Daniel C Beachler1, Alison G Abraham2, Michael J Silverberg3, Yuezhou Jing4, Carole Fakhry5, M John Gill6, Robert Dubrow7, Mari M Kitahata8, Marina B Klein9, Ann N Burchell10, P Todd Korthuis11, Richard D Moore12, Gypsyamber D'Souza13. 1. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe St., Baltimore, MD, USA. Electronic address: dbeachl1@jhu.edu. 2. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe St., Baltimore, MD, USA. Electronic address: aabraham@jhsph.edu. 3. Division of Research, Kaiser Permanente Northern California, 2000 Broadway, Oakland, CA, USA. Electronic address: Michael.j.silverberg@kp.org. 4. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe St., Baltimore, MD, USA. Electronic address: yjing@jhsph.edu. 5. Department of Otolaryngology - Head and Neck Surgery, Johns Hopkins Hospital, 601 N. Caroline St., Baltimore, MD, USA. Electronic address: cfakhry@jhmi.edu. 6. Department of Medicine, University of Calgary, 3330 Hospital Dr. NW., Calgary, Canada. Electronic address: john.gill@albertahealthservices.ca. 7. Cancer Prevention and Control Program, Yale School of Public Health and Yale School of Medicine, P.O. Box 208034, 60 College Street, New Haven, CT, USA. Electronic address: Robert.dubrow@yale.edu. 8. University of Washington, 325 9th Ave, Seattle, WA, USA. Electronic address: kitahata@uw.edu. 9. Division of Medicine, McGill University, 3655 Sir William Osler, Montreal, Quebec, Canada. Electronic address: marina.klein@mcgill.ca. 10. Division of Oncology, Ontario HIV Treatment Network, 1300 Yong St. Suite 600, Toronto, Ontario, Canada. Electronic address: ann.burchell@mail.mcgill.ca. 11. Department of Public Health/Preventive Medicine, Oregon Health & Science University, 3181 S.W. Sam Jackson Park Rd., Portland, OR, USA. Electronic address: korthuis@ohsu.edu. 12. Department of Medicine, Johns Hopkins University, 1830 E. Monument St., Baltimore, MD, USA. Electronic address: rdmoore@jhmi.edu. 13. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe St., Baltimore, MD, USA. Electronic address: gdsouza2@jhu.edu.
Abstract
OBJECTIVES: To examine the risk and trends of HPV-related and HPV-unrelated Head and Neck Squamous Cell Carcinoma (HNSCC) in HIV-infected individuals and assess whether immunosuppression (measured through CD4 cell count) and other risk factors impact HNSCC risk. MATERIALS AND METHODS: Incident HNSCCs at HPV-related and HPV-unrelated anatomic sites were detected in HIV-infected participants from pooled data from 17 prospective studies in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) between 1996 and 2009. HNSCC cases were validated using chart review or cancer registry matching. Risk factors for incident HPV-related and HPV-unrelated HNSCC were explored using mixed effects Poisson regression in a full prospective analysis, and the effect of CD4 prior to cancer diagnosis was examined in a nested case control analysis. RESULTS: 66 HPV-related and 182 HPV-unrelated incident HNSCCs were detected among 82,375 HIV-infected participants. Standardized incidence ratios (SIRs) for both HPV-related (SIR=3.2, 95%CI=2.5-3.4) and HPV-unrelated (SIR=3.0, 95%CI=2.5-4.1) HNSCC were significantly elevated in HIV-infected individuals compared with the US general population. Between 1996 and 2009, the age-standardized HPV-related HNSCC incidence increased non-significantly from 6.8 to 11.4per 100,000 person-years (p-trend=0.31) while the age-standardized incidence of HPV-unrelated HNSCC decreased non-significantly from 41.9 to 29.3 per 100,000 person-years (p-trend=0.16). Lower CD4 cell count prior to cancer diagnosis was significantly associated with increased HPV-related and HPV-unrelated HNSCC risk. CONCLUSION: The standardized incidence of HPV-related and HPV-unrelated HNSCC are both elevated in HIV-infected individuals. Immunosuppression may have a role in the development of both HPV-related and HPV-unrelated HNSCC.
OBJECTIVES: To examine the risk and trends of HPV-related and HPV-unrelated Head and Neck Squamous Cell Carcinoma (HNSCC) in HIV-infected individuals and assess whether immunosuppression (measured through CD4 cell count) and other risk factors impact HNSCC risk. MATERIALS AND METHODS: Incident HNSCCs at HPV-related and HPV-unrelated anatomic sites were detected in HIV-infectedparticipants from pooled data from 17 prospective studies in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) between 1996 and 2009. HNSCC cases were validated using chart review or cancer registry matching. Risk factors for incident HPV-related and HPV-unrelated HNSCC were explored using mixed effects Poisson regression in a full prospective analysis, and the effect of CD4 prior to cancer diagnosis was examined in a nested case control analysis. RESULTS: 66 HPV-related and 182 HPV-unrelated incident HNSCCs were detected among 82,375 HIV-infectedparticipants. Standardized incidence ratios (SIRs) for both HPV-related (SIR=3.2, 95%CI=2.5-3.4) and HPV-unrelated (SIR=3.0, 95%CI=2.5-4.1) HNSCC were significantly elevated in HIV-infected individuals compared with the US general population. Between 1996 and 2009, the age-standardized HPV-related HNSCC incidence increased non-significantly from 6.8 to 11.4per 100,000 person-years (p-trend=0.31) while the age-standardized incidence of HPV-unrelated HNSCC decreased non-significantly from 41.9 to 29.3 per 100,000 person-years (p-trend=0.16). Lower CD4 cell count prior to cancer diagnosis was significantly associated with increased HPV-related and HPV-unrelated HNSCC risk. CONCLUSION: The standardized incidence of HPV-related and HPV-unrelated HNSCC are both elevated in HIV-infected individuals. Immunosuppression may have a role in the development of both HPV-related and HPV-unrelated HNSCC.
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