Journal of the National Cancer Institute Advance Access originally published online on March 24, 2009
JNCI Journal of the National Cancer Institute 2009 101(7):475-487; doi:10.1093/jnci/djn510
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ARTICLES |
Human Papillomavirus Genotype Distributions: Implications for Vaccination and Cancer Screening in the United States
Affiliations of authors: Department of Molecular Genetics and Microbiology (CMW, WCH), Department of Obstetrics and Gynecology (CMW), Department of Pathology (NEJ, CRK), New Mexico Tumor Registry (CRK), School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM; DDL Diagnostic Laboratory, Voorburg, the Netherlands (WGVQ); Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD (PEC)
Correspondence to: Cosette M. Wheeler, PhD, House 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 (e-mail: cwheeler{at}salud.unm.edu).
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.
| CONTEXT AND CAVEATS Prior knowledge Vaccination of adolescent girls for the primary prevention of human papillomavirus (HPV) infection and methods to detect infection with carcinogenic HPV types have emerged as approaches for the prevention of cervical cancer. Population-based studies of HPV genotype prevalence are needed to predict how these approaches might influence cervical cancer prevention. Study design A case–control study of Hispanic and non-Hispanic white women in New Mexico to describe cervical cancer risk by HPV genotype, species, and risk groups. Contribution HPV16 and 18 caused the majority of cervical cancer in this population sample of US women. However, the proportion of HPV16-positive cancers declined over the last 20 years, and age at diagnosis of HPV16- and HPV18-related cancers was 5 years earlier than that of cancers caused by other carcinogenic HPV genotypes. Implications The earlier age at diagnosis of HPV16- and HPV18-related cancers suggests that the age at initiation of cervical screening could be delayed in populations that are vaccinated against those HPV types. Limitations The findings may not be generalizable to other populations. Relationships between outcomes and time were inferred. Misattribution of some cases of cervical disease to HPV16 and 18 was likely. From the Editors
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Manuscript received July 1, 2008; revised December 3, 2008; accepted December 23, 2008.
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J Natl Cancer Inst 2009 101: 437.
J Natl Cancer Inst 2009 101: 437.