No abstract available.
Child* ; Ductus Arteriosus, Patent* ; Humans

Epstein-Barr virus (EBV) has been linked to a spectrum of neoplastic conditions, including Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's disease, lymphoepithelioma-like carcinomas and malignant lymphomas in immunocompromised state. To determine the prevalence and the subtype of EBV in gatrointestinal malignancies, fifty cases of adenocarcinomas and seventeen cases of malignant lymphomas were analyzed by EBERs in situ hybridization and polymerase chain reaction using primers for EBNA-1, EBNA-2A and EBNA-2B, on the paraffin sections. In addition, immunohistochemical stain for p53 protein was performed to investigate the potential role of EBV infection on tumor suppressor gene, p53, during tumorigenesis. EBER was detected in 6 of 26 gastric adenocarcinomas, 2 of 24 colon adenocarcinomas, and 8 of 17 malignant lymphomas. EBER was more prevalent in malignant lymphoma arising in the intestine (6/6) than in the stomach (2/11), and was detected in both B and T cell phenotypes. EBNA-1 was positive in 11 of 16 EBER positive cases and the subtyping was possible in 8; both type 1 and 2 were detected in gastric cancers, whereas only type 2 was found in intestinal neoplasms. In adenocarcinomas the high rate of p53 protein overexpression was found in both EBER positive (8/8) and negative cases (32/42), whereas the positive rate was higher in EBER positive cases (7/8) than in EBER negative cases (4/9) of malignant lymphomas. From the results, it can be concluded that EBV infection and the p53 tumor suppressor gene are independently associated in a significant portion of the gastrointestinal malignancies, but the mechanism of action remains to be elucidated.
Adenocarcinoma* ; Burkitt Lymphoma ; Carcinogenesis ; Colon ; Epstein-Barr Virus Infections ; Gastrointestinal Tract ; Genes, Tumor Suppressor ; Herpesvirus 4, Human* ; Hodgkin Disease ; In Situ Hybridization ; Intestinal Neoplasms ; Intestines ; Lymphoma* ; Paraffin ; Phenotype ; Polymerase Chain Reaction ; Prevalence ; Stomach ; Stomach Neoplasms

OBJECTIVE: Although ovarian cancer is the leading cause of death among all cancers of the female reproductive tract, the genetic alterations involved in ovarian cancer remains largely unknown. Recently, mutations of the p53 gene have been documented in many types of human cancer including ovarian cancer. METHODS: In tbe present study, p53 gene mutation was examined in DNA samples extracted from paraffin embedded surgical specimens of ovarian cancer. Furthermore, clinicopathological parameters were examined in relation to p53 gene mutation in order to understand the role of p53 mutation in the development of ovarian cancer. Using the polymerase chain reaction(PCR) and single strand conformational polymarphism(PCR-SSCP), p53 gene mutation was examined and the mutations were confirmed by DNA scquencing in 17 cases of ovarian cancer. RESULTS: Abnormal bands indicating mutation were detected in 2/17(11.8%). DNA sequencing confirmed in 2 mutations and revealed C to T and A to T nucleotide chmges. In clinicopathological parameters, FIGO stage, grade, and recunence were not correlated with the p53 gene mutation. However, the recurrence rate was higher in patients with mutant p53 compared with those with wild type p53(50.0% vs 13.3%), altbough this is not statisticaUy significant. CONCLUSION: In conclusion, p53 gene mutation shows no correlation with stage, grade and recurrence, and p53 gene mutation does not appear to be a marker that predicts the biological behavior or the outmme of the disease. This study suggested useful data to elucidate the mechanism of chemotherapy-resistant ovarian cancer and further p53 expression assay would be mandatory for p53 nonfunctioning ovarian cancas.
Cause of Death ; DNA ; Female ; Genes, p53* ; Humans ; Ovarian Neoplasms* ; Paraffin ; Recurrence ; Sequence Analysis, DNA

No abstract available.
Drug Eruptions* ; Imatinib Mesylate*

No abstract available.
Hemangiosarcoma* ; Neoplasm Metastasis*

No abstract available.
Leukemia*

No abstract available.
Adenoma, Pleomorphic* ; Lip*

No abstract available.
Hand ; Hyperplasia

No abstract available.
Adult ; Hidradenitis ; Humans

A fluorescence bronchoscope system has been developed for detecting early lung cancer including dysplasia and carcinoma in situ. To determine the histologic findings and genetic alterations of the lung tissues, which were biopsied by the fluorescence bronchoscope, we analyzed 104 specimens from 62 heavy smokers for their histopathology, cell proliferation index, and genetic mutations of p53 and K-ras. We used immunohistochemistry for MIB-1 and p53, and PCR-SSCP and direct DNA sequencing for p53 and K-ras. The histology was variable from reactive conditions to invasive cancers, and consisted of basal cell hyperplasia (26.9%), dysplasia (4.8%), carcinoma in situ (1.9%), squamous cell carcinoma (7.7%), adenocarcinoma (4.8%), and small cell carcinoma (10.6%). The cellular proliferation index of the lesions increased as their aggressiveness increased. p53 and K-ras mutations were detected in 33.7% and 14.4% of all tissues, respectively. In dysplasia, p53 and K-ras mutations were observed in 3 of 5 and in 2 of 5 tissues, respectively. However, these genetic alterations were not found in carcinoma in situ. Interestingly, 28.6% of basal cell hyperplasia showed p53 mutations. In conclusion, these data suggest that the biopsy specimens using fluorescence bronchoscopy show variable histologic findings, ranging from reactive conditions to invasive cancers. In addition, some of the dysplastic lesions are related to p53 and K-ras mutations, although these genetic alterations are also seen in basal cell hyperplasia.
Adenocarcinoma ; Biopsy* ; Bronchoscopes ; Bronchoscopy* ; Carcinoma in Situ ; Carcinoma, Small Cell ; Carcinoma, Squamous Cell ; Cell Proliferation ; Fluorescence* ; Hyperplasia ; Immunohistochemistry ; Lung ; Lung Neoplasms ; Sequence Analysis, DNA