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Purpose Non-small cell lung carcinoma (NSCLC) comprises 75-85% of all lung cancers, and approximately 25% of all NSCLC patients develop brain metastasis. There are no reliable markers for predicting in which patients this metastasis will occur. DCUN1D1, also known as squamous cell carcinoma-related oncogene, is associated with tumor progression and poor outcomes in NSCLC. The objective of this study was to investigate the role of DCUN1D1 expression in cases of brain metastasis due to NSCLC. Materials and methods Primary tumor samples from a total of 71 cases of NSCLC, either with (n=40) or without (n=31) brain metastasis, were evaluated for DCUN1D1 expression by immunohistochemistry analysis. Results DCUN1D1 expression was detected in 16 patients (23%) and tended to correlate with T classification (15% of T1-2 tumors vs. 30% of T3-4 tumors, p=0.083). DCUN1D1 expression was significantly associated with tumor stage. It was observed in none of the patients with stage I disease, 10% of those with stage II disease, and 29% with stage III disease (p=0.009). In addition, 14 of 16 DCUN1D1-positive patients resulted in brain metastasis (p=0.01). The odds ratio of brain metastasis for patients with DCUN1D1 expression was 3.112 (p=0.009). Conclusion DCUN1D1 expression may play a role in tumor progression and development of brain metastasis in patients with NSCLC. Evaluation of DCUN1D1 expression may provide assistance in identifying those patients who are at higher risk for brain metastasis.

Breast carcinomas are an uncommon neoplastic condition in men, accounting for only 1% of all breast cancers, and less than 1% of all malignancies in men. A 70-year-old man who presented a right breast mass was found to have infiltrating ductal carcinoma. We herein report the case with a review of the literature.

PURPOSE Pregnancy and hCG treatments are considered essential for inhibiting breast cancer. The effect of hCG is accompanied by the synthesis of inhibin, a transforming growth factor involved in cell differentiation and proliferation. Inhibin is considered a tumor suppressor, but its role in the breast is unclear. The aim of this study was to determine the frequency and tissue distribution of the expressions of inhibin-alpha and beta-hCG in breast cancer, and their prognostic relevance with other biological parameters. MATERIALS AND METHODS 334 of formalin-fixed, paraffin embedded tissue blocks were selected, and then immunostained for inhibin-alpha and beta-hCG. The inhibin-alpha expression was compared with those of beta-hCG, ER, PR and HER-2/neu, as well as the tumor characteristics and recurrences. RESULTS Inhibin-alpha and beta-hCG were expressed in 87 (26.0%) and 44 cases (13.2%), respectively. Inhibin-alpha was found in 25.1% of infiltrating ductal carcinomas (67/267), 26.7% of intraductal carcinomas (8/30), 33.3% of lobular tumors (3/9), 80.0% of apocrine carcinomas (4/5) and 21.7% of the other types (5/23). Inhibin-alpha was correlated with beta-hCG (p

Purpose: c-myc, bcl-2 and p53 are known to regulate apoptosis. There has been growing interest in analyzing their contribution to the pathogenesis and prognosis in a variety of human cancers. This study was undertaken to investigate the expression of these proteins in pulmonary adenocarcinomas and to determine their relationship with clinicopathologic parameters and survival. Materials and Methods: Archival tumor tissues from 61 patients with adenocarcinoma of lung were analyzed by immunohistochemistry for the expression of c-myc, bcl-2 and p53 proteins. Clinical information was obtained through the computerized retrospect database from the tumor registry. Results: Of 61 patients, 32 were men and 29 women with the median age 63 years. 4 had stage I disease, 2 had stage II disease and 55 had stage III disease. The expression of c-myc protein was identified in 13% (8/61) tumors, bcl-2 protein was detected in 1.6% tumors (1/61) and p53 was detected in 77% (47/71) tumors. The association of the expression of c-myc, bcl-2 and p53 was not detected. The survival time was longer in patients expressing c-myc protein than in patients without the c-myc protein expression (p=.045). Neither bcl-2 nor p53 showed the correlation to clinicopathologic variables. Conclusion: Our data suggest the involvement of p53 alteration in the pathogenesis of lung adenocarcinoma. The c-myc expression in some tumors indicates that c-myc alone may not contribute critically to the development and/or the progression of these tumors. It, however, correlated to the survival time, suggesting the c-myc expression as a favorable prognostic factor possibly through the apoptosis pathway.