p53 mutations and human papillomavirus DNA in oral squamous cell carcinoma: correlation with apoptosis

Koh, J.; Cho, Nam-Pyo; Kong, Guangyao; Lee, J. D.; Yoon, Kyoungro

doi:10.1038/bjc.1998.498

Cited by 30 publications

(22 citation statements)

References 29 publications

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“…Therefore, the high percentage of HPV positivity of the control tissues in the present study is not unusual. Our finding of no correlation between AI and HPV was also in agreement with the results of Isacson et al [4] and Koh et al [20]. We have previously identified ABs in exfoliated cervicovaginal epithelial cells.…”

Section: Discussionsupporting

confidence: 93%

“…Although the E6 oncoprotein of HPV is implicated in the functional inactivation of p53 (a gene that regulates apop- tosis) [18], in two separate studies [4,19], however, the AI was not found to be correlated with HPV infection. Koh et al [20] suggested that the decrease in apoptosis is more closely related to p53 mutation rather than HPV infection. In the present study, the AI was also not found to be affected by HPV infection.…”

Section: Discussionmentioning

confidence: 99%

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Apoptotic Changes in Cervical Intraepithelial Neoplasia

Duttagupta

Basu

Ray

et al. 2001

Gynecol Obstet Invest

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We examined apoptosis in paraffin-embedded archival cervical tissues from cervical intraepithelial neoplasia (CIN) cases to determine whether the apoptotic process is involved in the cellular changes of CIN. Apoptotic bodies, determined by the Tunel method, were largely found at the surface epithelium in a few tissue specimens with no significant abnormality and in most tissues with CIN. Apoptotic bodies were also found within the stratified epithelium of CIN lesions and were altogether absent in specimens with no significant abnormalities. The apoptotic index was significantly associated with the severity of CIN and not with either age or human papillomavirus infection. Based on the findings of increased numbers of apoptotic bodies and their presence within the stratified epithelium in CIN tissues, we hypothesize that dysregulation in the exfoliation of apoptotic cells and resistance towards apoptosis may be prerequisites for the pathogenesis of CIN.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Apoptotic Changes in Cervical Intraepithelial Neoplasia

Duttagupta

Basu

Ray

et al. 2001

Gynecol Obstet Invest

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“…Yet, the method is risky to overlook mutations in case wt-p53 sequences of contaminating regular cells disturb the signal of the mutated cells. In studies reporting higher mutation rates single-strand conformation polymorphism (SSCP) was applied, a technique which has shown rather frequent false positive results (1).…”

Section: Discussionmentioning

confidence: 99%

“…More than 90% of these represent squamous cell carcinomas (HNSCC) (1). The main risk factors for developing HNSCC are the carcinogenic substances of tobacco smoke and alcohol.…”

Section: Introductionmentioning

confidence: 99%

Molecular and immunological aspects of p53 and p53-autoantibodies in head and neck squamous cell carcinoma

Cordes

Lingen²,

Görögh³

et al. 2009

Oncol Rep

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Abstract. The tumour suppressor protein p53 (wild-type = wt-p53) is of major importance in the genetic integrity of the cell. Mutations of the p53-gene (mt-p53) are the most frequent genetic aberrations identified in different tumour entities. As analyzed in a wide variety of human malignomas, mtp53 evokes a specific immune response. Yet, the possible occurrence of p53-autoantibodies in patients with head and neck squamous cell carcinomas (HNSCC) correlated to p53-mutations, p53 in sera and p53-overexpression in tissue has not been previously investigated. For the first time, the p53 status in 24 HNSCC patients was analyzed in the present study. The following parameters were investigated: analysis of mutation frequency of the p53-gene by direct sequencing of the exons 5-9, immunohistochemical detection of p53, measurement of the wt-and mt-p53-protein in sera by ELISA and p53-autoantibodies in sera by ELISA. Mutations of the p53-gene were detected in four (17%) patients. Overexpression of wt-p53 was detected by immunohistochemistry in 18 out of 24 (75%) tumours. In 8 (33%) patients the p53-protein was also detectable in sera, whereas in just one of these eight patients p53-autoantibodies were detectable simultaneously. Overall 6 out of 24 (25%) patients were found to be positive for serum p53-autoantibodies. Of these 6 cases, 5 could be assigned to tumours with immunohistochemically measurable wt-p53-overexpression. There was no correlation between p53-overexpression in tissue and p53-protein levels in sera or between p53-autoantibody levels in sera, nor in mutation frequency of the p53-gene and p53-overexpression in tissue. The results presented herein support the hypothesis that strong accumulation of p53 in the tissue is an important prerequisite for development of p53-autoantibodies. However, there must be further, yet unknown factors that influence the p53-autoantibody production because p53-autoantibodies were not identified in sera in each case of p53-accumulation in the tissue.

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“…Several studies demonstrated that the association between HPV infection and/ or p53 inactivation and the risk of oral cancer is implicated, although it is not a mutually exclusive event (69,70). Immunohistochemical detection of p53 protein clarified that HPV and p53 protein alteration coexisted in oral lesions, and p53 mutation was initiated during early events of HPV infection to lead to oral cancer (71).…”

Section: Hpv In Oral Lesionsmentioning

confidence: 99%

Human Papillomavirus in the Oral Cavity

Terai

Takagi

2001

Oral Med Pathol

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Human papillomavirus (HPV) cannot be efficiently propagated in tissue cultures or animal models. However, molecular biological technology has made it possible to clone viral genomes, which can then be compared and also used as reagents in clinical and epidemiological studies.Today HPV infections are recognized as being responsible for inducing cancers worldwide and it is expected that HPV-based technologies will provide the tools to prevent and treat HPV-induced cancers. In this review, we focus on the association between oral lesions and HPV infection and the natural history of HPV infection of the oral cavity. We also evaluate the HPV detection methods in this important and fundamental matter for the HPV studies. We then discuss the potential targeted molecular therapies and prevention of a variety of HPVinduced diseases of the oral cavity, including oral cancers. Key words: HPV, human papillomavirus, oral cavityCorrespondence : Minoru Takagi, Molecular Pathology, Oral Restitution, Oral Health Science, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113- 8549, JapanPhone: +81-3-5803-5451, Fax: +81-3-5803-0188 IntroductionHuman papillomavirus (HPV) is a small, nonenveloped and double stranded circular DNA virus, about 8,000 bp in length, with a well-known physical structure and gene organization (1). HPV belongs in the subfamily papillomavirus (PV) of the papovavirus family, which are widely distributed in nature and infect many higher vertebrates including cattle, rabbits and dogs (1). It is thought that the viruses may have co-evolved with their hosts (2). They are highly species-specific species, having one or more of its own PVs, and viruses of one species do not infect other species (1).HPV is classified into more than 100 types, including 84 clones and others detected by PCR (3). To be recognized as a distinct HPV genome, the full genome should be cloned and the sequence of the L1 gene should be no more than 90% similar to previously assigned and referenced HPVs (4). HPVs naturally fall into two groups: mucosal HPVs and cutaneous HPVs according to the anatomic site of infection and/or phylogenetic analysis (5). Some HPV infections can lead to malignant lesions depending on HPV genotypes and infection persistence. HPV is also broadly categorized into low, intermediate and highrisk types in accordance with their potential to induce or their association with malignant lesions (6). In oral lesions 24 genotypes have been identified 2,3,4,6,7,10,11,13,16,18,30,31,32,33,35,45,52,55,57,59,69,72 and 73) (7-27) ( Table 1).The HPV genome is comprised of early (E) genes that function primarily in episomal replication and late (L) genes that encode the viral capsid proteins. HPV 16 genome map is shown in Fig. 1. The L1 and L2 genes code for proteins that make up the viral major and minor capsid. The capsid encloses the viral genome and mediates viral entry into susceptible cells (28). Much of the immune response to infection is directed at the capsid protein (29). Based on experi...

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p53 mutations and human papillomavirus DNA in oral squamous cell carcinoma: correlation with apoptosis

Cited by 30 publications

References 29 publications

Apoptotic Changes in Cervical Intraepithelial Neoplasia

Apoptotic Changes in Cervical Intraepithelial Neoplasia

Molecular and immunological aspects of p53 and p53-autoantibodies in head and neck squamous cell carcinoma

Human Papillomavirus in the Oral Cavity

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