© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 8, 708-715,
April 21, 1999
© 1999 Oxford University Press
REPORTS |
Tobacco Smoking as a Risk Factor in Anal Carcinoma: an Antiestrogenic Mechanism?
Affiliations of authors: M. Frisch, J. Wohlfahrt, M. Melbye, Department of Epidemiology Research, Danish Epidemiology Science Center, Statens Serum Institut, Copenhagen, Denmark; B. Glimelius, Department of Oncology, Radiology, and Clinical Immunology, University Hospital, Uppsala, Sweden; H.-O. Adami, Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden, and Department of Epidemiology and Harvard Center for Cancer Prevention, Harvard University, Boston, MA.
Correspondence to present address: Morten Frisch, M.D., Ph.D., visiting scientist, Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Executive Plaza South, Rm. 8015, Bethesda, MD 20892 (e-mail: frischm{at}mail.nih.gov).
BACKGROUND: Human papillomavirus-associated anogenital carcinogenesis depends on
poorly defined cofactors. Smoking was recently suggested to increase the risk of anal cancer
more in premenopausal women than in postmenopausal women. Thus, we used our
population-based anal cancer case-control study in Denmark and Sweden to test this hypothesis.
METHODS: Our study included 417 patients (324 women and 93 men) who were diagnosed
with anal cancer (84% invasive cancer) from 1991 through 1994; it also included five
patients diagnosed in 1995. Two control groups were used: 1) 554 population control subjects
(349 women and 205 men) and 2) 534 patients with rectal adenocarcinoma (343 women and 191
men). Odds ratios (ORs), calculated from logistic regression analyses, were used as measures of
relative risk. All P values are two-sided. RESULTS: Compared with the risk for lifelong
nonsmokers, the risk of anal cancer was high among premenopausal women who currently
smoked tobacco (multivariate OR = 5.6; 95% confidence interval [CI]
= 2.4-12.7) and increased linearly by 6.7% per pack-year smoked (one pack-year is
equivalent to one pack of cigarettes smoked per day for 1 year) (P for trend <.001).
Smoking was not statistically significantly associated with anal cancer risk in postmenopausal
women or men. Women whose menstrual periods started late were at high risk (multivariate OR
= 3.6; 95% CI = 1.8-7.3, for 
17 years of age versus 
12 years of
age; P for trend <.001), and body mass index (weight in kg/[height in m]2) was inversely associated with risk among women (P<.001).
CONCLUSIONS: Because the risk of anal cancer associated with smoking was restricted to
premenopausal women and because higher risk was associated with late menarche and lean body
composition, female sex hormones may be a factor in anal cancer development in women. Since
the anal mucosa is an estrogen-sensitive area, we hypothesize an antiestrogenic mechanism of
action for smoking in anal carcinogenesis.
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