Human papillomavirus DMA in oral squamous cell carcinomas and normal mucosa

Abstract

Human papillomavirus (HPV) infections in oral carcinomas and normal oral mucosa were studied by consensus primer screening and typing for HPV types 6/11, 16 and 18 DNA. After polymerase chain reaction (PCR) the DNA species of interest were identified by Southern blot hybridization with digoxigenin-labeled oligonucleotide probes. Frozen tissue and scrapings were equally suitable for HPV testing and yielded high HPV detection rates in carcinomas. By comparison, HPV analysis of paraffin-embedded material was much less efficient. HPV were demonstrated in 61.5% (16/26) of oral squamous cell carcinomas, high risk HPV 16 and 18 being the preferential types. The frequency of HPV detection in non-neoplastic mucosa of tumor patients decreased clearly with increasing distance from the tumor (range 26.9-3.8%) suggesting focal HPV infections. In contrast, normal buccal mucosa of a group of healthy volunteers contained HPV DNA only in 1% (1/97).

Expression of cell cycle markers and human papillomavirus infection in oral squamous cell carcinoma: Use of fuzzy neural networks

“…33 Thus, other agents, such as viruses, are being investigated. 34 In particular, with regard to viral involvement, it is still highly controversial whether HR HPV can be considered an etiologic or a malignant risk factor in oral carcinogenesis: 14 some research groups 14,35,36 have identified HR HPV antigens and viral DNA in potentially malignant and malignant oral lesions, and others have defined HR HPV as playing an important role in OSCC, especially in the absence of common oral habits. 37 Historically, evidence of the carcinogenic role of HR HPVs is based on 2 oncoproteins: HPV-E6, which promotes degradation of the p53 tumor-suppressor gene product, 38 and HPV-E7, which modifies pRb tumor-suppressor gene product function, leading to increased cell proliferation and contributing to carcinogenesis.…”

A High Frequency of Allelic Loss in Oral Verrucous Lesions May Explain Malignant Risk

“…In a recent comprehensive study, Sidransky and co-workers reported a low rate of HPV in oral SCC (12% of cases) (Gillison et al, 2000). However, other studies have reported different frequencies (Ostwald et al, 1994;Snijders et al, 1996). HPV etiology for oral cancer may be better evaluated with improvements in the detection of different types of HPV.…”

Correlação da infecção viral pelo papilomavírus humano com as lesões papilomatosas e o carcinoma epidermóide na boca e orofaringe

“…Apesar da exposição da mucosa oral a vários carcinógenos, somente um pequeno percentual dos indivíduos desenvolvem câncer 1 . Lembrando que a carcinogênese é um processo multifatorial, a mutagênese é determinada também por agentes co-carcinogenéticos como o papilomavírus humano (HPV) 2,3 . O epitélio da cavidade oral e orofaringe é uma membrana mucosa com propensão para o desenvolvimento neoplásico, sendo exposto a vários carcinógenos nutricionais e ambientais, determinantes de lesões decorrentes de efeitos da infecção pelo HPV e mutagênese química, sendo que dos 77 tipos de HPV isolados, 41 deles apresentam maior tropismo pelas mucosas.…”

“…Isto ocorre a partir da síntese de três oncogens (oncoproteínas), sendo que a E5 estimula o fator de crescimento epidérmico (FCE), a E6 ligada ao p53 selvagem e a E7 ao Rb selvagem, todas encontradas nos HPV de alto risco (HPV16,18,31,33,35,39,42) para a mucosa oral 2,4 . Quanto à investigação do HPV humano como agente etiológico do CEC da boca e orofaringe, o mesmo foi detectado em lesões pré-malignas do trato genital feminino, onde predominou o mesmo tipo de neoplasia em localização anatômica sujeita a traumas e infecções contínuas 3 . Dentre os 77 HPV humanos (pequenos DNA vírus), os HPV 6 e 11 são encontrados nas doenças benignas e os HPV 16 e 18 são vírus de alto risco por estarem ligados em 30% com neoplasias malignas humanas 5 .…”