HPV now causes most throat cancers, and cases in men keep rising

Most cancers of the oropharynx — the tonsils and the base of the tongue — are now caused by human papillomavirus, the same virus behind cervical cancer, and they are rising fastest in men. In the most recent period a US registry study examined, 71.7% of oropharyngeal cancers tested positive for HPV, up from 16.3% two decades earlier [s1].

That shift, documented across population-based cancer registries, turned a cancer once tied mainly to tobacco and alcohol into one driven largely by a sexually transmitted infection. The trend has consequences for who gets the disease, how well they survive it, and what — if anything — can prevent it.

A virus-driven cancer, climbing in men

The landmark analysis came from the Surveillance, Epidemiology, and End Results residual-tissue programme, which tested all 271 oropharyngeal tumours it held from 1984 to 2004 for HPV. HPV prevalence rose from 16.3% in 1984-1989 to 71.7% in 2000-2004 [s1]. Once the observed prevalence was re-weighted to the wider registry population, the incidence of HPV-positive oropharyngeal cancers rose by 225% between 1988 and 2004 — from 0.8 to 2.6 per 100,000 — while HPV-negative cancers fell by 50%, from 2.0 to 1.0 per 100,000 [s1]. On those trajectories, the authors projected that the annual number of HPV-positive oropharyngeal cancers would surpass cervical cancers by 2020 [s1].

Later national data confirm the rise has not levelled off, and that it is concentrated in men. A study of all 50 states counted 260,182 oropharyngeal cancers from 2001 to 2017, of which 209,297 — 80% — occurred in men [s2]. Incidence rose 2.7% a year among men, and by more than 3% a year among non-Hispanic white men and men aged 65 and older, while the annual change among women, at 0.5%, was not statistically significant [s2]. Regional-stage disease — cancer that has spread to nearby lymph nodes — rose 3.1% a year in men (95% CI 2.4-3.8), nearly doubling, and accounted for 65% of all cases; the increases clustered in the Southeast and Midwest, which together held 55% of cases [s2]. Among men, incidence-based mortality also began climbing again, up 2.1% a year from 2006 to 2017 [s2].

Why survival is better here than the numbers suggest

HPV-positive throat cancers behave differently from the tobacco-linked kind, and generally better. In the SEER analysis, median survival was 131 months for patients with HPV-positive tumours against 20 months for HPV-negative tumours, an adjusted hazard ratio of 0.31 [s1]. That difference is one reason the two cancers, though they arise in the same tissue, are now staged and studied as distinct diseases. It is not a reason for complacency: the absolute number of cases, and of deaths, is still rising in men [s2].

What actually causes it, and what prevents it

The proximate cause is oral HPV infection, acquired sexually, which the vaccine studies describe as "the principal cause of HPV-positive oropharyngeal cancers" [s3]. That points to a prevention route already in wide use for cervical cancer — vaccination — and there is now population-level evidence it reaches the mouth as well as the cervix.

A cross-sectional study of US adults aged 18 to 33 found the prevalence of oral infection with HPV types 16, 18, 6 or 11 was 0.11% in people who had received at least one vaccine dose, versus 1.61% in the unvaccinated — an estimated 88.2% reduction after adjustment [s3]. Among vaccinated men specifically, the prevalence of those infections was zero, against 2.13% in unvaccinated men [s3].

The catch, the same study makes plain, is uptake. Only 18.3% of that age group reported any HPV vaccination before age 26 — 29.2% of women but just 6.9% of men — so the population-level effect on oral infection was 17.0% overall and only 6.9% in men, the group whose cancer rates are climbing [s3]. Because those men were largely too old to be vaccinated during the periods studied, the benefit for oropharyngeal cancer will take decades to appear, and depends on vaccinating boys as well as girls.

Two limits are worth stating plainly. The vaccine evidence here measures infection, not throat-cancer endpoints, which lie years downstream; no trial has yet shown a fall in oropharyngeal cancer itself [s3]. And unlike cervical cancer, which has an established screening pathway through the shift to primary HPV testing and self-collection, oropharyngeal cancer has no equivalent routine screen — prevention rests on the vaccine and on catching symptoms such as a persistent neck lump early.

The same virus links a cluster of cancers the site covers separately, including penile cancer and cervical cancer, where the vaccine's effect on cancer rates is already measurable. Oral HPV is also one of the infections that routine STI screening does not currently detect.