PURPOSE: Cyclins are groups of proteins that play a role as a major regulator of the G1 restriction point promoting inactivation of the retinoblastoma protein. The cyclin D1 gene, CCND1, is amplified in approximately 20% of breast carcinomas and the protein is reportedly overexpressed in 60~80% of all cases. Cyclin D1 overexpression was strongly correlated to estrogen receptor positivity and better histologic grade in breast cancer. The aim of this study was to correlate cyclin D1 overexpression using a well characterized antibody with estrogen receptor status and other clincopathologic parameters. METHODS: From March 1989 to December 1994, 85 patients with primary breast carcinoma were the subject in this study. We analyzed cyclin D1 expression by immnohistochemical staining using cyclin D1 antibody, cells were considered positive according to distinct nuclear staining. The correlation between cyclin D1 expression was compared with important clinicopathologic parameters (tumor size, axillary lymph node status, p53 expression, c-erbB2 expression, histologic grade, estrogen receptor status). RESULTS: Cyclin D1 expression was detected in 37 cases (43.5%). Cyclin D1 expression was high in patients with tumors that expressed estrogen receptor (58.5% vs 26.5%, P=0.019). Cyclin D1 was mainly overexpressed in the histologic grade I and II (75.0%), as compared with 65.2% in cyclin D1 negative tumor, however there was no statistical significance (P=0.067). There were no significant correlation with tumor size, axillary lymph node status, p53 expression, or c-erbB2 expression (P>0.05). CONCLUSION: Cyclin D1 expression in estrogen receptor (ER) positive patients was significantly higher than that seen in ER negative patients. There was a negative correlation between cyclin D1 and tumor histologic grade, however it was not statistically significant. Tumor size, axillary lymph node status, p53 expression, and c-erbB2 expression were not correlated with cyclin D1.
Breast Neoplasms* ; Breast* ; Cyclin D1* ; Cyclins* ; Estrogens* ; G1 Phase Cell Cycle Checkpoints ; Genes, bcl-1 ; Humans ; Lymph Nodes ; Retinoblastoma Protein

PURPOSE: Cyclins are groups of proteins that play a role as a major regulator of the G1 restriction point promoting inactivation of the retinoblastoma protein. The cyclin D1 gene, CCND1, is amplified in approximately 20% of breast carcinomas and the protein is reportedly overexpressed in 60~80% of all cases. Cyclin D1 overexpression was strongly correlated to estrogen receptor positivity and better histologic grade in breast cancer. The aim of this study was to correlate cyclin D1 overexpression using a well characterized antibody with estrogen receptor status and other clincopathologic parameters. METHODS: From March 1989 to December 1994, 85 patients with primary breast carcinoma were the subject in this study. We analyzed cyclin D1 expression by immnohistochemical staining using cyclin D1 antibody, cells were considered positive according to distinct nuclear staining. The correlation between cyclin D1 expression was compared with important clinicopathologic parameters (tumor size, axillary lymph node status, p53 expression, c-erbB2 expression, histologic grade, estrogen receptor status). RESULTS: Cyclin D1 expression was detected in 37 cases (43.5%). Cyclin D1 expression was high in patients with tumors that expressed estrogen receptor (58.5% vs 26.5%, P=0.019). Cyclin D1 was mainly overexpressed in the histologic grade I and II (75.0%), as compared with 65.2% in cyclin D1 negative tumor, however there was no statistical significance (P=0.067). There were no significant correlation with tumor size, axillary lymph node status, p53 expression, or c-erbB2 expression (P>0.05). CONCLUSION: Cyclin D1 expression in estrogen receptor (ER) positive patients was significantly higher than that seen in ER negative patients. There was a negative correlation between cyclin D1 and tumor histologic grade, however it was not statistically significant. Tumor size, axillary lymph node status, p53 expression, and c-erbB2 expression were not correlated with cyclin D1.
Breast Neoplasms* ; Breast* ; Cyclin D1* ; Cyclins* ; Estrogens* ; G1 Phase Cell Cycle Checkpoints ; Genes, bcl-1 ; Humans ; Lymph Nodes ; Retinoblastoma Protein

Klinefelter's syndrome (KS) is a genetic syndrome that presents with hypogonadism and is associated with metabolic syndrome. Patients demonstrating hypogonadism show a greater prevalence of metabolic syndrome due to changes in body composition. We aimed to determine the association between KS and dyslipidemia. The KS group comprised 55 patients who visited the infertility clinic for an infertility evaluation and were confirmed as having a diagnosis of KS. The control group comprised 120 patients who visited the clinic for health screening. Patient characteristics were compared between the two groups with respect to height, weight, body mass index (BMI), testosterone, total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, and triglyceride (TG) levels. Height and weight were significantly greater in patients belonging to the KS group, but no statistically significant difference was found with respect to the BMI. Testosterone levels in patients belonging to the KS group were significantly lower compared to the control group (2.4 ± 2.6 vs. 5.2 ± 1.8 ng/mL, P < 0.001). Compared to the control group, TG levels in patients belonging to the KS group were increased (134.9 ± 127.8 vs. 187.9 ± 192.1 mg/dL, P = 0.004) and HDL cholesterol was significantly decreased (51.2 ± 22.0 vs. 44.0 ± 9.5 mg/dL, P = 0.009). LDL cholesterol and total cholesterol were not significantly different between the two groups (P = 0.076 and P = 0.256, respectively). Significant differences were noted between patients belonging to the KS group and normal control group with respect to elevated TG and decreased HDL cholesterol levels.
Body Composition ; Body Weight ; Cholesterol ; Cholesterol, HDL ; Cholesterol, LDL ; Diagnosis ; Dyslipidemias* ; Humans ; Hypogonadism* ; Infertility ; Klinefelter Syndrome* ; Lipoproteins ; Mass Screening ; Prevalence ; Testosterone ; Triglycerides

Two autopsy cases of asphyxia due to oxygen deficiency are reported. The first case is that a 38-year-old man died in a storehouse. Many pears were stored in a storehouse and the its atmosphere was strictly controlled. The second case is that a 42-year-old man died in the boiler room of a fishing ship. Much amount of Freon gas escaped due to a defect of the refrigerator in the boiler room. The victim entered the boiler room because he repaired the refrigerator. But, the victim died when he entered the boiler room immediately. In this article, the autopsy findings and the contents of the investigation of scene of two cases are described.
Adult ; Anoxia* ; Asphyxia* ; Atmosphere ; Autopsy* ; Chlorofluorocarbons ; Humans ; Oxygen* ; Pyrus ; Ships ; United Nations

No abstract available.
Survival Rate* ; Uterine Cervical Neoplasms*

Epigenetic silencing is considered to be a major mechanism for loss of activity in tumor suppressors. Reversal of epigenetic silencing by using inhibitors of DNA methyltransferase (DNMT) or histone deacetylases (HDACs) such as 5-Aza-CdR and FK228 has shown to enhance cytotoxic activities of several anticancer agents. This study aims to assess the combinatorial effects of gene-silencing reversal agents (5-Aza-CdR and FK228) and oxaliplatin in gastric cancer cells, i.e., Epstein-Barr virus (EBV)-negative SNU-638 and EBV-positive SNU-719 cells. The doublet combinatorial treatment of 5-Aza-CdR and FK228 exhibited synergistic effects in both cell lines, and this was further corroborated by Zta expression induction in SNU-719 cells. Three drug combinations as 5-Aza-CdR/FK228 followed by oxaliplatin, however, resulted in antagonistic effects in both cell lines. Simultaneous treatment with FK228 and oxaliplatin induced synergistic and additive effects in SNU-638 and SNU-719 cells, respectively. Three drug combinations as 5-Aza-CdR prior to FK228/oxaliplatin, however, again resulted in antagonistic effects in both cell lines. This work demonstrated that efficacy of doublet synergistic combination using DNMT or HDACs inhibitors can be compromised by adding the third drug in pre- or post-treatment approach in gastric cancer cells. This implies that the development of clinical trial protocols for triplet combinations using gene-silencing reversal agents should be carefully evaluated in light of their potential antagonistic effects.
Antineoplastic Agents ; Cell Line ; DNA ; Drug Combinations ; Epigenomics* ; Herpesvirus 4, Human ; Histone Deacetylases ; Humans* ; Stomach Neoplasms* ; Triplets

PURPOSE: Studies on the incidence and mortality of refractures after primary osteoporotic fracture are limited by the relatively rare incidence of such refractures and small sample sizes. The objectives of this research were: 1) to determine the incidence of osteoporotic refractures and fracture locations and 2) to assess mortality rates associated with osteoporotic refracture over a median follow up of 3 years using nationwide claim database. MATERIALS AND METHODS: Patients over 50 years of age who had an osteoporotic fracture that was confirmed operationally were enrolled. Refracture was defined as that after 6 months of an untreated period. Mortality rate was calculated using the Charlson comorbidity index and was analyzed using Cox proportional hazards regression analysis. RESULTS: A total of 18956 first-time instances of osteoporotic fracture were reported between 2007 and 2012 after a median follow up of 3.1 years (range, 1 to 7 years). Among 18956 patients, 2941 (15.50%) experienced refracture. After follow up for 1 year, cumulative mortality rates for re-fracture and non-refracture groups were 9.1% and 7.2%, respectively. After adjusting for covriates, mortality rate was 1.2 times greater in patients with re-fracture than in patients without re-fracture over a median follow up of 3 years (hazard ratio: 1.20, 95% confidence interval: 1.08–1.34, p<0.001). CONCLUSION: The incidence of osteoporotic re-fracture in this nationwide study was 15.5%, and the mortality rate of re-fracture patients was 1.2 times higher than that of non-refracture patients over a median follow up of 3 years.
Comorbidity ; Follow-Up Studies ; Humans ; Incidence ; Korea ; Mortality ; Osteoporotic Fractures ; Sample Size

BACKGROUND: In recent years, numerous human tumor specific antigens such as melanoma antigen gene(MAGE) that is recognized by autologous cytotoxic T lymphocytes have been identified. MAGE is expressed in many human malignancies in various organs, such as lung, breast, stomach, esophagus and leukemia. Therefore MAGE has been studied widely for tumor diagnosis and immunotherapy. But, so far there were no clinical studies evaluating the role of MAGE in pleural effusion. We investigated the expression of MAGE in the patients with exudative pleural effusion for it's diagnostic utility and the RESULTS: were compared with those of cytologic examinations. METHODS: Diagnostic thoracentesis was performed in 44 consecutive patients with exudative pleural effusion during 6 months. We examined the expression of MAGE and cytology with the obtained pleural effusion. Expression of MAGE was interpreted by means of a commercial kit using RT-PCR method. Enrolled patients were divided into two groups such as malignant and benign and we analyzed its' sensitivity and specificity. RESULTS: There were no significant differences between two groups in age, sex, white blood cell counts in pleural fluid, pleural fluid/serum protein ratio and pleural fluid/serum LDH ratio. The sensitivity and specificity of MAGE were 72.2% and 96.2% respectively and the positive predictive value and negative predictive value of MAGE were also 92.9% and 83.3% respectively. The sensitivity and negative predictive value of cytologic examinations were 66.7% and 81.3% respectively. There were no significant differences between sensitivities of MAGE and cytologic examinations but false positive result of MAGE was found in 1 case of tuberculous pleurisy. CONCLUSION: MAGE is a sensitive and specific marker for the differential diagnosis between benign and malignant effusion in patients with exudative pleural effusion. And MAGE would provide the equal sensitivity compared with that of cytologic examination in patients with malignant pleural effusion if 5mL of the pleural fluid is examined.
Breast ; Diagnosis ; Diagnosis, Differential ; Esophagus ; Humans ; Immunotherapy ; Leukemia ; Leukocyte Count ; Lung ; Melanoma ; Pleural Effusion* ; Pleural Effusion, Malignant ; Sensitivity and Specificity ; Stomach ; T-Lymphocytes, Cytotoxic ; Tuberculosis, Pleural

PURPOSE: To evaluate the therapeutic activity and safety of paclitaxel and cisplatin combination chemotherapy in patients with advanced or metastatic gastric cancers that are unresponsive to primary chemotherapy. MATERIALS AND METHODS: Advanced or metastatic gastric cancer patients unresponsive to first line chemotherapy were entered into this trial. The treatment regimen consisted of paclitaxel, 175 mg/m(2) by 3-hour infusion on day 1, and cisplatin, 60 mg/m(2) by 1 hour infusion on day 1, with the treatment repeated every 3 weeks. RESULTS: 37 patients were entered in this study, with 32 fully evaluable for response. 4 (13%), 13 (40%) and 15 (47%) patients achieved a partial response, stable disease and progressed, respectively. The median time to progression was 4.0 months (95% CI: 2.0~6.0 months), and the median overall survival was 12.6 months (95% CI: 5.5~19.7 months), with a 1-year survival rate of 54%. Of a total of 135 cycles of chemotherapy, grades 3 and 4 hematological toxicities were neutropenia (14%) and anemia (3%). Grade > or =2 neuropathy was observed in 6 patients (17%). CONCLUSION: The combination of paclitaxel and cisplatin is an effective and tolerable salvage treatment modality for advanced gastric cancer.
Anemia ; Cisplatin* ; Drug Therapy ; Drug Therapy, Combination ; Humans ; Neutropenia ; Paclitaxel* ; Salvage Therapy* ; Stomach Neoplasms* ; Survival Rate

Imatinib mesylate is a selective Bcr/Abl kinase inhibitor and an effective anticancer agent for Bcr/Abl-positive chronic myelogenous leukemia. Most patients in chronic phase maintain durable responses; however, many in blast crisis fail to respond, or relapse quickly. Mutations within the BCR/ABL kinase domain are the most commonly identified mechanism associated with relapse. To overcome the imatinib resistance in CML, many investigators have tried to clarify molecular mechanism for imatinib resistance in cells of patients who failed to respond to imatinib. Our aim was to invesitigate underlying mechanism for imatinib resistance in SR-1 cells, which were derived from a CML patient in blast crisis. We detected the new mutation of BCR/ABL, resulting in premature termination and loss of BCR/ABL fusion protein expression, which might be possible mechanism for the resistance to imatinib in SR-1 cells.
Amino Acid Sequence ; Base Sequence ; Cell Line, Tumor ; Drug Resistance, Neoplasm/*genetics ; Fusion Proteins, bcr-abl/chemistry/*genetics ; Humans ; Leukemia, Myeloid/*genetics ; Molecular Sequence Data ; Mutagenesis, Insertional/*genetics ; Nucleotides/genetics ; Piperazines/*pharmacology ; Point Mutation/*genetics ; Pyrimidines/*pharmacology ; Research Support, Non-U.S. Gov't