Prevalence of high‐risk human papilloma virus types and its association with P53 codon 72 polymorphism in tobacco addicted oral squamous cell carcinoma (oscc) patients of Eastern India

Abstract

Key words: p53 polymorphism; HPV; oral cancerOral squamous cell carcinoma (OSCC) is the sixth most common malignancy and is a major cause of cancer morbidity and mortality worldwide. The overall survival percentage has not changed in recent years, despite extensive research on the biological and molecular aspects of oral SCC. Among the more pressing problems in clinical management are the lack of early detection and the high incidence of local-regional recurrence, even with aggressive surgical therapy. OSCC incidence accounts for up to 40% of all malignancies in India and South East Asia. 1 Moreover differences have been observed in the clinico-pathological and molecular pathological profile in the tobacco smoking and alcoholassociated oral cancers in the USA, UK, France, Japan, etc. and the chewing tobacco-associated oral cancers, particularly in the Indian sub-continent. 2 In India, oral leukoplakias have been reported to show a significant tendency to malignant transformation from 0.13 to 6% and rising to 14% or higher in cases of dysplasia. 3,4 Epidemiological studies reveal the betel quid and tobacco chewing habit as an important risk factor in the etiology of oral cancer in India. Since carcinogenesis is a multi-step process, therefore, in addition to insult by tobacco-associated intra oral carcinogens, several additional factors, such as genetic susceptibility of individuals and external agents, such as dietary factors and viruses (human papillomavirus, HPV, and Epstein-Baar virus, EBV), may play a synergetic role in oral tumorigenesis. [5][6][7][8] HPVs are a very heterogenous group of DNA viruses. Almost 90 HPV types have been described; 30 of these types are associated with anogenital cancers, forming either the high-risk types (HPV16 and HPV18) that are associated with anogenital invasive tumour and their precursor lesions or the low-risk types (HPV6 and HPV11) that rarely progress to malignancy. Analysis of viral genome has revealed that 2 early genes, E6 and E7, of high risk HPVs (16/18) are transforming genes that are responsible for maintenance of tumorigenic phenotype. 6,9,10 Genetic polymorphism at the genes involved in tumorigenesis may determine individual susceptibility of cancer. The genotype distribution of p53 codon 72 polymorphism is significantly different among ethnic groups. 11 Storey et al. 12 recently reported the probable correlation between p53 polymorphism and HPV associated cervical tumorigenesis. They showed that population homozygous for Arg-72 (arginine) is about 7 times more susceptible to development of cervical cancer than heterozygotes. However, this has been subject of much debate. Makni et al. 13 recently showed the substantial inter-laboratory variation in the proportion of Arg/Arg, Arg/Pro (proline) and Pro/Pro.In spite of its great relevance, so far only 2 contradictory reports have been proposed on the status of HPV in oral cancer on Indian population. The work on South Indian population has indicated 42% HPV-16 infection and 47% of HPV-18 infection, 7 whereas the r...

Association between p53 Gene Variants and Oral Cancer Susceptibility in Population from Gujarat, West India

“…They have observed that the Proline allele was more frequent in control population and no association was found between oral cancer risk and Arg72Pro polymorphism. Another study from east region of India noted that Arginine allele was more frequent in population (Nagpal et al, 2002). In the present study, Arginine allele was more frequent in this population.…”

“…The controls as well as the cases belonged to same ethnicity and were from the same geographic location. An allele frequency of Arg72Pro polymorphism has been reported to vary with respect to ethnicity and latitude (Nagpal et al, 2002). The allele frequency of proline at codon 72 varies from 0.12-0.69 worldwide (Francisco et al, 2011) whereas for the Indian population; it ranges from 0.42-0.72 (Nagpal et al, 2002;Tandle et al, 2001;Mitra et al, 2003;Mittal et al, 2011;Suresh et al, 2011).…”

No role for human papillomavirus infection in oral cancers in a region in southern India

“…The reported HPV prevalence in oral cancers in India varied from 0 to 100% in studies using biopsies in cases and PCR assay for HPV detection and genotyping. [14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] For the studies using a methodology similar to ours (oral brushing to collect epithelial cells instead of biopsy, combined with PCR for detection and genotyping), the prevalence reported for oral cancer cases was 31.5 26 and 32.4%. 15 Our results are in agreement with two studies conducted in Gujarat and Mumbai in West India, which reported a null prevalence of HPV in oral cancer using biopsies (in one of the studies, only HPV-16 and 18 were tested).…”

“…12 One-on-one semistructured interviews using a questionnaire and life grid technique, which has been shown to improve recall, 13 were conducted by three professionally trained dentists. Data collected included sociodemographic information, religious beliefs, environmental variables and sexual behavior including age at first sexual intercourse, number of sexual partners and oral sex practice frequency during three different life stages ( 16,(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30) and >30 years).…”

Correlation of Presence of Candida and Epithelial Dysplasia in Oral Mucosal Lesions

“…Although recent advancement in research methodologies as well as longitudinal follow up of the rate of incidence, confirms genetic factors as a major contributing factor in etiopathogenesis of such malignancies [3][4][5].…”