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      Changes in incidence and prevalence of human papillomavirus in tonsillar and base of tongue cancer during 2000‐2016 in the Stockholm region and Sweden

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          Abstract

          Tonsillar and base of tongue squamous cell carcinoma (TSCC/BOTSCC) has increased. In Stockholm, the proportion of human papillomavirus (HPV)-positive cases and the incidence of TSCC rose between 1970 and 2006 then stabilized. Here, HPV-prevalence, and TSCC/BOTSCC incidence 2000-2016, in Stockholm and Sweden were followed.

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          Most cited references37

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          Incidence trends for human papillomavirus-related and -unrelated oral squamous cell carcinomas in the United States.

          To investigate the impact of human papillomavirus (HPV) on the epidemiology of oral squamous cell carcinomas (OSCCs) in the United States, we assessed differences in patient characteristics, incidence, and survival between potentially HPV-related and HPV-unrelated OSCC sites. Data from nine Surveillance, Epidemiology, and End Results program registries (1973 to 2004) were used to classify OSCCs by anatomic site as potentially HPV-related (n = 17,625) or HPV-unrelated (n = 28,144). Joinpoint regression and age-period-cohort models were used to assess incidence trends. Life-table analyses were used to compare 2-year overall survival for HPV-related and HPV-unrelated OSCCs. HPV-related OSCCs were diagnosed at younger ages than HPV-unrelated OSCCs (mean ages at diagnosis, 61.0 and 63.8 years, respectively; P < .001). Incidence increased significantly for HPV-related OSCC from 1973 to 2004 (annual percentage change [APC] = 0.80; P < .001), particularly among white men and at younger ages. By contrast, incidence for HPV-unrelated OSCC was stable through 1982 (APC = 0.82; P = .186) and declined significantly during 1983 to 2004 (APC = -1.85; P < .001). When treated with radiation, improvements in 2-year survival across calendar periods were more pronounced for HPV-related OSCCs (absolute increase in survival from 1973 through 1982 to 1993 through 2004 for localized, regional, and distant stages = 9.9%, 23.1%, and 18.6%, respectively) than HPV-unrelated OSCCs (5.6%, 3.1%, and 9.9%, respectively). During 1993 to 2004, for all stages treated with radiation, patients with HPV-related OSCCs had significantly higher survival rates than those with HPV-unrelated OSCCs. The proportion of OSCCs that are potentially HPV-related increased in the United States from 1973 to 2004, perhaps as a result of changing sexual behaviors. Recent improvements in survival with radiotherapy may be due in part to a shift in the etiology of OSCCs.
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            Incidence of human papillomavirus (HPV) positive tonsillar carcinoma in Stockholm, Sweden: an epidemic of viral-induced carcinoma?

            In the county of Stockholm, between 1970 and 2002, we have previously reported a 3-fold parallel increase in the incidence of tonsillar squamous cell carcinoma (SCC) and the proportion of human papillomavirus (HPV) positive tonsillar SCC. Here, we have followed the above parameters in all patients (n = 120) diagnosed with tonsillar SCC during 2003-2007 in the same area, and also in correlation to our previous data. Ninety-eight pretreatment biopsies were available and presence of HPV DNA and HPV-16 E6 and E7 RNA were tested by polymerase chain reaction (PCR) and RT-PCR. Incidence data were obtained from the Swedish Cancer Registry. Data reported from 1970 to 2002 were also obtained for comparison. HPV DNA was present in 83 of 98 (85%) of the tonsillar SCC biopsies from 2003 to 2007 and 77 of these were HPV-16 positive. HPV-16 E6 and E7 RNA were found in 98% of 52 analyzed HPV-16 positive cases. The proportion of HPV-positive cancers had significantly increased both from 1970 to 2007 (p < 0.0001) as well from 2000 to 2007 (p < 0.01), with 68% (95% confidence interval (CI), 53-81) 2000-2002; 77% (95% CI, 63-87) 2003-2005; and 93% (95% CI, 82-99) 2006-2007. The incidence rate of HPV-positive tumors almost doubled each decade between 1970 and 2007, in parallel with a decline of HPV-negative tumors. In conclusion, the incidence of HPV-positive cancers is still increasing in the County of Stockholm, suggesting an epidemic of a virus-induced carcinoma, with soon practically all tonsillar SCC being HPV positive, as in cervical cancer. Copyright 2009 UICC.
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              Oral sexual behaviors associated with prevalent oral human papillomavirus infection.

              Oral human papillomavirus (HPV) infection is a cause of oropharyngeal cancer. We investigated whether sexual behaviors that elevated the odds of oropharyngeal cancer developing in a case-control study similarly elevated the odds of oral HPV infection developing among control patients. HPV infection was detected in 4.8% of 332 control patients from an outpatient clinic and in 2.9% of 210 college-aged men (age range, 18-23 years). Among control patients, the odds of infection developing independently increased with increases in the lifetime number of oral (P = .007, for trend) or vaginal sex partners (P = .003, for trend). Among college-aged men, the odds of oral HPV infection developing increased with increases in the number of recent oral sex partners (P = .046, for trend) or open-mouthed kissing partners (P = .023, for trend) but not vaginal sex partners. Oral sex and open-mouthed kissing are associated with the development of oral HPV infection.
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                Author and article information

                Journal
                Head & Neck
                Head & Neck
                Wiley
                1043-3074
                1097-0347
                February 2019
                June 2019
                December 24 2018
                June 2019
                : 41
                : 6
                : 1583-1590
                Affiliations
                [1 ]Department of Oncology‐PathologyKarolinska Institutet Stockholm Sweden
                [2 ]Department of Medical Epidemiology and BiostatisticsKarolinska Institutet Stockholm Sweden
                [3 ]CLINTECKarolinska Institutet Stockholm Sweden
                [4 ]Department of Clinical PathologyKarolinska University Hospital Stockholm Sweden
                Article
                10.1002/hed.25585
                30584688
                054e0516-920c-4b32-af46-6db11bd71160
                © 2019

                http://onlinelibrary.wiley.com/termsAndConditions#vor

                http://doi.wiley.com/10.1002/tdm_license_1.1

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