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      Infección por papiloma virus humano y carcinoma escamocelular bucal: diversas técnicas moleculares para detectar su presencia Translated title: Human papillomavirus infection. Relationship with oral squamous cancer: several techniques for detecting its presence

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          Abstract

          El cáncer bucal (CB) es una neoplasia maligna de comportamiento agresivo, que comprende el 4 al 5 % de todos los tumores, con una alta tasa de mortalidad, la gran mayoría son carcinomas escamocelulares (90%). Entre los factores de riesgo asociados al CB se describen el tabaquismo, predisposición genética, alcohol y últimamente se menciona algunos virus con el virus de papiloma humano (VPH) entre otros. El objetivo del presente artículo es revisar los reportes de literatura que dan cuenta de la relación que existe entre CB y VPH, específicamente se describe el comportamiento molecular de los VPH de alto riesgo, el mapa genómico del virus y su posible relación con CB. La evidencia científica muestra que entre el 15 al 30% de los CB están relacionados con HPV, específicamente el subtipo 16 considerado de alto riesgo oncogénico y que los individuos con presencia de VPH bucal tienen dos veces mayor riesgo de desarrollar un CB que aquel que no está expuesto al virus.

          Translated abstract

          Oral cancer (BC) is an aggressive malignancy that includes 4 to 5% of all tumors with a high mortality rate, the vast majority are squamous cell carcinomas (90%). Among the factors risk associated with CB are described smoking, genetic predisposition, alcohol and recently mentioned some virus papilloma virus (HPV) among others. The aim of this paper is to review literature reports that account for the relationship between CB and HPV, specifically describing the molecular behavior of HPV high risk, the genome map of the virus and its possible relationship with CB. The Scientific evidence shows that between 15 to 30% of CB are related to HPV, specifically the subtype 16 considered high risk oncogenic and that individuals with oral HPV presence are twice increased risk of developing a CB who is not exposed to the virus.

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          Most cited references131

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          The papillomavirus life cycle.

          Papillomaviruses infect epithelial cells, and depend on epithelial differentiation for completion of their life cycle. The expression of viral gene products is closely regulated as the infected basal cell migrates towards the epithelial surface. Expression of E6 and E7 in the lower epithelial layers drives cells into S-phase, which creates an environment that is conducive for viral genome replication and cell proliferation. Genome amplification, which is necessary for the production of infectious virions, is prevented until the levels of viral replication proteins rise, and depends on the co-expression of several viral proteins. Virus capsid proteins are expressed in cells that also express E4 as the infected cell enters the upper epithelial layers. The timing of these events varies depending on the infecting papillomavirus, and in the case of the high-risk human papillomaviruses (HPVs), on the severity of neoplasia. Viruses that are evolutionarily related, such as HPV1 and canine oral papillomavirus (COPV), generally organize their productive cycle in a similar way, despite infecting different hosts and epithelial sites. In some instances, such as following HPV16 infection of the cervix or cottontail rabbit papillomavirus (CRPV) infection of domestic rabbits, papillomaviruses can undergo abortive infections in which the productive cycle of the virus is not completed. As with other DNA tumour viruses, such abortive infections can predispose to cancer.
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            Prevalence and determinants of HPV infection among Colombian women with normal cytology

            Human papillomavirus is the principal risk factor associated with cervical cancer, the most common malignancy among women in Colombia. We conducted a survey, aiming to report type specific prevalence and determinants of human papillomavirus infection in women with normal cytology. A total of 1859 women from Bogota, Colombia were interviewed and tested for human papillomavirus using a general primer GP5+/GP6+ mediated PCR–EIA. The overall HPV DNA prevalence was 14.8%; 9% of the women were infected by high risk types, 3.1% by low risk types, 2.3% by both high risk/low risk types and 0.4% by uncharacterized types (human papillomavirus X). Thirty-two different human papillomavirus types were detected, being human papillomavirus 16, 58, 56, 81(CP8304) and 18 the most common types. The human papillomavirus prevalence was 26.1% among women younger than 20 years, 2.3% in women aged 45–54 years, and 13.2% in women aged 55 years or more. For low risk types the highest peak of prevalence was observed in women aged 55 years or more. Compared to women aged 35–44 years, women aged less than 20 years had a 10-fold increased risk of having multiple infections. Besides age, there was a positive association between the risk of human papillomavirus infection and number of regular sexual partners and oral contraceptive use. In women aged below 25 years, high educational level and having had casual sexual partners predicted infection risk. In conclusion, there was a broad diversity of human papillomavirus infections with high risk types being the most common types detected. In this population multiplicity of sexual partners and, among young women, high educational level and casual sexual partners seem to determine risk. British Journal of Cancer (2002) 87, 324–333. doi:10.1038/sj.bjc.6600442 www.bjcancer.com © 2002 Cancer Research UK
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              Oral human papillomavirus in healthy individuals: a systematic review of the literature.

              Human papillomavirus type 16 (HPV16) is a common infection in the anogenital tract. HPV16 DNA detected in oral specimens has recently been identified as a risk factor for some oropharyngeal cancers. The reported prevalence of oral HPV infection from individual studies is highly variable. We systematically reviewed and abstracted data from published studies (n = 18) that detected oral HPV DNA in 4581 cancer-free subjects to determine the pooled prevalence (and 95% confidence intervals [CI]) of HPV16, carcinogenic HPV, and any HPV. 1.3% (95% CI: 1.0-1.7%) of 3977 healthy subjects had oral HPV16, 3.5% (95% CI: 3.0-4.1) of 4441 subjects had carcinogenic HPV, and 4.5% (95% CI: 3.9-5.1) of 4070 subjects were positive for any HPV. Oral HPV16 accounted for 28% of all HPV detected in the oral region. Men (47 of 1017) and women (117 of 3690) had nearly exactly the same prevalence of any oral HPV detected (4.6% vs. 4.4%, respectively). HPV-16, a common anogenital infection, was rarely detected in oral specimens. However, a small but noteworthy proportion of healthy individuals have oral HPV infections with types known to cause cancer in the oral region.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Journal
                odonto
                Avances en Odontoestomatología
                Av Odontoestomatol
                Ediciones Avances, S.L. (Madrid, Madrid, Spain )
                0213-1285
                2340-3152
                April 2014
                : 30
                : 2
                : 69-78
                Affiliations
                [03] orgnameGITOUC Grupo interdisciplinario de Investigaciones y Tratamientos Odontológicos (GITOUC)
                [01] Cartagena orgnameUniversidad de Cartagena
                [02] orgnameGrupo de investigación Universitaria de Medicina (GINUMED)
                Article
                S0213-12852014000200003
                10.4321/s0213-12852014000200003
                5c69dc6e-5730-495a-b895-7f230e0f195b

                This work is licensed under a Creative Commons Attribution-NonCommercial 3.0 International License.

                History
                : 26 January 2012
                : 15 May 2012
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 82, Pages: 10
                Product

                SciELO Spain


                Papillomavirus humano 6,carcinoma de células escamosas,transformación celular neoplásica,Human Papilloma Virus,carcinoma squamous cell,Neoplastic transformation

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