Leptin is higher in Females with Papillary Cancer compared to Benign Thyroid Nodules and Normal Controls

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 471-496-Thyroid Neoplasia & Case Reports
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-485
Ossama M.Z. Al-Taher* and Whitney S Goldner
University of Nebraska Medical Center, Omaha, NE
Background: Papillary thyroid carcinoma is the most common type of thyroid cancer comprising 80 to 90% of the cases. Thyroid cancer incidence has risen significantly in the United States since the early 1980s. In parallel, the rate of obesity has preceded this and there is evidence that obesity can predispose to an increased risk of thyroid cancer in both men and women. Leptin is elevated in obesity and it has been proposed that leptin is associated with thyroid cancer mediated by the leptin receptor long isoform. Leptin plays a role in the pathogenesis of papillary thyroid carcinoma through inhibiting apoptosis by activation of phosphatidylinositol3' kinase (PI3K)/protein kinase B (AKT) signaling pathway, and stimulating molecules such as CyclinD1, CDK2, and c-Myc resulting in cell cycle progression and proliferation. To date, we are not aware of studies evaluating leptin in age and BMI matched patients with papillary thyroid carcinoma versus benign thyroid nodules and ultrasound proven normal thyroid glands.

Method: We recruited 18 females with structurally and biochemically normal thyroids proven by ultrasound and TSH and Free T4 (CG). We used the Thyroid Tumor Cancer Collaborative Register (TCCR) at the University of Nebraska Medical Center for the age, gender, and BMI matched papillary thyroid carcinoma (PTCG n = 36) and benign thyroid nodules (BNG n = 18) participants. We analyzed leptin utilizing an ELISA Leptin kit. The correlation between leptin and BMI, TSH, free T4, and age were examined using a Spearman’s correlation coefficient.  Correlation of PTCG with TNM scores, stage, active, and inactive disease was evaluated using the Kruskal-Wallis test.

Results: Leptin levels were not significantly different between groups; however, there was a trend for higher leptin levels in the PTCG cohort (p = 0.0730; CG [10 to 23.3 ng/ml]; BNG [8.2 to 22.2 ng/ml]; PTCG [13.5 to 46.55 ng/ml]). Interestingly, leptin between CG and BNG was nearly identical (10 to 23.3 and 8.2 to 22.2 ng/ml respectively). As expected, leptin was significantly correlated with both BMI (p = <.0001) and age (p = 0.0006).

Conclusions: Although differences in leptin levels were not statistically significant between groups, a clear trend towards higher leptin levels was seen in PTCG compared to both CG and BNG. The levels between BNG and CG were similar. This warrants a larger prospective trial to ascertain if Leptin can be used clinically as a biomarker to help stratify benign nodules from malignant nodules.

Nothing to Disclose: OMZA, WSG

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm