Shinji Kitahama

A case of primary mucoepidermoid carcinoma of the thyroid: molecular evidence of its origin

Primary mucoepidermoid carcinoma (MEC) of the thyroid is very rare, and its origin has not been fully determined. We report a case of MEC, the origin of which was demonstrated by thyroid specific genes expressed in a metastatic lymph node. A 52‐year‐old male presented with chest pain, weight loss and diffuse goitre. Ultrasonography showed the thyroid to be diffusely enlarged with numerous small calcifications. The tumour was found to be infiltrating the thyroid, lung, lymph nodes and first thoratic vertebra. A variant type of papillary thyroid carcinoma was suspected by fine needle aspiration cytology of the thyroid. An open biopsy specimen from an axillary lymph node revealed the tumour to be composed of three distinct cell types: mucin‐producing cells, intermediate cells and a small amount of epidermoid cells with scattered psammoma bodies. Immunohistochemical studies showed the tumour cells to be negative for thyroglobulin and calcitonin, but positive for CEA. To examine the primary origin of the tumour, the expression of thyroid specific genes in the lymph node specimen was examined by RT‐PCR. TTF‐1, TTF‐2, Pax‐8, Na‐I symporter and thyroid peroxidase mRNA were detected. The presence of these thyroid‐specific mRNAs indicates that this MEC originated from thyroid follicular epithelium. This is the first molecular evidence of dedifferentiation from thyroid follicular cells to MEC.

Serum substances that interfere with thyroid hormone assays in patients with chronic renal failure

Serum thyroid hormone concen_trations in patients with chronic renal failure are usually low, despite normal serum TSH levels. We investigated the effect on thyroid hormone assays of serum dialysable organic acids that are elevated in uraemic patients.

Regulation of Calcitonin Receptor by Glucocorticoid in Human Osteoclast-Like Cells Prepared in Vitro Using Receptor Activator of Nuclear Factor-κB Ligand and Macrophage Colony-Stimulating Factor1

Using mouse osteoclast-like cells (OCs), we have shown that treatment with glucocorticoids (GCs) resulted in an increase in calcitonin (CT) binding by enhancing CT receptor (CTR) gene transcription. Additionally, treatment with GCs demonstrated increased sensitivity to CT. There is, however, scant information on the effects of GC or CTR regulation by GCs in human osteoclasts. In this study we examined CTR regulation by GCs and the effects of GCs and CT together in human OCs. OCs were prepared by treatment of peripheral blood mononuclear cells in vitro with soluble receptor activator of nuclear factor-κB ligand and macrophage colony-stimulating factor. Treatment of mature OCs with dexamethasone (Dex) resulted in a dose- and time-dependent increase in [125I]salmon CT (sCT) binding capacity. Treatment with Dex enhanced CTR messenger RNA (mRNA) expression, suggesting that CTR up-regulation is at least partly due to an increase in de novo CTR synthesis. Triamcinolone and prednisolone reproduced the Dex effect ...