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Risk of second cancer among women with breast cancer

✍ Scribed by Lene Mellemkjær; Søren Friis; Jørgen H. Olsen; Ghislaine Scélo; Kari Hemminki; Elizabeth Tracey; Aage Andersen; David H. Brewster; Eero Pukkala; Mary L. McBride; Erich V. Kliewer; Jon M. Tonita; Chia Kee-Seng; Vera Pompe-Kirn; Carmen Martos; Jon G. Jonasson; Paolo Boffetta; Paul Brennan


Publisher
John Wiley and Sons
Year
2006
Tongue
French
Weight
111 KB
Volume
118
Category
Article
ISSN
0020-7136

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✦ Synopsis


Abstract

A large number of women survive a diagnosis of breast cancer. Knowledge of their risk of developing a new primary cancer is important not only in relation to potential side effects of their cancer treatment, but also in relation to the possibility of shared etiology with other types of cancer. A cohort of 525,527 women with primary breast cancer was identified from 13 population‐based cancer registries in Europe, Canada, Australia and Singapore, and followed for second primary cancers within the period 1943–2000. We used cancer incidence rates of first primary cancer for the calculation of standardized incidence ratios (SIRs) of second primary cancer. Risk of second primary breast cancer after various types of nonbreast cancer was also computed. For all second cancer sites combined, except contralateral breast cancer, we found a SIR of 1.25 (95% CI = 1.24–1.26) on the basis of 31,399 observed cases after first primary breast cancer. The overall risk increased with increasing time since breast cancer diagnosis and decreased by increasing age at breast cancer diagnosis. There were significant excesses of many different cancer sites; among these the excess was larger than 150 cases for stomach (SIR = 1.35), colorectal (SIR = 1.22), lung (SIR = 1.24), soft tissue sarcoma (SIR = 2.25), melanoma (SIR = 1.29), non‐melanoma skin (SIR = 1.58), endometrium (SIR = 1.52), ovary (SIR = 1.48), kidney (SIR = 1.27), thyroid gland (SIR = 1.62) and leukaemia (SIR = 1.52). The excess of cancer after a breast cancer diagnosis is likely to be explained by treatment for breast cancer and by shared genetic or environmental risk factors, although the general excess of cancer suggests that there may be additional explanations such as increased surveillance and general cancer susceptibility. © 2005 Wiley‐Liss, Inc.


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