Oral Sex Increases Throat Cancer Risk Scientists Say

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Main Category: Sexual Health / STDs
Also Included In: Cancer / Oncology;  Ear, Nose and Throat;  Cervical Cancer / HPV Vaccine
Article Date: 10 May 2007 - 0:00 PDT

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In a new study, US scientists suggest that people who have oral sex with 5 or more partners during their lifetime have a much greater chance of having throat cancer and they suspect the cause is a well known strain of the Human papillomavirus (HPV) that is linked to a number of anogenital cancers.

The study is published in today's issue of the New England Journal of Medicine which also includes a number of other articles on HPV.

The research was conducted by Dr Maura Gillison of Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland, US, and colleagues.

Scientists already knew that HPV was doing something at the molecular level to help trigger a type of throat cancer known as oropharyngeal squamous-cell carcinoma, but consistent epidemeological evidence was still missing.

Dr Gillinson and colleagues recruited 100 patients with newly diagnosed oropharyngeal cancer and 200 control patients without cancer in a hospital-based case controlled study. They used logistic regression models to look for links between results from the patients' blood and saliva samples and lifestyle variables such as their sexual behaviour, consumption of alcohol and smoking habits. The lifestyle data was collected via anonymous questionnaire.

The results showed that:

• Patients who had a lifetime number of 6 or more oral-sex partners were 3.4 times more likely to have oropharyngeal cancer
• Those who had 26 or more vaginal-sex partners during their lifetime were 3.1 times more likely to have oropharyngeal cancer.
• The link became stronger as the number of lifetime oral and vaginal sex partners went up.
• Oropharyngeal cancer was significantly linked with oral infection with HPV type 16 (HPV-16), with any of the 37 types of HPV, and with having been exposed in the past to HPV, as measured by seropositivity for the HPV-16 L1 capsid protein.
• The odds ratio for these three events were found to be 14.6, 12.3 and 32.2 respectively.
• DNA from HPV-16 was found in 72 per cent of tumour specimens and 64 per cent of patients tested positive for presence of one or more cancer-related proteins produced by HPV-16 (oncoproteins E6, E7, or both).

The results suggested that once the link with HPV is present, there is no added risk from tobacco use and alcohol consumption, usually regarded as the highest risk factors for this type of throat cancer.

Dr Gillinson and colleagues suggest that HPV "drives" the cancer and once the cell is sufficiently disrupted to cause cancer, the impact of tobacco and alcohol is unlikely to contribute any more risk.

The researchers concluded that:

"Oral HPV infection is strongly associated with oropharyngeal cancer among subjects with or without the established risk factors of tobacco and alcohol use."

In an accompanying editorial, Dr Stina Syrjänen from the University of Turku in Finland suggested that this study raises important clinical and public health issues.

For instance, should heavy smokers and drinkers be screened for HPV-related throat infection? Should throat cancers with a suspected HPV origin be treated differently to those with no HPV link and most likely caused by smoking and drinking?

And the question that must be in the minds of many currently focused on the HPV vaccination debate, would HPV vaccination give people protection against some throat and mouth cancers?

Article.

Information on symptoms and treatment of throat cancer (patient information from NIH Medline plus).

Written by: Catharine Paddock
Writer: Medical News Today
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today