Background and aims:Precise pathological diagnosis is essential for optimal treatment of thyroid tumors. Ancillary diagnostic markers may be helpful in some cases. The purpose of this study was to compare and evaluate the diagnostic value of CD56, cytokeratin 19 (CK19), and galectin-3 immunohistochemical stainings in distinguishing between papillary carcinoma (PC) and other thyroid malignancies and benign lesions. Methods: The expressions of the three markers were evaluated in PC (n = 67), follicular carcinoma (FC, n = 23), medullary carcinoma (MC, n = 18), anaplastic carcinoma (AC, n = 4), follicular adenoma (FA, n = 15), and nodular hyperplasia (NH, n = 21). Results: Statistical analysis showed significantly different expressions of CD56, galectin-3, and CK19 in PC versus other lesions of the thyroid gland, with the exception of AC. Especially, the sensitivity and specificity of CD56 for diagnosing PC were 92.5% and 86.4%, respectively. The diagnostic specificity of CD56 was higher than that of galectin-3 or CK19 in differentiating PC from other lesions of the thyroid gland. However, its sensitivity was lower than that of galectin-3 or CK19. Conclusion: CD56 turns out to be a good negative marker for diagnosing PC. We suggest that immunohistochemical panels directed at the diagnosis of PC should include CD56 together with galectin-3 and CK19.

A 24-year-old man was admitted due to an incidentally detected mass in his left testis, which showed radiopaque calcification on plain X-ray film. Left orchiectomy was performed, and the resected testis contained a well-demarcated, hard mass measuring 1.1 cm. Histological analysis revealed that the tumor was composed of neoplastic cells, fibrotic stroma, and laminated or irregularly shaped calcific bodies. The individual cells had abundant eosinophilic or clear cytoplasm with round nuclei, each of which contained one or two conspicuous nucleoli. They were arranged in cords, trabeculae, clusters, and diffuse sheets. There were several foci of intra-tubular growth patterns, with thickening of the basal lamina. Immunohistochemically, the neoplastic cells were positive for S-100 protein and vimentin, focally positive for inhibin alpha, and negative for cytokeratin, CD10, and Melan-A. In addition to reporting this rare case, we also review the relevant literature regarding large cell calcifying Sertoli cell tumors.

Background :The epithelial mesenchymal transition (EMT) is intimately associated with tumor hypoxia. The present study was conducted to investigate the immunohistochemical relationship between hypoxic and EMT-related molecules in non-small cell lung carcinoma (NSCLC). Methods : Immunohistochemical staining for hypoxia inducible factor (HIF)-1a, carbonic anhydrase (CA) IX, TWIST, and E-cadherin proteins was performed in 146 cases of NSCLC (80 cases of adenocarcinoma and 66 cases of squamous cell carcinoma) using tissue microarray blocks. Results : HIF-1a, TWIST, CA IX, and E-cadherin were expressed in 58 (40%), 90 (62%), 82 (56%), and 36 (25%) of 146 NSCLC cases, respectively. TWIST expression was positively correlated with HIF-1a expression (p = 0.03) and inversely correlated with E-cadherin expression (p < 0.01). TWIST and CA IX expression were not significantly interrelated, but each showed a relationship with histological tumor grade. However, the expression of these molecules had no significant effect on clinical staging or patient survival. Conclusions : Although TWIST expression was correlated positively with HIF-1a expression and inversely correlated with E-cadherin, HIF-1a expression was not associated with E-cadherin expression. However, considering the relationship between HIF-1a and TWIST expression, further studies should be performed to demonstrate the role of hypoxia-induced EMT in NSCLC.

Myoepitheliomas are well-established to occur in the salivary glands, but they have also been described in the breast, upper aerodigestive tract, skin, and soft tissues. We report here on a unique case of primary myoepithelioma that occurred in the right testis of a 28-year-old man. The tumor was entirely confined to the testis and it was clearly separated from the epididymis. Histopathology revealed mixed architectural patterns in which the reticular areas merged into the chondromyxoid stroma. The tumor cells, which were focally immunoreactive to pancytokeratin and S-100 protein, were round to ovoid and spindly arranged in cords, strands, and fascicles. They showed mild nuclear pleomorphism, sparse mitotic figures and a low Ki-67 proliferative index. There was no ductal differentiation in the tumor. To the best of our knowledge, there has been only one case report of a primary testicular myoepithelioma in the English medical literature.

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Background and aims:Atherosclerosis is a systemic disorder that develops in any blood vessel of the body. Atherosclerosis can result in fatal complications such as myocardial infarction or stroke. The aim of this study was to compare the severity of atherosclerosis between the coronary arteries and other peripheral arteries. To our knowledge, no such morphometric tissue studies through autopsy samples so far are available in Korea. Methods: The left anterior descending artery, right coronary artery and bilateral carotid, renal and femoral arteries were obtained from 50 autopsies during the period from June to October 2008. Detailed gross examination of the each arteries was performed to look for the most severe site of luminal narrowing. Results: There was a significant correlation between the maximal carotid artery intima-media thickness and the largest plaque area of the coronary artery (P < 0.05). However, some discordant cases were also noted. Seven cases had more severe coronary atherosclerosis compared to the carotid artery. Conclusions:The careful examination of peripheral arteries including the carotid artery can be helpful in clinical prediction of coronary artery disease. However, such prediction should include other risk factors such as age, hypertension, diabetes and dyslipidemia and other relevant clinical conditions.

Abstract. DNA hypermethylation is common and plays a critical role in the regulation of gene expression. It is considered a major cause of carcinogenesis. High-throughput profiling method has been developed to analyze the methylation status of hundreds of pre-selected genes simultaneously. The aim of this study was to analyze promoter hypermethylation profiles of each subtype of ovarian epithelial cancer (OEC), to improve the understanding of the role of epigenetic silencing in carcinogenesis. DNA hypermethylation profiles on fresh frozen tissue samples of 5 serous, 3 mucinous, 5 endometrioid and 4 clear cell types of OEC, as well as 5 normal ovarian tissue samples as control. We used a highthroughput method for analyzing the hypermethylation status of 1,505 CpG loci selected from 871 genes simultaneously by GoldenGate Methylation Cancer Panel I (Illumina Human-6 v2 Expression BeadChip). Methylation status of seven genes was verified by methylation specific PCR (MSP). We identified 20, 37, 15 and 56 hypermethylated CpG locations in serous, mucinous, endometrioid and clear cell type OEC compared to control. Only 6 CpG loci were commonly hypermethylated across all subtypes of OEC. Hypermethylated loci of serous 17 (81.0%) and endometrioid type 10 (71.4%) were identical to that of clear cell type. However, mucinous type showed 17 peculiar loci (43.6%) out of 39 hypermethylated loci. The unique DNA hypermethylation patterns identified in different OEC subtypes suggest that their cause may involve different epigenetic mechanisms and the Bead chip used in this study is a useful tool to analyze DNA hypermethylation. IntroductionOvarian cancer is the fourth leading cause of cancer death in women (1). Patients (70%) have advanced disease (stage III or IV) upon presentation, with a 5-year survival between 15 and 20% at best with aggressive treatment. Ovarian epithelial cancer (OEC) accounts for over 90% of all cases and includes the following major histological subtypes: serous, mucinous, endometrioid and clear cell carcinomas. Cytogenetic and molecular analyses indicated that multiple genetic alterations were involved in the pathogenesis of ovarian cancer. BRCA1 and BRCA2 mutations are associated with increased ovarian cancer risks (2). Some studies have showed that p16 loss was associated with ovarian cancer prognosis (3). However, it remains unclear how genetic alterations lead to development and subsequent progression of ovarian cancer. Better understanding of the molecular mechanisms responsible for ovarian cancer development and progression will improve diagnosis and treatment of this disease.DNA methylation is an epigenetic alteration that plays an important role in carcinogenesis (4). The importance of aberrant CpG island methylation as an alternative mechanism to inactivate tumor suppressor genes has been recognized recently. Addition of a methyl group to the cytosine residues of CpG dinucleotide clusters in the 5' regulatory regions of genes occurs frequently in cancer cells, but seldom in nonmalignant cells. Ab...