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Review
. 2016 Dec;42(6):327-336.
doi: 10.5125/jkaoms.2016.42.6.327. Epub 2016 Dec 27.

Human papilloma virus in oral cancer

Soung Min Kim  1
Affiliations
Review

Human papilloma virus in oral cancer

Soung Min Kim. J Korean Assoc Oral Maxillofac Surg. 2016 Dec.

Abstract

Cervical cancer is the second most prevalent cancer among women, and it arises from cells that originate in the cervix uteri. Among several causes of cervical malignancies, infection with some types of human papilloma virus (HPV) is well known to be the greatest cervical cancer risk factor. Over 150 subtypes of HPV have been identified; more than 40 types of HPVs are typically transmitted through sexual contact and infect the anogenital region and oral cavity. The recently introduced vaccine for HPV infection is effective against certain subtypes of HPV that are associated with cervical cancer, genital warts, and some less common cancers, including oropharyngeal cancer. Two HPV vaccines, quadrivalent and bivalent types that use virus-like particles (VLPs), are currently used in the medical commercial market. While the value of HPV vaccination for oral cancer prevention is still controversial, some evidence supports the possibility that HPV vaccination may be effective in reducing the incidence of oral cancer. This paper reviews HPV-related pathogenesis in cancer, covering HPV structure and classification, trends in worldwide applications of HPV vaccines, effectiveness and complications of HPV vaccination, and the relationship of HPV with oral cancer prevalence.

Keywords: HPV vaccine; Human papilloma virus; Oral cancer; Uterine cervical cancer; Virus-like particle.

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Conflict of interest statement

No potential conflict of interest relevant to this article was reported.

Figures

Fig. 1
Fig. 1. Schematic drawing comparing normal and human papilloma virus (HPV)-infected epithelia. Virions are released from the stratum corneum and granulosum and directly infect the basal layer, involving capsid synthesis and late and early promoter activation.
Fig. 2
Fig. 2. Viral protein expression after human papilloma virus (HPV) infection showing integration between E1 and E2 and between E6 and E7.
Fig. 3
Fig. 3. A sample microscopic view of focal epithelial hyperplasia. There are a few mitosoid cells among the normal keratinocytes and chromatin peripheralization with inclusion bodies in the stratum granulosum (A), stratum spinosum (B), and stratum basale (C) (original magnification, ×400).
See this image and copyright information in PMC

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