Public Lecture on Oncogenic Human Papillomavirus & Oral and Oropharyngeal Carcinogenesis

PL-DecIt is our pleasure to invite you to our event as follows;

Public Lecture on:

ONCOGENIC HUMAN PAPILLOMAVIRUS & ORAL AND OROPHARYNGEAL CARCINOGENESIS 

  • Date    : 18th December 2013
  • Time    : (1.00pm – 2.00pm)
  • Venue : Auditorium Level 11, Postgraduate & Research Tower,Faculty of Dentistry, UM

Should you have further inquiries, do feel free to contact DRMC at:

03-7967 6454 or email at najmi@um.edu.my

Registration : Kindly RSVP before 17th December 2013

Your attendance to this programme would be highly valuable and we do hope all of you will be able to attend the program. 

Below is information on program;

Speaker:

Saman Warnakulasuriya OBE, BDS, FDSRCS, Dip Oral Med, PhD, DSc

Saman Warnakulasuriya is Professor of Oral Medicine at King’s College and a consultant to two NHS Trusts in London based at King’s and Guy’s Hospitals. He has published over 200 scientific peer reviewed articles and lectured extensively on the subject of oral cancer and precancer from the levels of basic science to the management. He is an authority on global aspects of risk factors and screening for oral cancer, having conducted several innovative field surveys in different population groups on screening for oral cancer using the primary health care model. He was the principal investigator of an epidemiological study on oral cancer in young people, the largest reported so far from Europe.

His popular reviews include Global epidemiology of oral cancer, Nomenclature and classification of potentially malignant disorders of the oral mucosa, Oral epithelial dysplasia classification systems, Clinical, pathological, cellular and molecular lesions caused by oral smokeless tobacco, Oral lichenoid contact lesions to mercury and amalgam, Squamous cell carcinoma and precursor lesions: prevention, Screening for oral cancer: contributing to the debate, Global inequalities in incidence and outcome for oral cancer: causes & solutions, Molecular markers in oral epithelial dysplasia and Oral health risks of tobacco use and effects of cessation.

His current research interests are (1) developing tumour and genetic markers for diagnosis and examining risks for oral cancer in different populations, (2) the delivery of interventional programmes directed at cessation of tobacco and areca nut usage and (3) Early diagnosis, screening for and management of potentially malignant oral disorders.

He is the director of the WHO Collaborating Centre for Oral Cancer and Precancer in the United Kingdom and is on the editorial boards of Oral Oncology, J Oral Pathology and Medicine, International Journal of Clinical Dentistry, World Journal of Dentistry, International Journal of Head and Neck Surgery and Head and Neck Oncology.  He was the President of British Dental Association Metropolitan Branch in 2012 and is a scientific advisor to the Ben Walton Trust.

Abstract

Human papillomavirus associated oropharyngeal and tongue cancers constitute an important subgroup of head and Neck cancers (HNC).  Particularly among a high proportion of young people diagnosed with tongue and oropharyngeal cancers (OPC) human papillomavirus (HPV) is an emerging risk factor. HPV is detectable in approximately a quarter of all HNC and a particularly higher prevalence (~40%) is noted in OPCs.  In global terms, the reported rates though vary widely. Patients with HPV positive HNCs tend to be younger in age and US data indicate that HPV-positive HNC cases are associated with a higher number of sexual partners.

More than 100 types of HPVs – a member of papillomaviridae family – have been identified.  Only about 15 types have been identified as high-risk types with oncogenic potential. High risk HPV type 16 accounts for over 75% of all HPV +ve OPCs, while types 18, 31 and 33 are noted in a few. After infection of a keratinocyte the HPV genome may remain episomal or become integrated into the host genome.

Active transcription of HPV with generation of E6 and E7 oncoproteins results in tumour cell proliferation, suppression of apoptosis, and ultimately carcinogenesis. HPV proteins E6 and E7 promote carcinogenesis by blocking the action of p53 protein and pRB respectively. Expression of p16 can be detected by immunohistochemistry (IHC) and is strongly and diffusely expressed in HPV-associated tumours but absent in HPV negative cancers.

HPV-positive tumours arising from the oropharynx are more likely to be poorly differentiated and have a basaloid morphology more in keeping with tonsilar crypt morphology. HPV positivity is an independent prognostic factor for improved survival and locoregional control in HNCs. This is particularly noted for transcriptionally active HPV infections with detectable E6/E7 mRNA and with positive p16 expression.

Differences in the detection rates of HPV positivity reported in the literature could be due to 1) population differences 2) sample distribution from various HNC sites (oral vs OPC) and 3) different analytical methods used.   Combined methods to detect causative HPV in oral and oropharyngeal SSC, by p16 IHC, consensus PCR HPV-DNA and in situ hybridization has recently been proposed.   Even cases that are PCR positive if they are negative for E6 or E7 m RNA expression could be molecularly similar to HPV negative tumours.  National Comprehensive Cancer Network Guidelines suggests p-16 IHC as a screening method for HPV detection.

HPV can be detected in normal human oral mucosa and through all stages of carcinogenesis from oral dysplasia (OD) and orpharyngeal epithelial dysplasia (OPD) to invasive carcinoma. A recent meta analysis based on data from US, Europe and Japan reported a prevalence of HPV 16/18 in OD & OPD in 24.5% [CI 14.4-41.5] cases. This suggested that HPV is involved in early phases of carcinogenesis, though such infections could be transient and causality is not certain.  The rates were however, higher in dysplasia compared with normal samples, higher in younger people and males. Large prospective studies are needed in South Asia to critically understand HPV-associated carcinogenesis through normal to dysplasia to carcinoma. Prophylactic vaccination may in the future reduce the risk of HPV 16/18 infection and availability of HPV vaccination should be included in countries’ strategic cancer control policies. HPV testing for OPCs should be considered in routine diagnostic settings.

— Thank you & we look forward to seeing you soon!