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J Natl Cancer Inst. 2009 Apr 1;101(7):475-87. doi: 10.1093/jnci/djn510. Epub 2009 Mar 24.

Human papillomavirus genotype distributions: implications for vaccination and cancer screening in the United States.

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  • 1House of Prevention Epidemiology, Department of Molecular Genetics and Microbiology, School of Medicine, University of New Mexico Health Sciences Center, 1816 Sigma Chi Rd Bldg 191, Albuquerque, NM 87131, USA. cwheeler@salud.unm.edu

Abstract

BACKGROUND:

Limited data are available describing human papillomavirus (HPV) genotype distributions in cervical cancer in the United States. Such studies are needed to predict how HPV vaccination and HPV-based screening will influence cervical cancer prevention.

METHODS:

We used the New Mexico Surveillance, Epidemiology, and End Results Registry to ascertain cases of in situ (n = 1213) and invasive (n = 808) cervical cancer diagnosed during 1985-1999 and 1980-1999, respectively, in the state of New Mexico. HPV genotyping was performed using two polymerase chain reaction-based methods on paraffin-embedded tissues from in situ and invasive cancers and on cervical Papanicolaou test specimen from control subjects (ie, women aged 18-40 years attending clinics for routine cervical screening [n = 4007]). Relative risks for cervical cancer were estimated, and factors associated with age at cancer diagnosis and the prevalence of HPV genotypes in cancers were examined.

RESULTS:

The most common HPV genotypes detected in invasive cancers were HPV type 16 (HPV16, 53.2%), HPV18 (13.1%), and HPV45 (6.1%) and those in in situ cancers were HPV16 (56.3%), HPV31 (12.6%), and HPV33 (8.0%). Invasive cancer case subjects who were positive for HPV16 or 18 were diagnosed at younger ages than those who were positive for other carcinogenic HPV genotypes (mean age at diagnosis: 48.1 [95% confidence interval {CI} = 46.6 to 49.6 years], 45.9 [95% CI = 42.9 to 49.0 years], and 52.3 years [95% CI = 50.0 to 54.6 years], respectively). The proportion of HPV16-positive in situ and invasive cancers, but not of HPV18-positive cancers, declined with more recent calendar year of diagnosis, whereas the proportion positive for carcinogenic HPV genotypes other than HPV18 increased.

CONCLUSIONS:

HPV16 and 18 caused the majority of invasive cervical cancer in this population sample of US women, but the proportion attributable to HPV16 declined over the last 20 years. The age at diagnosis of HPV16- and HPV18-related cancers was 5 years earlier than that of cancers caused by carcinogenic HPV genotypes other than HPV16 and 18, suggesting that the age at initiation of cervical screening could be delayed in HPV-vaccinated populations.

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PMID:
19318628
[PubMed - indexed for MEDLINE]
PMCID:
PMC2664090
Free PMC Article

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