of ovarian cancer, nonetheless many uncertainties remain. Future studies need to establish whether the association is causal with a clear temporal relation, or merely association due to exposure to shared risk factors. Additionally, risk stratiﬁcation algorithms should be judged not only on how well they help with disease detection when present, but also on how accurately they protect patients from the danger of a false-positive result. We declare that we have no conﬂicts of interest.
*Sun-Wei Guo, Marya D Zilberberg, Lone Hummelshoj [email protected]
Shanghai Hospital, Fudan University, Shanghai, China (S-WG); EviMed Research Group, LLC, Goshen, MA, USA (MDZ); University of Massachusetts, Amherst, MA, USA (MDZ); and Endometriosis.org, London, UK (LH) 1
Pearce CL, Templeman C, Rossing MA, et al. Association between endometriosis and risk of histological subtypes of ovarian cancer: a pooled analysis of case–control studies. Lancet Oncol 2012; 13: 385–94. Risch HA. Hormonal etiology of epithelial ovarian cancer, with a hypothesis concerning the role of androgens and progesterone. J Natl Cancer Inst 1998; 90: 1774–86. Cottreau CM, Ness RB, Modugno F, Allen GO, Goodman MT. Endometriosis and its treatment with danazol or lupron in relation to ovarian cancer. Clin Cancer Res 2003; 9: 5142–44. Rogers PA, D’Hooghe TM, Fazleabas A, et al. Priorities for endometriosis research: recommendations from an international consensus workshop. Reprod Sci 2009; 16: 335–46. Surveillance Epidemiology and End Results. SEER stat fact sheets: ovary. http://seer.cancer. gov/statfacts/html/ovary.html (accessed Feb 28, 2012).
Authors’ reply Both Vercellini and colleagues and Guo and colleagues raise concerns about screening, with which we agree. Our ﬁndings should not suggest to clinicians or the public
that screening for ovarian cancer should be implemented for women with endometriosis. Rather, we hope that our work stimulates further research that can reﬁne risk groups related to endometriosis on the basis of anatomical site, epidemiological risk factors, or molecular features. Vercellini and colleagues raise an interesting point about atypical endometriosis, but this diagnosis is not standardised or commonly used and can not be addressed in epidemiological studies. Estimation of the prevalence of endometriosis in the general population—as represented by the controls in our studies—is diﬃcult, as outlined by Eskenazi and Warner.1 Guo and colleagues suggest that our ﬁndings should be questioned because the prevalence reported in our control groups was less than 10% in 12 of 13 studies. They maintain that 10% is the benchmark used for prevalence of endometriosis in the population and cite Rogers and coworkers2 to support this statement, who in turn cite Eskenazi and Warner1 to support this prevalence estimate. In fact, Eskenazi and Warner1 state that the best estimate of prevalence in the general population comes from a study done in the USA by Houston and co-investigators,3 which suggests that prevalence is 6·2–8·2%. These ﬁgures are in line with the prevalence in controls reported in our Article.4 Thus lower reporting of endometriosis in controls in our studies than in the general population—ie, recall bias—is unlikely to explain our ﬁndings. Guo and colleagues suggest that the results we presented in table 4 of our Article to address the potential
of detection bias bring the reported associations into question because the magnitude of the odds ratio goes down in relation to the length of time between endometriosis diagnosis and diagnosis of ovarian cancer. To our knowledge, no evidence exists to indicate that increasing time since endometriosis diagnosis is associated with risk for ovarian cancer. Surgical treatment of endometriosis might be more common in women who have been diagnosed with the disease for longer than in those diagnosed more recently. An explanation for the attenuation noted could possibly be that surgery for endometriosis reduces the risk of endometriosisassociated ovarian cancer and is more common in women who have been diagnosed with endometriosis for a long period of time. Regardless, the attenuated associations remain statistically signiﬁcant. We declare that we have no conﬂicts of interest.
*Celeste Leigh Pearce, Andrew Berchuck [email protected]
University of Southern California, Los Angeles, CA, USA (CLP); and Duke University, Durham, NC, USA (AB) 1
Eskenazi B, Warner ML. Epidemiology of endometriosis. Obstet Gynecol Clin North Am 1997; 24: 235–58. Rogers PA, D’Hooghe TM, Fazleabas A, et al. Priorities for endometriosis research: recommendations from an international consensus workshop. Reprod Sci 2009; 16: 335–46. Houston DE, Noller KL, Melton LJ 3rd, Selwyn BJ, Hardy RJ. Incidence of pelvic endometriosis in Rochester, Minnesota, 1970–1979. Am J Epidemiol 1987; 125: 959–69. Pearce CL, Templeman C, Rossing MA, et al. Association between endometriosis and risk of histological subtypes of ovarian cancer: a pooled analysis of case-control studies. Lancet Oncol 2012; 13: 385–94.
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