Human papillomavirus type 38 infection in oral squamous cell carcinomas

Kojima, Akiko; Maeda, Hideaki; Sugita, Yoshihiko; Tanaka, Seiya; Kameyama, Yôichiro

doi:10.1016/s1368-8375(01)00112-9

Cited by 50 publications

(48 citation statements)

References 42 publications

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“…These detection rates are lower than some reports in the literature, with PCNA expression up to 94.7% in HPV-positive OSCC; [53][54][55][56] furthermore, OSCCs with HPV-positive genotype 16/18 53-55 or 38 9 have been associated with more intense expression of PCNA. PCNA is an accessory protein of DNA polymerase-delta, associated with cell cycle progression and detectable in the replicating cells of normal tissues, reaching an expression peak during the S phase of the cell cycle.…”

Section: Discussionmentioning

confidence: 61%

“…6 Besides the relevance of studies on several markers, it was mandatory to investigate the risk factors of continued use of tobacco, alcohol misuse, diet and viral infections. 7 In particular, it has been generally hypothesized that HPV infection may play a role in the occurrence of potentially malignant oral lesions and/or in their malignant transformation, [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] even if the detection rate of HPV DNA reported in carcinomas of the oral cavity is very discordant. 19 A previous study, carried out in our geographic area (southern Italy), determined that HPV prevalence was 61.5% in carcinomas, 27.1% in potentially malignant lesions, 26.5% in erosive ulcerative lesions and 5.5% in controls.…”

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confidence: 99%

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

Muzio

D’Angelo

Procaccini

et al. 2005

Intl Journal of Cancer

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Our aim was to evaluate in oral squamous cell carcinoma (OSCC) the relationship between some cell cycle markers and HPV infection, conditionally to age, gender and certain habits of patients, and to assess the ability of fuzzy neural networks (FNNs) in building up an adequate predictive model based on logic inference rules. Eighteen cases of OSCC were examined by immunohistochemistry for MIB-1, PCNA and survivin expression; presence of HPV DNA was investigated in exfoliated oral mucosa cells by nested PCR (nPCR, MY09-MY11/GP5-GP6), and HPV genotype was determined by direct DNA sequencing. Data were analyzed by traditional statistics (TS) and FNNs. HPV DNA was found in 9/18 OSCCs (50.0 %) without any significant higher risk of HPV infection with respect to the sociodemographic variables considered ( p > 0.2), apart from tobacco smoking, reported in 44.4% of OSCC HPV-positive vs. 100% HPV-negative subjects ( p = 0.029). Regarding cell cycle markers, TS and FNN revealed that survivin was expressed significantly more in HPV-negative than in HPVpositive OSCC [root mean-square error (RMSE) = 5.89 3 10 -6 , % predicted 100.0]; furthermore, smoking played a protective role for survivin expression in HPV-positive cases (OR = 0.019, 95%CI 0.001-0.723, RMSE = 0.20, % of prevision 94.4). FNN, although on a small sample size, allowed us to confirm data by TS and to hypothesize a different cell cycle pattern for HPV-positive vs. HPV-negative OSCC. In the latter cases, the relevance of apoptotic vs. proliferative markers suggested that they may be related to the different supposed outcome of HPV-negative OSCC and that HPV may have a protective role in the expression level of survivin, especially in tobacco smokers. ' 2005 Wiley-Liss, Inc.Key words: human papillomavirus; survivin; oral squamous cell carcinoma; fuzzy neural network; carcinogenesis OSCC is rapidly increasing in incidence and represents the most frequent malignant oral tumor. The incidence of metastasis depends on the degree of cellular differentiation, deep invasion and site of the primary tumor; however, outcome is difficult to predict if only standard clinicopathologic parameters are taken into account. Biologic markers that can help to identify lesions with an aggressive phenotype and worse prognosis need to be identified.Since the majority of human neoplasms are characterized by an imbalance of the regulatory cell cycle control processes, the study of OSCC using the expression of proteins involved in the critical checkpoints of cell apoptosis and growth starts by elucidating the processes of carcinogenesis and appears to have good prognostic value. 1 Indeed, we know that apoptosis, or programmed cell death, and its suppression are involved in the carcinogenesis of several tumors; this process, mediated by caspases and cysteine proteinases present as proenzymes, is inhibited by several proteins, such as those of the Bcl-2 and IAP families. Survivin is an IAP protein, which is abundantly expressed in most solid and hematologic malignancies but undetectable in ...

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Section: Discussionmentioning

confidence: 61%

mentioning

confidence: 99%

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

Muzio

D’Angelo

Procaccini

et al. 2005

Intl Journal of Cancer

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“…Além disso, os autores usaram o anticorpo imunoistoquímico antígeno nuclear de proliferação celular (PCNA), enquanto nós utilizamos o Ki-67, que, segundo a literatura, é superior àquele (9,10,28) . Utilizando uma metodologia mais semelhante à do presente estudo, Kojima et al (7) , diferentemente dos nossos resultados, encontraram um progressivo e significativo aumento dos índices de proliferação celular entre mucosa oral normal, OSCC HPV-38-negativo e OSCC HPV-38-positivo, empregando PCR e PCNA. El-Mofty e Lu (4) também encontraram escores aumentados de marcação pelo Ki-67 em carcinomas de células escamosas de cabeça e pescoço HPV-positivos em relação aos HPV-negativos.…”

Section: Discussionunclassified

“…Tendo em vista o papel das oncoproteínas virais (principalmente E6 e E7) dos HPVs de alto risco na desregulação do controle da proliferação celular, estudos têm avaliado se lesões cancerizáveis e malignas HPV-positivas exibem níveis de proliferação celular aumentados em relação às HPV-negativas (3,4,7,17) . Um dos métodos mais comuns entre os patologistas para se detectar e quantificar as células em proliferação é a imunoistoquímica, sendo o Ki-67 o anticorpo mais utilizado (10,27) .…”

Section: Introductionunclassified

Análise comparativa da proliferação celular entre carcinomas de células escamosas orais HPV-positivos e HPV-negativos

Rocha¹,

Souza²,

Pinto³

2007

J. Bras. Patol. Med. Lab.

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Introdução: O carcinoma de células escamosas oral (OSCC) representa a neoplasia maligna mais freqüente em boca, e, entre os agentes etiológicos implicados, o papilomavírus humano (HPV) tem sido extensivamente estudado nos últimos anos. Objetivo: Analisar comparativamente os índices de proliferação celular em OSCCs HPV-negativos e HPV-positivos. Material e método: A amostra consistiu em 11 casos de OSCCs HPV-positivos (10 infectados por HPV-18 e um por HPV-16 e 18) e 13 HPVnegativos, previamente analisados quanto à presença ou ausência, bem quanto à tipagem viral por proteína C reativa (PCR) (primers GP5+/GP6+) e hibridização dot blot, respectivamente. No método imunoistoquímico utilizou-se a técnica da estreptoavidina-biotina, com anticorpo para a proteína nuclear Ki-67. Resultados: O teste estatístico não-paramétrico de Mann-Whitney revelou que não houve diferença estatisticamente significativa entre os grupos HPV-positivo e HPV-negativo (p = 0,72). Discussão: Os estudos semelhantes a estes são poucos e não são concordantes em demonstrar maior atividade proliferativa tumoral nos casos HPV-positivos em relação aos HPV-negativos, seja através da análise da expressão de proteínas relacionadas ao ciclo celular, seja na análise direta da fração proliferativa tumoral. Conclusão: Não houve diferença no índice de proliferação celular entre os grupos de OSCCs HPV-positivo e HPV-negativos. abstract resumo Background: Oral Squamous Cell Carcinoma (OSCC) is the most common malignant tumor in the mouth, and the human papillomavirus (HPV) has been hardly studied as a possible etiologic agent. Objectives: The aim of this study was to compare the rates of cell proliferation in HPV-positive and HPV-negative OSCC, using the immunohistochemical antibody Ki-67. Material and method: The sample consisted of 11 cases HPV-positive OSCC (10 cases infected with HPV-18 and 1 case infected with HPV-16 and 18) and 13 cases HPV-negative OSCCs, previously analyzed regarding the presence or absence of HPV, as well as the viral type, using PCR (primers GP5+/GP6+) and dot blot hybridization, respectively. Immunohistochemical study was performed by streptoavidin-biotin technique with antibody against nuclear protein

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“…A remarkable example is the study by Kojima et al (23) , in which ISH-tyramide exposed an elevated prevalence of HPV-38 (35/53 [66%]), a genotype rarely investigated in other studies. Meanwhile, Pannone et al (37) detected genotypes 44, 53, and 70, by DNA sequencing following PCR, but were not successful with the ISH method, as the available commercial kits do not include the corresponding probes: they are designed to detect high-risk genotypes associated with anogenital lesions.…”

Section: Considerations About Viral Detectionmentioning

confidence: 99%

Association between human papillomavirus (HPV) and the oral squamous cell carcinoma: a systematic review

Lima¹,

Silva

Rabenhorst³

2014

J. Bras. Patol. Med. Lab.

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The human papillomavirus (HPV) is an epitheliotropic agent whose high-risk genotypes have a well-established link with the development of cervical cancer. Although the relation of HPV to the oral squamous cell carcinoma (OSCC) has been studied since the beginning of the 1980s, its role in the oral carcinogenesis and the probable underlying molecular mechanisms are still not fully elucidated. We performed a systematic review of the worldwide scientific literature, published until the preparation of the present paper, concerning the association of HPV with OSCC, scrutinizing the samples, prevalence levels, the techniques utilized and relevant findings of the studies. The results showed that HPV is associated with approximately one quarter of OSCCs. Another interesting feature is the distinct pattern of infection in these oral tumors, including the participation of genotypes that are uncommon in cervical malignant lesions, such as HPV-38, 44, 53 and 70. Equally interesting is the possibility of carcinogenic action without the occurrence of viral integration, verified by the high expression of messenger ribonucleic acid (mRNA) of E6 and E7 from high-risk genotypes in cases whose virus remain in the episomal form. These findings support the assumption of HPV involvement in the genesis of OSCC, whereas warn about the possibility of unexpected viral behaviors that sometimes are not perceived or understood due to the technological limitations of the time and to the shortage of studies with the adequate approaches.

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Human papillomavirus type 38 infection in oral squamous cell carcinomas

Cited by 50 publications

References 42 publications

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

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

Análise comparativa da proliferação celular entre carcinomas de células escamosas orais HPV-positivos e HPV-negativos

Association between human papillomavirus (HPV) and the oral squamous cell carcinoma: a systematic review

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