Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.25.1 (proteasome)
 28,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tuberculosis of the thyroid gland is extremely uncommon. The infection may present first in the thyroid gland or appear secondary to a tuberculous process elsewhere in the body. The diagnosis is rarely made clinically because the different presentations of the disease often mimick malignancy or euthyroid nodular goitre. It is of interest to report a case of tuberculosis of the thyroid associated with papillary microcarcinoma of the gland. No tuberculous process elsewhere in the body has been found. The frequency of MCP on thyroidectomy specimens suggest that this association is incidental.
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PMID:[Thyroid tuberculosis associated with papillary microcarcinoma of the thyroid gland: a case report]. 1179 65

The specific pathogenesis of nodular goiter and the role of apoptosis in goitrogenesis are not known. We sought to examine the regulation of the TNF-related apoptosis-inducing ligand (TRAIL) and Fas ligand (FasL)-induced apoptosis pathways in primary thyroid cells from 17 patients with nodular goiter, using 10 normal thyroids as controls. Both goitrous and normal thyroid cells were resistant to recombinant human TRAIL and an agonist anti-Fas antibody under basal conditions. However, all normal thyrocytes could be sensitized by TNFalpha/IL-1beta or interferon gamma/IL-1beta to undergo apoptosis in response to TRAIL or FasL, respectively. In contrast, the majority of goiter-derived cells remained resistant to TRAIL (12 of 17 samples) or FasL (9 of 17 samples) after cytokine pretreatment; 14 of 17 goiter nodules were resistant to at least one death ligand. Goiter size was inversely correlated with the sensitivity to TRAIL-mediated apoptosis. The resistance of goiter cells to TRAIL did not appear to be due to transcriptional regulation or cell surface expression of death and decoy receptors. However, increased proteasome activity was found in a subset of goiter cells resistant to both death ligands, and proteasome inhibitors could sensitize these goiter cells to TRAIL-mediated apoptosis. In conclusion, goiter-derived thyroid cells are resistant to TRAIL and/or Fas-induced apoptosis in vitro, and this may represent a new aspect of aberrant growth regulation in goiter nodules. The increased proteasome activity associated with this resistance suggests that the proteasome may be an important regulator of apoptosis in nodular goiter.
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PMID:Aberrant apoptosis in thyroid epithelial cells from goiter nodules. 1221 83