|
Advertisement |
|
|
||
 |
|
|||||
|
|||||
|
 |
||||||
|
||||||
|
||||||
|
Originally published as JCO Early Release 10.1200/JCO.2009.22.5706 on May 11 2009 © 2009 American Society of Clinical Oncology.
Reply to P.A. LeppäluotoDivision of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD
Danish Cancer Society, Copenhagen, Denmark
University of Iowa, Iowa City, IA
Karolinska Institutet, Stockholm, Sweden
Cancer Registry of Norway, Oslo, Norway
Finnish Cancer Registry, Helsinki, Finland
Karolinska Institutet, Stockholm, Sweden
Danish Cancer Society, Copenhagen, Denmark
Cancer Registry of Norway, Oslo, Norway
Helsinki University Central Hospital, Helsinki, Finland
University of Rochester Medical Center, Rochester, NY
Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD We thank Leppäluoto1 for his interest in our study,2 in which we evaluated second cancer risks among 85,109 survivors of cervical squamous cell carcinoma (SCC) and 10,280 survivors of cervical adenocarcinoma (AC) over more than 40 years of follow-up. We calculated standardized incidence ratios (SIRs) to compare cancer incidence among survivors of cervical SCC or AC with incidence among women in the general population. We observed that risk of second primary lung cancers was significantly elevated among both survivors of cervical SCC (SIR, 2.69; 95% CI, 2.57 to 2.83) and survivors of cervical AC (SIR, 2.18; 95% CI, 1.82 to 2.61) when compared with women in the general population. The increased lung cancer risk among survivors of cervical AC was observed for the major lung cancer histologies (SCC and AC) and was apparent up to 20 years after cervical cancer diagnosis, arguing against misclassified metastases as a potential explanation for the increased risk. Because smoking is not believed to be a risk factor for cervical AC (ie, at cervical AC diagnosis, prevalence of smoking—past or current—is similar in women with cervical AC and women in the general population3), we concluded that the increased lung cancer risk among survivors of cervical AC pointed to the role of nonsmoking-related factors. As Leppäluoto1 describes, long-term use of oral contraceptives (OCs) is associated with increased risk of cervical SCC and cervical AC (ie, the prevalence of past or current OC use is higher among women with cervical SCC or AC than among women in the general population).4–6 Leppäluoto goes on to suggest that the known association between OC use and smoking could explain the elevated risk of lung cancer that we observed among survivors of cervical AC.2 Specifically, some OC users classified as nonsmokers should have been considered nonsmokers only for the duration of their OC use; some of these OC users would have been smokers either before or after their OC use. As a result, the prevalence of current or past smoking among survivors of cervical AC would have been higher than that among women in the general population, which could have led to increased lung cancer risk among survivors of cervical AC. We did not have information on smoking behaviors of the survivors of cervical cancer in our study,2 either before or after their cervical cancer diagnosis. Nonetheless, we believe that the scenario Leppäluoto1 suggests is unlikely, given that several previous case-control studies3,6 have shown that cervical AC risk is unrelated to cigarette smoking (measured using different metrics, including whether participants had ever smoked, past smoking, current smoking, and duration and intensity of smoking). In a recent pooled analysis3 of 23 case-control studies, including 1,191 patients with invasive cervical AC and 16,245 noncancer control participants, neither current smoking nor past smoking was found to be significantly related to cervical AC risk (relative risk for current smoking, 0.92; 95% CI, 0.78 to 1.07; relative risk for past smoking, 0.84; 95% CI, 0.68 to 1.03). Likewise, duration and intensity of smoking were unrelated to cervical AC risk. Importantly, cigarette smoking was not related to cervical AC risk in either unadjusted analyses or analyses adjusted for OC use. These results argue both against confounding by OC use of the association between smoking and AC risk and against differential reporting of smoking behaviors among OC users. These analyses3 show that at cervical AC diagnosis, past as well as current smoking behaviors are similar for women with cervical AC and women in the general population. Therefore, the elevated lung cancer risk among survivors of cervical AC when compared with women in the general population could not have arisen from increased smoking.2 Because it is unlikely that survivors of cervical AC would have preferentially initiated cigarette smoking after cervical cancer diagnosis, we believe that differences in smoking behaviors did not account for their increased lung cancer risk. In summary, our observation of a more than two-fold increased lung cancer risk among survivors of cervical AC suggests a role for factors other than smoking. AUTHORS' DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST The author(s) indicated no potential conflicts of interest. REFERENCES
1. Leppäluoto PA: Nonsmoking: A surrogate factor in primary lung cancer in survivors of cervical adenocarcinoma? J Clin Oncol 27:3065, 3066; 2009. 2. Chaturvedi AK, Kleinerman RA, Hildesheim A, et al: Second cancers after squamous cell carcinoma and adenocarcinoma of the cervix. J Clin Oncol 27:967, 973; 2009. 3. Appleby P, Beral V, Berrington de González A, et al: Carcinoma of the cervix and tobacco smoking: Collaborative reanalysis of individual data on 13,541 women with carcinoma of the cervix and 23,017 women without carcinoma of the cervix from 23 epidemiological studies. Int J Cancer 118:1481, 1495; 2006.[CrossRef][Medline] 4. Moreno V, Bosch FX, Munoz N, et al: Effect of oral contraceptives on risk of cervical cancer in women with human papillomavirus infection: The IARC multicentric case-control study. Lancet 359:1085, 1092; 2002.[CrossRef][Medline] 5. Lacey JV Jr, Brinton LA, Abbas FM, et al: Oral contraceptives as risk factors for cervical adenocarcinomas and squamous cell carcinomas. Cancer Epidemiol Biomarkers Prev 8:1079, 1085; 1999. 6. Castellsagué X, Díaz M, de Sanjosé S, et al: Worldwide human papillomavirus etiology of cervical adenocarcinoma and its cofactors: Implications for screening and prevention. J Natl Cancer Inst 98:303–315, 2006.
Related Articles
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
|
|||||||||||
|
|||||||||||
|
|
Copyright © 2009 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
|
