis of all published data on this topic with our results. This ended up in SNP distribution data from 177 cases and 1149 controls. Overall, there were also no significant differences in the allelic distribution of the p53 codon 72 SNP between either cases and controls (p=0,914) or HPV-positive and HPV-negative cases (p=0,486). From this most comprehensive data available to date we conclude that there is no influence of the p53 codon 72 SNP on the risk of development of penile carcinoma in Caucasians even in the presence of HPV.

Dataset Information

P53 polymorphism and association of human papillomavirus in oral submucous fibrosis and oral squamous cell carcinoma: A case-control study.

Publications

p53 polymorphism and association of human papillomavirus in oral submucous fibrosis and oral squamous cell carcinoma: A case-control study.

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