By Wojciech Golusiński, C. René Leemans, Andreas Dietz
This booklet is phenomenal in proposing an interdisciplinary method of the topic of human papillomavirus (HPV) an infection within the context of head and neck melanoma. best specialists within the box talk about the epidemiology and molecular biology of HPV-positive head and neck squamous phone carcinoma, HPV trying out, the nonsurgical and surgical operation of HPV-positive tumors, predictive elements for consequence and caliber of existence, and ongoing trials at the effectiveness of vaccination in ailment prevention. It additionally offers options for checking out, prognosis therapy and vaccination. Otolaryngologists, head and neck surgeons, scientific oncologists, radiation oncologists, molecular biologists and pathologists will locate this e-book a priceless resource.
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Extra info for HPV Infection in Head and Neck Cancer
2010). In brief, formalin-ﬁxed, parafﬁn-embedded cancer tissues of the oral cavity, pharynx and larynx were collected from pathology archives in 29 countries worldwide. All samples were subjected to central histopathological evaluation, DNA quality control, and HPV-DNA detection. Samples containing HPV-DNA were further tested for HPV E6*I mRNA detection and expression of p16INK4a, pRb, p53, and Cyclin D1 by immunohistochemistry. A total of 3,680 samples yielded valid results: 1,374 pharyngeal, 1,264 oral cavity, and 1,042 laryngeal cancers.
All cervical cancers are considered HPV-driven (Walboomers et al. 1999), the quantitative assessment of the etiological involvement of HPVs in HNCs is challenged by their multifactorial etiology largely attributed to tobacco and alcohol use (IARC 1988, 2004; Gillison et al. 2012). Consequently, the unequivocal fraction of HPV-DNA-positive HNCs for which HPV infection is indeed the truly triggering carcinogenic event is unknown and its estimation remains a challenge (Herrero et al. 2003). Further, the mere presence of HPV DNA in HNCs is not sufﬁcient to prove viral causation as it might just reflect a transient infection unrelated to the carcinogenic process (Holzinger et al.
1996; Tabor et al. 2001; Leemans et al. 2011) and are considered as the earliest genetic changes. In HPV+ve HNSCC, these same pathways are likely also the ﬁrst to be inactivated by the viral E6 and E7 oncoproteins, assuming that HPV infection is the initial carcinogenic event. Although it has been postulated that abrogation of p53 is one of the ﬁrst causative genetic hits by either somatic mutation or expression of HPV-E6, not all HPV-ve tumors do contain mutant p53. Approximately 60 % of HNSCC harbour a mutation in TP53 and 20 % contain transcriptionally active HPV (Braakhuis et al.
HPV Infection in Head and Neck Cancer by Wojciech Golusiński, C. René Leemans, Andreas Dietz