Bisphosphonates are traditionally used for treatment of osteoporosis and more recently for treatment and prevention of bone metastases in various malignancies. The use of 2nd-generation oral bisphosphonates has been reported to reduce the risk of developing breast and colon cancer but their influence on cancer survival has not been studied. Methods Two large cohorts of consecutively diagnosed cases with breast or colorectal cancer were studied for the association between use of 2nd-generation oral bisphosphonates and cancer survival. Using computerized prescription records, sustained use of alendronate/risedronate was assessed in postmenopausal women with newly diagnosed breast (n = 2,843) or colorectal cancer (n = 1,706). Overall survival and cancer-specific survival were evaluated using time dependent analysis. Results Postmenopausal women with breast cancer previously unexposed to bisphosphonates who used 2nd-generation bisphosphonates after diagnosis for at least one year had a significantly better survival than non-users, adjusted for age, tumor stage and grade (Overall survival: HR = 0.53, 0.33-0.86, breast cancer-specific survival: HR = 0.26, 0.10-0.71, p = 0.009). A similar advantageous hazard ratio was found in users with ER positive, ER negative and HER2neu positive tumors. A similar significantly better survival was noted for colorectal cancer after adjustment for age, tumor stage and grade (Overall survival: HR = 0.53, 0.33-0.85, colorectal cancer-specific survival: HR = 0.44, 0.21-0.88, p = 0.02). Women who used bisphosphonates before diagnosis did not exhibit a significant survival benefit. Pharmacogenetic studies of F(D)PPS (Farnesyl Pyrophosphate Synthase), a gene coding a key step in the mevalonate pathway revealed direct correlation between a minor homozygous status and survival in bisphosphonate users. Conclusions The use of 2nd-generation bisphosphonates initiated after diagnosis was associated with a significant improvement in overall and in cancer-specific survival of postmenopausal women with breast or colon cancers. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P3-06-03.
Introduction: Statins and aspirin have been shown to reduce the risk of venous thromboembolic events (VTE's) in the general population in randomized trials. Aim: To assess whether statins and aspirin reduce the incidence of deep vein thrombosis and pulmonary embolism in patients diagnosed with breast cancer. Methods: The Breast Cancer in Northern Israel Study (BCINIS) is an on-going population-based case-control study of consecutive breast cancer cases and matched controls diagnosed in the northern part of Israel since 2000. Only cases insured by the Clalit Health Services (64%) were included in this analysis. Data on medication use and VTE were extracted from the computerized database. Patients taking Warfarin or LMWH were excluded. Statistical analysis was performed using SPSS (v 18). Use of medications was analyzed as a time dependent covariate in a Cox Regression model. Results: Of 3552 patients 261 (7.3%) had a VTE during a median follow up of 4.7 years. In a multivariate analysis age (HR 1.03, 95% CI 1.02–1.04), BMI (HR 2.12, 95% CI 1.43–3.14 for BMI >30), chemotherapy (HR 3.87, 95% CI 2.50–5.98) and metastatic disease (HR 2.27, 95% CI 1.10–6.53) were associated with an increased risk for VTE's. Statins, mainly simvastatin and pravastatin, were used by 55.7% of the patients, and 45.7% used aspirin. Neither statins nor aspirin were associated with a significantly reduced risk for a VTE. After controlling for age, BMI, stage, chemotherapy and tamoxifen use the HR for statins was 0.80, CI 0.56–1.13, p = 0.2, and the HR for aspirin was 1.004, CI 0.74–1.76, p = 0.98. Conclusion: In contrast to the findings in the general population, statin and aspirin use were not associated with a reduced risk for VTE's in our cohort of breast cancer patients. Our results might be explained by an alternate mechanism of VTE formation in breast cancer and the use of low potency statins (simvastatin and pravastatin) in this cohort. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P6-14-03.
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