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Aetiology of Head and Neck Cancer
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Recent studies have shown a dramatic change in the aetiology of oropharyngeal cancer from a cancer caused by smoking and alcohol to a cancer now predominantly caused by HPV. The increase in tonsil and base of tongue cancer over the last decade is largely due to HPV infection of the palatine and lingual tonsils, and it has been called an epidemic of HPV-associated oropharyngeal cancer.
Aetiology of Head and Neck Cancer
Published in John C Watkinson, Raymond W Clarke, Terry M Jones, Vinidh Paleri, Nicholas White, Tim Woolford, Head & Neck Surgery Plastic Surgery, 2018
Pablo H. Montero, Snehal G. Patel, Ian Ganly
Recent studies have shown a dramatic change in the aetiology of oropharyngeal cancer from a cancer caused by smoking and alcohol to a cancer now predominantly caused by HPV.3 Cancer of the oropharynx is the third most common head and neck cancer after larynx and oral cavity. It is estimated that in 2013 there will be 13 930 new cases of oropharynx cancer in the United States, 11 200 male and 2730 female.2 In the UK, it has an increasing incidence, reported in near 6% annual percentage change, especially among men.67, 68 Raised incidence rates are observed in Netherlands, India, France and Italy.69–71 This increase in tonsil and base of tongue cancer over the last decade is largely due to HPV infection of the palatine and lingual tonsils, and has been called an epidemic of HPV-associated oropharyngeal cancer.72, 73
Human Papillomavirus
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Mustaffa Junaid, Hisham M. Mehanna
Recently a geographic variation in prevalence has been demonstrated, with high prevalence in oropharyngeal cancers demonstrated in Western Europe (37%) compared with Eastern Europe (6%) and Asia (2%).29 The increasing prevalence of HPV-related cancers can be attributed to changes in sexual practices. Risk factors for high-risk HPV infection in oropharyngeal cancer include younger age group (<20 years), higher number of sexual partners, early sexual contact, oral-genital and oral-anal sex.30-31
Days alive and out of hospital a validated patient-centred outcome to be used for patients undergoing transoral robotic surgery: protocol and perspectives
Published in Acta Oto-Laryngologica, 2021
Mikkel Hjordt Holm Larsen, Susanne Irene Scott, Henrik Kehlet, Christian von Buchwald
Worldwide more than 92,000 patients are diagnosed with oropharyngeal cancer annually [8]. Since 2000 the incidence has been rising, due to a rise in Human Papillomavirus (HPV) associated cancer [9]. Traditionally treatment has consisted of radiotherapy with or without chemotherapy, which is associated with less morbidity compared to open surgery with a mandibular split. However, In 2009 the use of Transoral Robotic surgery (TORS) was approved by the U.S. Food and drug administration for the treatment of early-stages oropharyngeal cancer [10]. TORS is less invasive than open surgery and studies are currently comparing radiotherapy vs TORS with regards to functional outcomes and quality of life. TORS enables the surgeon to perform a safe transoral en-bloc resection of the oropharyngeal lesion with improved visualization and maneuverability compared to normal line of sight surgery.
Distinct microbial communities colonize tonsillar squamous cell carcinoma
Published in OncoImmunology, 2021
Angelina De Martin, Mechthild Lütge, Yves Stanossek, Céline Engetschwiler, Jovana Cupovic, Kirsty Brown, Izadora Demmer, Martina A. Broglie, Markus B. Geuking, Wolfram Jochum, Kathy D. McCoy, Sandro J. Stoeckli, Burkhard Ludewig
Patients diagnosed with a primary, untreated and histologically confirmed squamous cell carcinoma of the tonsil (n = 28) were prospectively included into the study cohort 2 between August 2017 and February 2020. Patients with previous radiotherapy or surgery due to oropharyngeal cancer were excluded. Two punch biopsies from tonsillar crypts were taken directly after removal of the tumor-affected tonsil and two crypt biopsies were acquired from the contralateral tonsil during surgery. In cases when tumor tonsils were not resected, crypt biopsies were acquired in situ by punch biopsy. Each biopsy was acquired using a fresh sterile biopsy punch and a separate sterile pair of scissors and forceps. Tissue biopsies were placed in sterile tubes on ice and stored at −80°C within 30 min until further analysis.
The value of immunotherapy in head and neck cancer
Published in Expert Opinion on Biological Therapy, 2019
Paolo Manca, Luis E. Raez, Matthew Salzberg, Jorge Sanchez, Brian Hunis, Christian Rolfo
Human papillomavirus (HPV), especially genotype 16, is present in many patients with HNSCC and is felt to be in part responsible for the pathogenesis of these tumors. It is most commonly associated with SCC of the oral cavity and can be found in 40–80% of patients in Western countries [33,34]. Recently, there has been a rise of oropharyngeal cancer in younger individuals from Western countries, which is believed to be due to a reflective of a rise in HPV disease [35]. HPV (+) HNSCCs have different characteristics and actually have a more favorable prognosis. In fact, there appears to be a 60–80% reduction in OS in HPV (+) HNSCC patients when compared to matched HPV (−) patients [24]. PD-L1 expression seems to be correlated to higher OS and PFS in the subgroup of patients with HPV (+) HNSCC and to have an opposite effect in HPV (−) patients [36]. Although no differences in PD-L1 expression were reported when comparing HPV (+) and HPV (−) HNSCCs [36], the former were found to have an immune infiltrate richer of PD1+CD4+ and CD8+ lymphocytes [37]. The use of HPV circulating tumor DNA (ctDNA) as a monitoring tool for the response to anti PD-1 therapy in a patient with squamous anal cancer has been recently reported and may hold promise for HPV (+) HNSCC monitoring [38]. Finally, HPV infection doesn’t seem to affect the mutation burden of HNSCC [22].