[Islet cell antibodies].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Tetsuro Kobayashi.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The histogenesis of sarcomatoid transformation in hepatocellular carcinomas (HCCs) and cholangiocellular carcinomas (CCCs) remains unclear. In the current case, microsatellite loss of heterozygosity (LOH) assay and mutational analysis of the p53 gene with immunohistochemical examination were performed to investigate the histogenesis of each component. The tumor was composed of two parts: one part comprised poorly differentiated HCC (HCC portion), while the other part included undifferentiated, sarcomatoid HCC and CCC (combined portion). LOH at D8S555 was detected in both portions. 1-bp cytosine was deleted at codon 241 of exon 7 of the p53 gene in the combined portion. Immunohistochemically, p53 accumulated in the nuclei of undifferentiated, sarcomatoid HCC and CCC cells, suggesting that the p53 gene mutation might be common in these components. These results support the hypothesis that undifferentiated, sarcomatoid HCC and CCC could be offspring from the original HCC.
PURPOSE: We evaluated the accuracy of magnetic resonance imaging (MRI) in predicting esophageal invasion by thyroid carcinomas and established an optimal criterion for diagnosing esophageal invasion. METHOD: The MRI findings (size and margins of tumor, ratio of tumor contact to the esophagus, shape and displacement of the esophagus, and tumor invasion to the outer and inner layers of the esophagus) in 67 patients with thyroid carcinomas were retrospectively reviewed and correlated with surgical and pathologic findings. Logistic modeling was used to determine the significant factors for predicting esophageal invasion. RESULTS: Seventeen (34%) of the 67 patients had pathologically or surgically verified esophageal invasion. The logistic modeling revealed that outer layer invasion (P < 0.001) and poorly defined margins (P = 0.001) were the significant factors. The outer layer invasion showed the highest accuracy of 91%, with 82% sensitivity and 94% specificity. The addition of poorly defined margins to this criterion did not improve its accuracy. CONCLUSION: Esophageal invasion by thyroid carcinoma was accurately predicted with MRI, and an MRI finding of outer layer invasion was optimal for diagnosing esophageal invasion.
The aim of this study was to clarify the genetic alterations in anaplastic transformation of the thyroid cancer. A total of 17 thyroid cancers including 7 anaplastic and 10 papillary cancers were analyzed for loss of heterozygosity (LOH) on chromosome 16p and 18q. All the samples from anaplastic cancer showed LOH at one or more loci out of ten markers on 16p, and only two showed one LOH at two loci out of five markers on 18q. No LOH was found on either 16p or 18q in papillary cancers. D16S423, D16S418 and D16s406 on 16p13.3 were the most frequently deleted loci in anaplastic cancers, and the region around these may harbor the putative tumor suppressor gene related to anaplastic transformation of thyroid cancer.