scholarly journals Oral Bisphosphonate Use and Risk of Postmenopausal Endometrial Cancer

2015 ◽  
Vol 33 (10) ◽  
pp. 1186-1190 ◽  
Author(s):  
Polly A. Newcomb ◽  
Michael N. Passarelli ◽  
Amanda I. Phipps ◽  
Garnet L. Anderson ◽  
Jean Wactawski-Wende ◽  
...  

Purpose Bisphosphonates are common medications used for the treatment of osteoporosis and are also used to reduce metastases to bone in patients with cancer. Several studies, including the Women's Health Initiative (WHI), have found that use of bisphosphonates is associated with reduced risk of developing breast cancer, but less is known about associations with other common malignancies. This study was aimed at examining the effects of bisphosphonates on the risk of endometrial cancer. Methods We evaluated the relationship between use of oral bisphosphonates and endometrial cancer risk in a cohort of 89,918 postmenopausal women participating in the WHI. A detailed health interview was conducted at baseline, and bisphosphonate use was ascertained from an inventory of regularly used medications at baseline and over follow-up. All women had an intact uterus at the time of study entry. Results During a median follow-up of 12.5 years, 1,123 women were diagnosed with incident invasive endometrial cancer. Ever use of bisphosphonates was associated with reduced endometrial cancer risk (adjusted hazard ratio, 0.80; 95% CI, 0.64 to 1.00; P = .05), with no interactions observed with age, body mass index, or indication for use. Conclusion In this large prospective cohort of postmenopausal women, bisphosphonate use was associated with a statistically significant reduction in endometrial cancer risk.

2012 ◽  
Vol 20 (1) ◽  
pp. 151-160 ◽  
Author(s):  
Cher M Dallal ◽  
Louise A Brinton ◽  
Douglas C Bauer ◽  
Diana S M Buist ◽  
Jane A Cauley ◽  
...  

Endometrial cancer risk is strongly influenced by obesity, but the mechanisms of action remain unclear. Leptin and adiponectin, secreted from adipose tissue, reportedly play a role in such carcinogenic processes as cell proliferation, angiogenesis, and insulin regulation. In this case–control study, nested within the Breast and Bone Follow-up of the Fracture Intervention Trial (n=15 595), we assessed pre-diagnostic serum leptin, total adiponectin, and high-molecular-weight (HMW) adiponectin in relation to endometrial cancer among postmenopausal women. During the 10-year follow-up, 62 incident endometrial cases were identified and matched to 124 controls on age, geographical site, time of fasting blood draw at baseline (1992–1993), and trial participation status. Adipokines and C-peptide were measured by ELISA. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated via conditional logistic regression, with exposures categorized in tertiles (T). Multivariable models considered C-peptide, BMI (kg/m2), and estradiol (E2) as potential confounders. Endometrial cancer risk was significantly associated with higher leptin levels, adjusted for E2 and C-peptide (ORT3 vs T1=2.96; 95% CI, 1.21–7.25; P trend <0.01). After further adjustment for BMI, the estimates were attenuated and the positive trend was no longer statistically significant (ORT3 vs T1=2.11; 95% CI, 0.69–6.44; P trend=0.18). No significant associations were observed with adiponectin or HMW adiponectin and endometrial cancer. Our findings with leptin suggest that the leptin–BMI axis might increase endometrial cancer risk through mechanisms other than estrogen-driven proliferation. Continued exploration of these pathways in larger prospective studies may help elucidate mechanisms underlying observed obesity–endometrial cancer associations.


2016 ◽  
Vol 25 (7) ◽  
pp. 1081-1089 ◽  
Author(s):  
Louise A. Brinton ◽  
Britton Trabert ◽  
Garnet L. Anderson ◽  
Roni T. Falk ◽  
Ashley S. Felix ◽  
...  

2005 ◽  
Vol 8 (7) ◽  
pp. 912-919 ◽  
Author(s):  
Stephanie AN Silvera ◽  
Thomas E Rohan ◽  
Meera Jain ◽  
Paul D Terry ◽  
Geoffrey R Howe ◽  
...  

AbstractObjectiveHigh-glycaemic-load diets may increase endometrial cancer risk by increasing circulating insulin levels and, as a consequence, circulating oestrogen levels. Given the paucity of epidemiological data regarding the relationship between dietary glycaemic index and glycaemic load and endometrial cancer risk, we sought to examine these associations using data from a prospective cohort study.Design, setting and subjectsWe examined the association between dietary glycaemic load and endometrial cancer risk in a cohort of 49 613 Canadian women aged between 40 and 59 years at baseline who completed self-administered food-frequency questionnaires between 1982 and 1985. Linkages to national mortality and cancer databases yielded data on deaths and cancer incidence, with follow-up ending between 1998 and 2000.ResultsDuring a mean of 16.4 years of follow-up, we observed 426 incident cases of endometrial cancer. Hazard ratios for the highest versus the lowest quartile level of overall glycaemic index and glycaemic load were 1.47 (95% confidence interval (CI) = 0.90–2.41; P for trend = 0.14) and 1.36 (95% CI = 1.01–1.84; P for trend = 0.21), respectively. No association was observed between total carbohydrate or total sugar consumption and endometrial cancer risk. Among obese women (body mass index > 30 kg m−2) the hazard ratio for the highest versus the lowest quartile level of glycaemic load was 1.88 (95% CI = 1.08–3.29; P for trend = 0.54) and there was a 55% increased risk for the highest versus the lowest quartile level of glycaemic load among premenopausal women. There was also evidence to support a positive association between glycaemic load and endometrial cancer risk among postmenopausal women who had used hormone replacement therapy.ConclusionsOur data suggest that diets with high glycaemic index or high glycaemic load may be associated with endometrial cancer risk overall, and particularly among obese women, premenopausal women and postmenopausal women who use hormone replacement therapy.


2013 ◽  
Vol 28 (10) ◽  
pp. 2813-2821 ◽  
Author(s):  
L. A. Brinton ◽  
C. L. Westhoff ◽  
B. Scoccia ◽  
E. J. Lamb ◽  
B. Trabert ◽  
...  

Nutrients ◽  
2011 ◽  
Vol 3 (11) ◽  
pp. 937-950 ◽  
Author(s):  
Ayush Giri ◽  
Susan R. Sturgeon ◽  
Nicole Luisi ◽  
Elizabeth Bertone-Johnson ◽  
Raji Balasubramanian ◽  
...  

2008 ◽  
Vol 98 (9) ◽  
pp. 1582-1585 ◽  
Author(s):  
K Lindemann ◽  
L J Vatten ◽  
M Ellstrøm-Engh ◽  
A Eskild

2020 ◽  
Author(s):  
Pik Fang Kho ◽  
Sally Mortlock ◽  
Peter A.W. Rogers ◽  
Dale R. Nyholt ◽  
Grant W. Montgomery ◽  
...  

AbstractThe non-cancerous gynecological diseases, endometriosis, polycystic ovary syndrome (PCOS) and uterine fibroids, have been proposed as endometrial cancer risk factors; however, disentangling their relationships is complicated due to their shared risk factors and comorbidity. Using genome-wide association study (GWAS) summary data, we have explored the relationship between these non-cancerous gynecological diseases and endometrial cancer risk, assessing genetic correlations, causal relationships and shared genetic risk regions. Firstly, we found significant genetic correlation between endometrial cancer and PCOS (rG = 0.36, se = 0.12, P = 1.6×10−3), and uterine fibroids (rG = 0.24, se = 0.09, P = 5.4×10−3). Adjustment for genetically predicted body mass index (BMI; a risk factor for PCOS, uterine fibroids and endometrial cancer) substantially attenuated the genetic correlation between endometrial cancer and PCOS, but not uterine fibroids. Despite the observed genetic correlation, genetic causal inference tests (latent causal variable and Mendelian randomization analyses) did not support a causal relationship between any of the non-cancerous gynecological diseases and endometrial cancer. Gene-based association analysis revealed four shared endometriosis and endometrial cancer risk loci (9p21.3, 15q15.1, 17q21.32 and 3q21.3) and two shared uterine fibroid and endometrial cancer risk loci (5p15.33 and 11p13). In summary, we have shown that PCOS and uterine fibroids are genetically correlated with endometrial cancer, although the genetic architecture shared between endometrial cancer and PCOS likely relates to BMI. Furthermore, shared genetic risk regions, and thus potentially shared causal genes, were identified between the risk for endometrial cancer and endometriosis, and uterine fibroids.


2015 ◽  
Vol 138 (5) ◽  
pp. 1129-1138 ◽  
Author(s):  
Mireia Obón-Santacana ◽  
Heinz Freisling ◽  
Petra H. Peeters ◽  
Leila Lujan-Barroso ◽  
Pietro Ferrari ◽  
...  

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