No abstract available.
Biomarkers* ; Child* ; Hepatitis B* ; Hepatitis* ; Humans ; Prevalence*

No abstract available.
Hepatitis B virus* ; Hepatitis B* ; Hepatitis*

No abstract available.
Hepatitis B virus* ; Hepatitis B* ; Hepatitis*

Cancer is considered to occur through abnormal growth and differentiation processes, in which oncogenes and tumor suppressor genes are deeply related. Cellular responses to DNA-damaging agents are believed to be critical determinants of human tumorigenesis. Cell cycle arrests and DNA repair following DNA damage require the coordination of multiple gene products that, as a whole, serve to maintain the integrity of the genome. Within the cell cycle, both G1-S and G2-M phase transitions are under constant surveillance by checkpoint genes for the protection of cells from either exogenous or endogenous DNA-damaging agents. p53 tumor suppressor gene mediates cell cycle perturbations in response to DNA damage, and play a role in cell death, genetic stability, and cancer susceptibility. Recently, gene therapy with p53 tumor suppressor gene is expected as a new effective therapeutic strategy in many kinds of cancer. By using retroviral vector system, we transduced p53 tumor suppressor gene into human osteosarcoma cells, and analysed its growth suppression and apoptosis inducing effects. Combined effects of p53 gene therapy with chemotherapeutic agent or radiation were also analysed. Titer of ecotrophic p53 retrovirus was 5.0x10/ml, and that of amphotrophic p53 retrovirus was 2.0x10/ml when NIH3T3 cells were used as target cells. Human osteosarcoma cells infected with amphotrophic p53 retroviruses showed increased p21waf1 gene expression, which acts as a major cyclin-dependent kinase inhibitor in DNA damage responses. In normal DMEM media, human skin fibroblasts infected with amphotrophic p53wt retroviruses showed very slow growing (1.7 fold increase in doubling time) and very low saturation density (50% decrease in cell density). In media containing chemotherapeutic agent, human osteosarcoma cells infected with p53wt retroviruses died rapidly; 75% of them died within 4 days and all of them died within 10 days of incubation with chemotherapeutic agent. Their DNAs were extracted and electrophoresed in agarose gel, and we identified DNA ladders characteristic of apoptotic cell death. When human osteosarcoma cells infected with p53 retroviruses were irradiated with ultraviolet light, more than 95% of cancer cells died within 1 day; whereas mock infected cells showed only less than 5% of cell death. These findings suggest that retroviral vector mediated p53 tumor suppressor gene transfer into cancer cells can suppress tumor cell growth and decrease tumor cell density effectively. These findings also suggest that effective induction of tumor cell apoptosis can be obtained when p53 gene therapy is used in combination with chemotherapy or radiotherapy.
Apoptosis ; Carcinogenesis ; Cell Count ; Cell Cycle ; Cell Cycle Checkpoints ; Cell Death ; DNA ; DNA Damage ; DNA Repair ; Drug Therapy ; Fibroblasts ; Gene Expression ; Genes, p53 ; Genes, Tumor Suppressor* ; Genetic Therapy* ; Genome ; Humans ; Oncogenes ; Osteosarcoma ; Phase Transition ; Phosphotransferases ; Radiotherapy ; Retroviridae* ; Sepharose ; Skin ; Ultraviolet Rays ; Zidovudine

OBJECTIVE: The purpose of this study was to identify the clinicopathologic characteristics, treatments and overall 5-year survival and to analyze the prognostic factors affecting the survival in patient with ovarian tumors. METHODS: We reviewed retrospectively the outcome of 116 patients with ovarian cancer and 64 patients with borderline malignant ovarian tumor, who had been treated at Department of Obstetrics and Gynecology, Korea University Anam Hospital from Jan. 1991 to Dec. 2001. Univariate and multivariate analysis for survival were conducted to test the prognostic significance of several clinicopathologic factors. RESULTS: The mean age of the patients with borderline malignant ovarian tumor was 39.9 years old, and nulliparity was most common (42.2%). Mucinous tumor was the most common histologic subtype (68.8%). The FIGO stage distribution of borderline malignancy were 89.1%, 1.6%, 9.3% for stage I, II, and III, respectively. The overall 5-year survival rate of patients with borderline malignancy was 98.4%. The mean age of the patients with ovarian cancer was 50.1 years old. The incidence of ovarian cancer according to histologic type were 74.1%, 12.9%, 11.2%, 0.9%, 0.9%, in epithelial ovarian cancer, Sex-cord stromal tumor, malignant germ cell tumor, metastatic carcinoma of the ovary, and small cell carcinoma, respectively. The FIGO stage distribution of ovarian cancer were 40.5%, 12.1%, 42.2%, 5.2% for stage I, II, III, and IV, respectively. The overall 5-year survival rate of patients with ovarian cancer was 60.9%. In multivariate analysis, FIGO stage was identified as a significant independent prognostic factor in this study. CONCLUSION: In this study, patients with borderline malignancy of the ovary have good prognosis and the overall 5-year survival rate was 98.4%. Otherwise, the overall survival rate of patients with ovarian cancer was 60.9% and the stage was most important prognostic factor.
Carcinoma, Small Cell ; Female ; Gynecology ; Humans ; Incidence ; Korea ; Mucins ; Multivariate Analysis ; Neoplasms, Germ Cell and Embryonal ; Obstetrics ; Ovarian Neoplasms ; Ovary ; Parity ; Prognosis ; Retrospective Studies ; Survival Analysis* ; Survival Rate

No abstract available.
Cachexia* ; Ductus Arteriosus, Patent* ; Heart Failure* ; Heart* ; Humans ; Infant*

We report a case of atypical eruption due to chemotherapeutic agent in a 60-year-old man who presented with asymptomatic, erythematous, 0.5cm in diameter, confluent, and elevated papules and plaques confined to the face. The patient was previously diagnosed with small cell carcinoma of the lung with liver metastasis. Two months after the diagnosis, a first course of chemotherapy including etoposide was started. Five days after starting the chemotherapy, the patient developed a facial eruption. Histopathologic examination demonstrated increased epidermal mitotic figures, cells in metaphase arrest, basal cell layer hyperpigmentation, prominent dyskeratosis, and squamous atypia. The most distinctive histologic feature was the presence of starburst cells, which are markedly enlarged pale staining keratinocytes containing small basophilic fragments of nuclear debris haphazardly scattered throughout the cytoplasm in a starburst pattern.
Basophils ; Carcinoma, Small Cell ; Cytoplasm ; Diagnosis ; Drug Therapy ; Etoposide ; Humans ; Hyperpigmentation ; Keratinocytes ; Liver ; Lung ; Metaphase ; Middle Aged ; Neoplasm Metastasis

PURPOSE: To characterize strain-specific differences in radiation response in murine tissues with different radiosensitivity. MATERIALS AND METHODS: Six-week old male mice of 2 strains, C57Bl/6J and C3H/HeJ, were given whole body gamma-radiation with a single dose of 10 or 25 Gy. At different times after irradiation, mice were killed and tissues with different radiosensitivity, thymus and liver, were collected. Each tissue sample was stained with hematoxylin and eosin and apoptotic cells were scored. Expression of p53, Bcl-2, Bcl-x, and Bax was analysed by western blotting and densitometry. RESULTS: Radiation induced massive apoptosis in thymus with a peak level at 8 h after radiation. With 10 Gy irradiation, apoptotic indices in C57Bl/6J and C3H/HeJ were 81.0 2.5% and 59.4 4.0%, respectively (p<0.05). Radiation upregulated the expression of p53, Bcl-x, and Bax, but not Bcl-2; p53 with a peak level of 2.5 fold (C57Bl/6J) and 1.4 fold (C3H/HeJ) at 4 h, Bax with a peak level of 2.6 fold (C57Bl/6J) and 1.3 fold (C3H/HeJ) at 8 h, and Bcl-x with a peak level of 11.1 fold (C57Bl/6J) and 8.2 fold (C3H/HeJ) at 8 h after radiation. In liver, however, radiation-induced apoptosis was minimal (peak apoptotic index of 2.1% in C57Bl/6J and 1.7% in C3H/HeJ). None of p53, Bcl-2, Bcl-x, and Bax was significantly increased. CONCLUSIONS: Induction of apoptosis and regulation of related genes by radiation were tissue specific. Strain difference of radiation-induced apoptosis was well coupled with theinduction of related genes in thymus, a radiosensitive tissue. This study shows that quantitative difference of radiation induced apoptosis by strain is regulated at the gene level with the involvement of multiple genes.
Animals ; Apoptosis* ; Blotting, Western ; Densitometry ; Eosine Yellowish-(YS) ; Hematoxylin ; Humans ; Liver ; Male ; Mice ; Radiation Tolerance ; Thymus Gland

Hyperkeratosis of the nipple and areola is a rare condition. We report a case of hyperkeratosis of the nipple and areola occurrinp in man with no underlying endocrirop thy or synthetic estrogenic drug therapy. The patient was not associated with epidermal nevus orichthyosis and so fitted into the nevoid form of hyperkeratosis of the nipple and areola. The clinical appearance and histological findings of the lesion were the same as those reported before. He showed a slight improvement in the color and hyperkeratcsis of the nipple and areola with 6 months use of a topical keratolytic agent and corticosteroid crearn.
Drug Therapy ; Estrogens ; Humans ; Nevus ; Nipples*

PURPOSE: We analyzed the gene status of p16INK4A, p15INK4B and MTAP (methylthio adenosine phophorylase) in Korean hepatdegrees Cellular carcinoma (HCC) to investigate whether the inactivation of these genes participated in hepatdegrees Carcinogenesis, and evaluated MTAP-targeted chemotherapy in MTAP-deficient cell lines. MATERIAL AND METHODS: We examined eleven primary HCC and 8 SNU cell lines using PCR, Southern blot analysis, PCR-SSCP, DNA sequencing, methylation-specific PCR, Western blot analysis, MTT assay, and crystal violet staining. RESULTS: Mutations or deletion of the p16INK4A, 15INK4B, and MTAP genes were rare, but methylation of the p16INK4A promoter region was common in HCC. The base alterations of 3' untranslated region of p16INK4A exon 3 were also detected in 3 samples. In SNU cells, p16INK4A was not detectable, when treated with demethylating agent, high levels of re-expressed p16INK4A protein were detected. In MTAP-targeted chemotherapy experiment, methylthioadeno sine (MTA) was able to rescue MTAP positive cell lines but not MTAP negative cell lines from growth inhibition by depletion of methionine and MTX treatment. CONCLUSION: These results suggest that de novo methylation of the p16INK4A promoter region seems to play an important role in the pathogenesis of HCC. And treatment of MTX, combined with methionine depletion in the presence of MTA, may be a high selective treatment for MTAP negative HCC.
3' Untranslated Regions ; Adenosine ; Blotting, Southern ; Blotting, Western ; Carcinogenesis ; Cell Line ; Cyclin-Dependent Kinase Inhibitor p16 ; Drug Therapy ; Exons ; Gentian Violet ; Methionine ; Methylation ; Polymerase Chain Reaction ; Promoter Regions, Genetic ; Sequence Analysis, DNA ; Pemetrexed