492 European Journal of Cancer Prevention 2014, Vol 23 No 5
Fig. 1
(a) (b)
(c) (d)
(b)
(c)
(d)
(e)
(f)
(g)
(a) Moderately differentiated invasive ductal carcinoma with a mixed pattern of growth (H&E, whole-mount section); (b–d) the lesion showing usual (b), cribriform (c), and papillary (d) patterns (H&E); (e) immunostain for the estrogen receptor; (f) immunostain for the progesterone receptor; (g) immunostain for HER2 protein.
Conflicts of interest
There are no conflicts of interest.
References Dimitrakakis C, Gosselink L, Gaki V, Bredakis N, Keramopoulos A (2004). Phytoestrogen supplementation: a case report of male breast cancer. Eur J Cancer Prev 13:481–484. Eisenberg DM, Davis RB, Ettner SL, Appel S, Wilkey S, Van Rompay M, Kessler RC (1998). Trends in alternative medicine use in the United States, 1990–1997: results of a follow-up national survey. JAMA 280:1569–1575. Lakhani SR, Ellis IO, Schnitt SJ, Tan PH, van de Vijver MJ (2012). WHO classification of tumours of the breast. Lyon: IARC. Messina M, McCaskill-Stevens W, Lampe JW (2006). Addressing the soy and breast cancer relationship: review, commentary, and workshop proceedings. J Natl Cancer Inst 98:1275–1284. Murkies AL, Wilcox G, Davis SR (1998). Clinical review 92: phytoestrogens. J Clin Endocrinol Metab 83:297–303.
Rice S, Whitehead SA (2006). Phytoestrogens and breast cancer – promoters or protectors? Endocr Relat Cancer 13:995–1015. Thompson LU, Robb P, Serraino M, Cheung F (1991). Mammalian lignan production from various foods. Nutr Cancer 16:43–52. Tindle HA, Davis RB, Phillips RS, Eisenberg DM (2005). Trends in use of complementary and alternative medicine by US adults: 1997–2002. Altern Ther Health Med 11:42–49.
A critique to a review on the relationship between asbestos exposure and the risk of mesothelioma Benedetto Terracinia, Dario Mirabellia, Corrado Magnanib, Daniela Ferranteb, Francesco Barone-Adesia,d and Marinella Bertolottib,c, a Department of Cancer Epidemiology, University of Turin and CPO Piemonte, Turin, bDepartment of Cancer Epidemiology, University of Eastern Piedmont and CPO Piemonte, Novara, cSanti Antonio e Biagio e Cesare Arrigo Hospital,
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Letters to the Editor 493
Alessandria, Italy and dDepartment of Population Health Sciences and Education, St George’s University of London, London, UK Correspondence to Benedetto Terracini, MD, Department of Cancer Epidemiology, University of Turin and CPO Piemonte, Via Santena 7, 10126, Turin, Italy Tel: +39 0116 336966; fax: +39 0116 336960; e-mail: [email protected] Received 7 February 2014 Accepted 15 May 2014
The review published by La Vecchia and Boffetta (2012) concluded by refuting that the risk of mesothelioma is influenced by subsequent exposures to asbestos or by stopping exposure. A leading European daily newspaper (Foucart, 2013), together with an interview with one of us, has recently reported that such conclusions were in part based on misinterpretation of our findings (Magnani et al., 2008). The present letter aims to provide a correct interpretation of our results and also to point out other possible issues in La Vecchia and Boffetta’s paper. First of all, it is useful to underline that La Vecchia and Boffetta did not carry out a systematic review of the literature, but presented selected results from selected papers. Comments on the specific results reported by La Vecchia and Boffetta follow. In our study on the cohort of workers employed at the Eternit plant of Casale Monferrato, we estimated the trends in mortality from pleural cancer by calculating rate ratios (RRs) by duration of exposure to asbestos and time since start (latency) and cessation of exposure. Multivariable statistical models were constructed by introducing all relevant variables (sex, age at first exposure, calendar period, duration, latency, time since exposure cessation) and retaining only those contributing significantly toward model fit. La Vecchia and Boffetta reported in their review that, in the Eternit study, the RR among workers who stopped exposure less than 3 years before death from mesothelioma was almost identical to that of individuals stopping more than 30 years before death. They considered this finding as supporting their hypothesis, but they overlooked the fact that the first category also included the person-years accrued during employment. As, while employed, individuals were necessarily alive, the risk of mesothelioma in the first category appears to be artificially lower than it would be in an analysis restricted to individuals who quit employment. In fact, there is a suggestion of a decreasing trend of RR with longer time since cessation of exposure in the other three categories (Table 1). Moreover, La Vecchia and Boffetta failed to report another result from the same analysis that is important when evaluating the role of recent exposures to asbestos. The original Table 5 of our study showed a steady increase in RR with duration of exposure, adjusted by latency and time since exposure cessation. Indeed, we reported in our paper that when the model was fitted by including duration as a continuous variable, every year of exposure was associated with a 5% increase in the risk of
Cohort study of asbestos-cement workers: analysis of mortality using Poisson regression, pleural malignant neoplasms (see also text for explanation on statistical modeling)
Table 1
Number of cases Time since exposure start (years) < 10 1 10–19 8 20–29 23 30–39 48 40–49 40 50 + 19 Time since exposure end (years) 30 16 Duration of exposure (years)
Fig. 1
(a) (b)
(c) (d)
(b)
(c)
(d)
(e)
(f)
(g)
(a) Moderately differentiated invasive ductal carcinoma with a mixed pattern of growth (H&E, whole-mount section); (b–d) the lesion showing usual (b), cribriform (c), and papillary (d) patterns (H&E); (e) immunostain for the estrogen receptor; (f) immunostain for the progesterone receptor; (g) immunostain for HER2 protein.
Conflicts of interest
There are no conflicts of interest.
References Dimitrakakis C, Gosselink L, Gaki V, Bredakis N, Keramopoulos A (2004). Phytoestrogen supplementation: a case report of male breast cancer. Eur J Cancer Prev 13:481–484. Eisenberg DM, Davis RB, Ettner SL, Appel S, Wilkey S, Van Rompay M, Kessler RC (1998). Trends in alternative medicine use in the United States, 1990–1997: results of a follow-up national survey. JAMA 280:1569–1575. Lakhani SR, Ellis IO, Schnitt SJ, Tan PH, van de Vijver MJ (2012). WHO classification of tumours of the breast. Lyon: IARC. Messina M, McCaskill-Stevens W, Lampe JW (2006). Addressing the soy and breast cancer relationship: review, commentary, and workshop proceedings. J Natl Cancer Inst 98:1275–1284. Murkies AL, Wilcox G, Davis SR (1998). Clinical review 92: phytoestrogens. J Clin Endocrinol Metab 83:297–303.
Rice S, Whitehead SA (2006). Phytoestrogens and breast cancer – promoters or protectors? Endocr Relat Cancer 13:995–1015. Thompson LU, Robb P, Serraino M, Cheung F (1991). Mammalian lignan production from various foods. Nutr Cancer 16:43–52. Tindle HA, Davis RB, Phillips RS, Eisenberg DM (2005). Trends in use of complementary and alternative medicine by US adults: 1997–2002. Altern Ther Health Med 11:42–49.
A critique to a review on the relationship between asbestos exposure and the risk of mesothelioma Benedetto Terracinia, Dario Mirabellia, Corrado Magnanib, Daniela Ferranteb, Francesco Barone-Adesia,d and Marinella Bertolottib,c, a Department of Cancer Epidemiology, University of Turin and CPO Piemonte, Turin, bDepartment of Cancer Epidemiology, University of Eastern Piedmont and CPO Piemonte, Novara, cSanti Antonio e Biagio e Cesare Arrigo Hospital,
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Letters to the Editor 493
Alessandria, Italy and dDepartment of Population Health Sciences and Education, St George’s University of London, London, UK Correspondence to Benedetto Terracini, MD, Department of Cancer Epidemiology, University of Turin and CPO Piemonte, Via Santena 7, 10126, Turin, Italy Tel: +39 0116 336966; fax: +39 0116 336960; e-mail: [email protected] Received 7 February 2014 Accepted 15 May 2014
The review published by La Vecchia and Boffetta (2012) concluded by refuting that the risk of mesothelioma is influenced by subsequent exposures to asbestos or by stopping exposure. A leading European daily newspaper (Foucart, 2013), together with an interview with one of us, has recently reported that such conclusions were in part based on misinterpretation of our findings (Magnani et al., 2008). The present letter aims to provide a correct interpretation of our results and also to point out other possible issues in La Vecchia and Boffetta’s paper. First of all, it is useful to underline that La Vecchia and Boffetta did not carry out a systematic review of the literature, but presented selected results from selected papers. Comments on the specific results reported by La Vecchia and Boffetta follow. In our study on the cohort of workers employed at the Eternit plant of Casale Monferrato, we estimated the trends in mortality from pleural cancer by calculating rate ratios (RRs) by duration of exposure to asbestos and time since start (latency) and cessation of exposure. Multivariable statistical models were constructed by introducing all relevant variables (sex, age at first exposure, calendar period, duration, latency, time since exposure cessation) and retaining only those contributing significantly toward model fit. La Vecchia and Boffetta reported in their review that, in the Eternit study, the RR among workers who stopped exposure less than 3 years before death from mesothelioma was almost identical to that of individuals stopping more than 30 years before death. They considered this finding as supporting their hypothesis, but they overlooked the fact that the first category also included the person-years accrued during employment. As, while employed, individuals were necessarily alive, the risk of mesothelioma in the first category appears to be artificially lower than it would be in an analysis restricted to individuals who quit employment. In fact, there is a suggestion of a decreasing trend of RR with longer time since cessation of exposure in the other three categories (Table 1). Moreover, La Vecchia and Boffetta failed to report another result from the same analysis that is important when evaluating the role of recent exposures to asbestos. The original Table 5 of our study showed a steady increase in RR with duration of exposure, adjusted by latency and time since exposure cessation. Indeed, we reported in our paper that when the model was fitted by including duration as a continuous variable, every year of exposure was associated with a 5% increase in the risk of
Cohort study of asbestos-cement workers: analysis of mortality using Poisson regression, pleural malignant neoplasms (see also text for explanation on statistical modeling)
Table 1
Number of cases Time since exposure start (years) < 10 1 10–19 8 20–29 23 30–39 48 40–49 40 50 + 19 Time since exposure end (years) 30 16 Duration of exposure (years)
