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Human papillomavirus, smoking, and sexual practices in the etiology of anal cancer
Article first published online: 2 JUN 2004
Copyright © 2004 American Cancer Society
Volume 101, Issue 2, pages 270–280, 15 July 2004
How to Cite
Daling, J. R., Madeleine, M. M., Johnson, L. G., Schwartz, S. M., Shera, K. A., Wurscher, M. A., Carter, J. J., Porter, P. L., Galloway, D. A. and McDougall, J. K. (2004), Human papillomavirus, smoking, and sexual practices in the etiology of anal cancer. Cancer, 101: 270–280. doi: 10.1002/cncr.20365
- Issue published online: 2 JUL 2004
- Article first published online: 2 JUN 2004
- Manuscript Accepted: 20 APR 2004
- Manuscript Revised: 13 APR 2004
- Manuscript Received: 22 OCT 2003
- National Cancer Institute. Grant Number: PO1 CA 42792
- The Cancer Surveillance System of the Fred Hutchinson Cancer Research Center. Grant Numbers: NO1-CN-05230, NO1-PC-67009
- Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute
- Fred Hutchinson Cancer Research Center
- State of Washington Department of Health
- human papillomavirus (HPV);
- anal neoplasms;
- cigarette smoking;
- sexual risk factors;
The incidence of anal cancer has increased among both men (160%) and women (78%) from 1973 to 2000 in the U.S. The authors conducted a population-based case–control study of anal cancer to examine factors that may account for this increase.
Men (n = 119 patients) and women (n = 187 patients) who were diagnosed with anal cancer between 1986 and 1998 in the Seattle area were ascertained through the local Surveillance, Epidemiology, and End Results registry. Control participants (n = 1700) were ascertained through random-digit telephone dialing. Participants were interviewed in person and provided blood samples. Archival tumor tissue was tested for human papilloma virus (HPV) DNA, and serum samples were tested for HPV type 16 (HPV-16).
Overall, 88% of tumors (all histologies) in the study were found to be positive for HPV. HPV-16 was the most frequent HPV type detected (73% of all tumors), followed by HPV-18 (6.9%), regardless of gender. However, 97.7% of tumors from men who were not exclusively heterosexual contained HPV DNA. The risk of anal cancer increased among men (odds ratio [OR], 5.3; 95% confidence interval [95% CI], 2.4–12.0) and women (OR, 11.0; 95% CI, 5.5–22.1) who had ≥ 15 sexual partners during their lifetime. Among men who were not exclusively heterosexual and women, receptive anal intercourse was related strongly to the risk of anal cancer (OR, 6.8 [95% CI, 1.4–33.8] and OR, 2.2 [95% CI, 1.4–3.3], respectively). Current smokers among men and women were at particularly high risk for anal cancer, independent of age and other risk factors (OR, 3.9 [95% CI, 1.9–8.0] and OR, 3.8 [95% CI, 2.4–6.2], respectively).
The high proportion of tumors with detectable HPV suggests that infection with HPV is a necessary cause of anal cancer, similar to that of cervical cancer. Increases in the prevalence of exposures, such as cigarette smoking, anal intercourse, HPV infection, and the number of lifetime sexual partners, may account for the increasing incidence of anal cancer in men and women. Cancer 2004. © 2004 American Cancer Society.