Risks for incident human papillomavirus infection and low-grade squamous intraepithelial lesion development in young females.

By A. Moscicki, N. Hills, S. Shiboski, K. Powell, N. Jay, E. Hanson, S. Miller, L. Clayton, S. Farhat, J. Broering and 2 more. Journal of the American Medical Association (JAMA), 2001

606 citations recorded by the source corpus.

Subfields: Epidemiology, Otorhinolaryngology, Surgery

View Paper: https://www.semanticscholar.org/paper/21442085f8a9209a56923342500d00641a4f6911

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Luisa Lina Villa
2. S. Kjaer
3. Mark Schiffman
4. S. de Sanjosé
5. X. Castellsagué
6. M. Stanley
7. E. Burd

In Otorhinolaryngology

1. S. de Sanjosé
2. X. Castellsagué

In Surgery

1. Luisa Lina Villa
2. S. Kjaer
3. Mark Schiffman
4. M. Stanley

Citations in the corpus

• Cervical human papillomavirus prevalence in 5 continents: meta-analysis of 1 million women with normal cytological findings. (2010, background): “The detection of HPV infection in women has been found to start consistently with a peak just after the onset of sexual relations, usually from 15 years of age [20], reaching prevalences up to 80% in some populations [16], mostly at the expense of transient infections that clear rapidly [21].”
• The natural history of cervical HPV infection: unresolved issues (2007, background): “Although several investigators have reported the distribution of exposure times necessary for disease to occu”
• Chapter 3: Cofactors in human papillomavirus carcinogenesis--role of parity, oral contraceptives, and tobacco smoking. (2003, neutral): “vs. never [10] 7.5 (1.2 to 46) [−20] 3.2 (1.0 to 9.7) [−19] 2.0 (1.2 to 3.3) [ 10 ] 2.0 (1.0 to 3.8) [20] 1.9 (1.0 to 3.5) [>20] 0.8 (0.3 to 2.7) [20] 3.1 (1.6 to 6.2)”
• Persistent human papillomavirus infection as a predictor of cervical intraepithelial neoplasia. (2001, methodology): “Among those studies that evaluated oncogenic HPV infection status through consecutive scheduled visits,(2-4,7-9) few investigated the RR association for incidence of cervical neoplasia following a repeated HPV infection.(2,4,8,9) Using a nonamplified hybridization method for typing HPVs, Koutsky et ”
• Chapter 2: Natural history of anogenital human papillomavirus infection and neoplasia. (2003, background): “It is still not known whether microscopically evident abnormalities represent a separate natural history stage from HPV detected by DNA testing alone ( 20 ,21).”
• 2012 updated consensus guidelines for the management of abnormal cervical cancer screening tests and cancer precursors. (2013, background): “Cervical cancer risk remains low through age 25 years (35), HPV is common (36), and lesions often regress (37).”
• Genital human papillomavirus infection: incidence and risk factors in a cohort of female university students. (2003, neutral): “Clinic-based studies achieve higher participation rates (4, 8, 9) but must contend with the fact that young women attending such clinics often do so because of signs or symptoms of a genital tract infection.”