Background: Over 200 million people worldwide are affected by thyroid proliferative diseases, including cancer, adenoma, and goiter, annually. The incidences of thyroid malignancies are three to four times higher in women, suggesting the possible involvement of estrogen. Based on this observed sex bias, we hypothesize that estrogen modulates the growth and metastatic propensity of thyroid cancer cells. Methods: In this study, two thyroid cell lines (Nthy-ori 3-1 and BCPAP) were evaluated for the presence of estrogen receptor (ER) by Western blot analysis and estrogen responsiveness by using a cell proliferation assay. In addition, the effect of estradiol (E 2 ) on modulation of metastatic phenotype was determined by using in vitro adhesion, migration, and invasion assays. Results: Thyroid cells expressed a functionally active ER-a and ER-b as evidenced by 50-150% enhancement of proliferation in the presence of E 2 . E 2 also enhanced adhesion, migration, and invasion of thyroid cells in an in vitro experimental model system that, based on our results, is modulated by b-catenin. Conclusion: Our data provide evidence that the higher incidence of thyroid cancer in women is potentially attributed to the presence of a functional ER that participates in cellular processes contributing to enhanced mitogenic, migratory, and invasive properties of thyroid cells. These findings will enable and foster the possible development of antiestrogenic therapy targeting invasion and migration, thus affecting metastatic propensity.

Postoperative recovery following intracapsular adenotonsillectomy in children with obstructive sleep apnea is significantly earlier with use of either the coblator or microdebrider versus traditional extracapsular tonsillectomy with electrocautery. Microdebrider and coblator were comparable in all other areas except for shorter operative time and less cost for the microdebrider.

Background: The incidence of thyroid cancer is four to five times higher in women than in men, suggesting a role for estrogen (E 2 ) in the pathogenesis of thyroid proliferative disease (TPD) that comprises cancer and goiter. The objective of this study was to investigate the antiestrogenic activity of 3,3 0 -diindolylmethane (DIM), a bioactive compound derived from cruciferous vegetables, in patients with TPD. Methods: In this limited phase I clinical trial study, patients found to have TPD were administered 300 mg of DIM per day for 14 days. Patients subsequently underwent a total or partial thyroidectomy, and tissue, urine, and serum samples were collected. Pre-and post-DIM serum and urine samples were analyzed for DIM levels as well as estrogen metabolites. DIM levels were also determined in thyroid tissue samples. Results: DIM was detectable in thyroid tissue, serum, and urine of patients after 14 days of supplementation. Urine analyses revealed that DIM modulated estrogen metabolism in patients with TPD. There was an increase in the ratio of 2-hydroxyestrones (C-2) to 16a-hydroxyestrone (C-16), consistent with antiestrogenic activity that results in more of C-2 product compared with C-16. Conclusion: Our data suggest that DIM enhances estrogen metabolism in TPD patients and can potentially serve as an antiestrogenic dietary supplement to help reduce the risk of developing TPD. The fact that DIM is detected in thyroid tissue implicates that it can manifest its antiestrogenic activity in situ to modulate TPD.

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Metastasis of cancer is a multifactorial disease and is the main cause of death in patients with malignancy. This disease demands treatments which may target multiple dysregulated cellular pathways in cancer cells. The anti-tumor and anti-metastatic properties of natural products in cancer prevention have been confirmed by several epidemiological studies, with cruciferous vegetables being especially protective against many cancers. In this study, we evaluated the anti-carcinogenic effects of 3,3'-diindolylmethane (DIM), which is a bioactive compound present in cruciferous vegetables and a widely used dietary supplement, on events commonly observed during metastasis using in vitro adhesion, migration and invasion assays. Our results indicate that DIM inhibits human cancer cell in vitro proliferation, adhesion, migration and invasion. Western blot analyses show that this inhibition of cell proliferation by DIM is exerted by combined suppression of AKT and ERK pathways. Furthermore, DIM also leads to down-regulation of G1-S cell cycle markers: cyclin D1, cdk6 and cdk4. These findings may lead to development of a novel preventive and/or therapeutic dietary supplement for patients diagnosed with cancer or predisposed to developing certain cancers.