Skip to Content

Publications Search - Abstract View

Title: Obesity-related hormones and endometrial cancer among postmenopausal women: a nested case-control study within the B~FIT cohort.
Authors: Dallal CM,  Brinton LA,  Bauer DC,  Buist DS,  Cauley JA,  Hue TF,  Lacroix A,  Tice JA,  Chia VM,  Falk R,  Pfeiffer R,  Pollak M,  Veenstra TD,  Xu X,  Lacey JV,  B~FIT Research Group,  Bauer DC,  Hue TF,  Litwack-Harrison S,  Rubin S,  Tice JA,  Buist DS,  LaCroix AZ,  Harris E,  Haskell WL,  Barrett-Connor E,  Torner JC,  Hochberg MC,  Levis S,  Cauley JA,  Satterfield S,  Quandt SA,  Brinton LA,  Lacey JV
Journal: Endocr Relat Cancer
Date: 2013 Feb
Branches: BB, EBP, HREB
PubMed ID: 23222000
PMC ID: PMC4038326
Abstract: 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/m(2)), and estradiol (E2) as potential confounders. Endometrial cancer risk was significantly associated with higher leptin levels, adjusted for E2 and C-peptide (OR(T3 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 (OR(T3 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.