Coffee Consumption and CYP1A2*1F Genotype Modify Age at Breast Cancer Diagnosis and Estrogen Receptor Status
- 1Department of Oncology, Clinical Sciences, Lund University; Departments of 2Surgery and 3Oncology, Lund University Hospital, Lund, Sweden; and 4Faculty of Health and Society, Malmö University, Malmö, Sweden
- Requests for reprints:
Helena Jernström, Lund University Hospital, Barngatan 2B, SE-221 85 Lund, Sweden. Phone: 46-4617-7619. E-mail: Helena.Jernstrom{at}med.lu.se
Abstract
CYP1A2 plays a key role in the metabolism of both estrogen and coffee. Women with higher coffee intake and the CYP1A2*1F A/A genotype have a ratio of high 2-hydroxyestrone (2-OHE1) to 16α-OHE1. 2-OHE1 is a weak estrogen and may even block the estrogen receptor (ER), whereas 16α-OHE1 is procarcinogenic. We hypothesized that moderate to high coffee consumption (≥2 cups per day) combined with the CYP1A2*1F A/A genotype would be associated with a later age at diagnosis and a greater proportion of ER-negative (ER−) tumors among patients with breast cancer. We genotyped 458 patients with breast cancer (age, 25-99 years) in Lund, Sweden, for CYP1A2*1F. Information on lifestyle factors and tumor characteristics were obtained from preoperative questionnaires and pathology reports. Among patients with CYP1A2*1F A/A (51.3%), moderate to high consumption was associated with a later age at diagnosis compared with low coffee consumption (59.8 versus 52.6 years, P = 0.0004). These patients were also more likely to have ER− tumors than patients with low consumption (14.7% versus 0%, P = 0.018). Coffee was not associated with ER status or age at diagnosis in patients with at least one C allele. Age at diagnosis was not associated with ER status in patients with CYP1A2*1F A/A, but younger patients (<50 years) with at least one C allele were more likely to have ER− tumors compared with older patients (odds ratio, 4.2; 95% confidence interval, 1.9-9.3; P = 0.0002). These findings raise the hypothesis that coffee slows the growth of ER-positive tumors in patients with CYP1A2*1F A/A and may have implications for breast cancer if confirmed. (Cancer Epidemiol Biomarkers Prev 2008;17(4):895–901)
Footnotes
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Grant support: Swedish Cancer Society, Mrs. Berta Kamprad Cancer Foundation, Lund University Hospital Fund, Crafoord Foundation, G. Nilsson Foundation, Swedish Research Council (K2001-27GX-14120-01A), GA's Donation for Breast Cancer Research, 1049 Fund at the Lund Oncology Clinic, Region Skåne ALF, Medical Faculty of Lund University, and an unrestricted grant by Novartis. E. Bågeman's position was supported by grants from the Swedish Cancer Society, the G. Nilsson Foundation, and the Swedish Research Council (K2001-27GX-14120-01A). C. Ingvar and C. Rose were financially supported through their clinical positions. H. Jernström's position was supported by the Swedish Research Council (K2002-27GP-14104-02B), the Medical Faculty of Lund University, and the Faculty of Health and Society of Malmö University.
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- Accepted February 1, 2008.
- Received June 18, 2007.
- Revision received January 8, 2008.
