Hypothesis: Some controversy exists concerning the appropriate surgical management for patients with thyroid cancer invading the laryngotracheal wall. We have used shaving of the wall when cancer invasion was confined to the perichondrium, and extensive resection when it invaded further. Preoperative assessment of the depth and length of laryngotracheal invasion is important when choosing an appropriate surgical procedure.

Abstract.We reported previously that vitamin D deficiency is a causal mechanism of postoperative tetany in patients with Graves' disease. The aim of the present study was to determine the prevalence of vitamin D deficiency by reviewing serum 25(OH)D levels in 208 patients with Graves' disease (146 women, 62 men) during a 1 year period. Serum 25(OH)D levels were significantly lower (p <0.001) in female Graves' patients (31.8± 13.3 nmol/1) than in male patients (41.3 ± 15.0 nmol/1). Vitamin D deficiency (defined as a serum 25(OH)D value below 25 nmol/l) was found in 40% of female patients and in 18% of male patients (p<0.005).There was a significant seasonal variation in the 25(OH)D concentrations in female patients [amplitude 6.38 (95% CI, 5.42-7.56)], with values below 25 nmol/1 found in 58% of female patients during the winter months. There were significant (p <0.001) differences in serum 25(OH)D levels between age groups in the female patients.The concentrations were lowest in patients in their twenties (25.1 ±8.2 nmol/1) and highest in patients in their fifties and sixties (43.2± 13.7 nmol/1). Serum 25(OH)D concentrations might be monitored in patients with Graves' disease during antithyroid drug therapy, and vitamin D and/or calcium supplements are recommended for patients with vitamin D deficiency.

Expression of genes in the Rb-E2F signaling pathway is controlled by E2F transcriptional factors originally defined as molecules that bind to the promoter of E2 adenovirus. The E2F gene family consists of six members and is designated E2F1-6. The Rb-E2F signaling pathway is among the main regulators of the cell cycle, hence its importance in differentiation and oncogenesis. We document here up-regulation of E2F1, but not other members of the E2F gene family, in 15 of 18 primary papillary thyroid cancers examined (83%) in comparison to corresponding noncancerous thyroid tissues and in all of 11 anaplastic thyroid cancer (ATC) cell lines (100%). The E2F4gene, however, was downregulated in 12 of the papillary thyroid cancers (67%). Immunohistochemical analysis with antibody to E2F1 revealed prominent intracellular E2F1 protein in most of the primary papillary cancers (16 of 18; 89%) but was not detectable in normal thyroid tissues. These data indicated that increased expression of the E2F1 gene might play a significant role in human thyroid carcinogenesis through derangement of the Rb-E2F signaling pathway.

Objective: The aim of this study was hypermethylation of multiple genes for papillary thyroid carcinomas (PTCs). Methods: We examined 39 lesions using methylation-specific PCR to assess hypermethylation in genes, including p16^INK4a, p14^ARF, RB1, p27^Kip1and 0⁶-MGMT. Homozygous deletions of p16^INK4a and p14^ARF were investigated by differential PCR, all with reference to clinicopathological factors. Results: We foundmethylation of p16^INK4a in 35.9% (14/39); p14^ARF in 2.6% (1/39); RB1 in 23.1% (9/39); p27^Kip1 in 15.4% (6/39),and 0⁶-MGMT in 15.4% (6/39). Hypermethylation of at least one of these genes was apparent in 66.7% (26/39). Homozygous deletions of p14^ARF and p16^INK4a were detected in 7.7 (3/39) and 2.6% (1/39), respectively. In cases with p16^INK4a alterations, tumors were significantly increased. A history of chronic thyroid disease and lymphocytic infiltration was significantly associated with p14^ARF alterations, without regional lymph node metastases. Conclusions: Our data suggest that alterations in p16^INK4a, mainly hypermethylation, may be linked to tumor growth but not tumor development, while alterations in p14^ARF may contribute to the induction of chronic inflammation-related PTCs.

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