No abstract available.
Genes, Neoplasm*

No abstract available.
Genes, Neoplasm*

Diseases caused by dioxine include mainly various types of cancers and p53 is one important gene in carcinogenesis-suppressing gene family. Objectives: This research's goal is detecting p53 gene's ratio in the high risk group of exposure to dioxine. Methods: In this study we detected p53 ratio in 50 cases in the group of high risk of exposure to dioxine and the control group of 30 cases. Gene p53 was detected by PCR technique. Results: The study showed that in the control group (no exposure to dioxine), p53 prevalence is 100% compared with 82% in high - risk group (p <0.05). Conclusions: p53 was not detected in 18% of the group of high risk exposure to dioxin, suggesting that there were serious damages in p53 gene (deletion...)
Genes, p53

The second step of immunoglobulin gene alteration consists of somatic hypermutation and class switch recombination. 80th are regulated by activation-induced cytidine deaminase (AID). Methods: Study on possible application of class switch recombination assays for immunoglobulin gene alteration via AID. Cell based assays using AID B lymphocyte and NIH3T3 cell carrying switch substrate; gene transfer using retrovirus system; FACS analysis; PCR and ELISA. Results: DNA sequencing for S region and gamma1CT are the most sensitive and accurate assays. However, gamma1CT assay seemed to be more reliable and applicable. Others are accurate assays but less applicable. Conclusion: gamma1CT determination is the best class switch recombination assay for immunoglobulin gene alteration via AID.
Immunoglobulins, Genes

Mutation of the p53 gene frequently results in overexpression of the p53 protein and loss of its tumor-suppressing properties. The overexpression of the p53 gene could be an indicator of rapid proliferation, poor differentiation, advanced stages, or poor prognosis. The prognostic value of the overexpression of the p53 gene in colorectal carcinoma is equivocal. The presence of DNA aneuploidy has been described as a powerful adverse prognostic indicator in relation to survival. To investigate the prognostic significance of p53 expression, and the relationship with DNA ploidy, 92 cases of colorectal carcinomas were analyzed. The overexpression of p53 gene product was present in 50(54.4%) of 92 cases. p53 expression only correlated with recurrence or metastasis during the follow-up periods (p=0.045). DNA aneuploidy was observed in 32(39.1%) of 82 cases. DNA ploidy was strongly associated with lymph node invasion(p=0.005), Dukes' stage(p=0.003), TNM classification (p=0.003), and recurrence or metastasis during the follow-up periods (p=0.045). The frequency of DNA aneuploidy was higher in the p53-positive colorectal carcinomas(58.3%) than in the p53-negative colorectal carcinomas (21.6%) (p=0.003). p53-positive colorectal carcinomas had a higher rate of cell proliferation than p53-negative cases(p<0.001). These results suggest that checking the p53 expression and DNA ploidy could be useful prognostic indicators of colorectal carcinoma.
Neoplasm Metastasis ; Genes, p53

No abstract available.
Genes, ras* ; Humans

p53 gene alterations in the ovarian cancers are regarded as early events in the whole process of carcinogenesis. This study is intended to compare p53 protein expression rate in the ovarian surface epithelial tumors according to histologic types, degree of malignancy and differentiation. 134 cases of ovarian epithelial tumors including 26 cases of serous cystadenoma, 7 cases of serous borderline malignancy, 15 cases of serous cystadenocarcinoma, 40 cases of mucinous cystadenoma, 21 cases of mucinous borderline malignancy, 20 cases of mucinous cystadenocarcinoma, 4 cases of endometrioid carcinoma, and 1 case of clear cell carcinoma were studied. Immunohistochemistry using monoclonal p53 antibody(DO-7) was applied to the routine formalin-fixed paraffin embedded tissue. The results were as follows; 1. No immunohistochemical positivity of p53 protein was found in all 66 cases of benign serous and mucinous tumors studied. 2. There was no significant difference of p53 protein expression between serous and mucinous malignant tumors. 3. The expression rate of p53 protein exhibited a statistically significant difference between borderline(42%) and malignant(74%) ovarian surface epithelial tumors (p<0.05). 4. The expression rate of p53 protein of poorly differentiated carcinomas(100%) was higher than those of moderately (88%) and well differentiated carcinomas(60%), but there was no statistical significance. In summary, p53 protein expression might be a good indicator of malignant transformation of the ovarian surface epithelial tumors.
Ovarian Neoplasms ; Genes, p53

BACKGROUND: Aberrant methylation of CpG islands in promoter regions is one of the major mechanisms for silencing of tumor suppressor genes in various types of human cancers including non-Hodgkin's lymphomas (NHL). In this study, we investigated the aberrant promoter methylation status of known or suspected tumor suppressor genes in NHLs and compared the methylation profiles between B-cell and T/NK-cell NHLs. METHODS: 54 cases of B-cell NHLs and 16 cases of T/NK-cell NHLs were examined for the methylation status of eight genes using methylation specific PCR. RESULTS: CpG islands methylation was variously found in eight genes as follows; DAPK (71%), MT1G (70%), p16 (53%), CDH1 (53%), THBS1 (56%), MGMT (27.1%), COX2 (13%), and RUNX3 (11.4%). In six cases (8 %), methylation was not observed in any of these genes. Overall methylation index of B-cell NHLs (0.48) was significantly higher than that of T/NK-cell NHLs (0.32). Of eight genes tested, THBS1 and CDH1 methylations were much more prominent in diffuse large B-cell lymphomas than in T/NK-cell NHLs or other B-cell NHLs. CONCLUSION: This study suggests that aberrant CpG island methylation is a frequent event in NHLs, and diffuse large B-cell lymphomas show overlapping but distinct methylation profiles.
Humans ; Genes, Tumor Suppressor

Lymphomatoid papulosis is an enigmatic disease entity which is clinically benign and histologically malignant. Although sporadic cases have been reported, we could not find any comprehensive report on the combined clinical and histologic features of lymphomatoid papulosis in the literature. Perhaps the most controversial aspect of lymphomatoid papulosis is its pathogenesis and categorization as a benign versus a malignant entity. To date, there are no reports on p53 and bcl-2 protein expression in lymphomatoid papulosis. We analysed the clinico-pathological findings of 18 cases with lymphomatoid papulosis during the 10 year period from 1984 to 1995 and examined the prevalence of immunoreactivity for CD30(DAKO, Ber-H2), p53(DAKO, DO-7), and bcl-2(DAKO, 124) using an immunohistochemical(ABC) method. The results obtained are summarized as follows. 1) Age distribution ranged from 20 to 65, with a mean age of 45 years and a sex distribution which showed a male predominence(8:1). The lesions were located on the trunk and extremities(8cases), extremities (7cases), and trunk(3 cases). The morphology of the lesions were papules or plaques(12 cases), and nodules(6 cases). 2) Histopathologic types were classified into 3 types: type A(4 cases), type B(8 cases) and mixed type (6 cases). 3) Positive immunoreactivity for CD30 was seen in 17%(3 of 18cases): type A(2 of 3) and mixed type(1 of 3). 4) The positive immunoreactivity for p53 and bcl-2 was observed in 29%(5 of 18) and 11%(2 of 18), respectively. 5) Cases showing positive immunoreactivity for P53 were type A(1 of 5), type B(1 of 5), and mixed type(3 of 5). 6) Cases showing positive immunoreactivity for bcl-2 were mixed type(2 of 2). One case developed into Ki-1 lymphoma. These results support the idea that lymphomatoid papulosis and Ki-1 lymphoma represent a continuum. The role of p53 gene mutation and bcl-2 activation in the development of lymphomatoid papulosis is currently unknown. But, our results suggest that p53 gene mutation and bcl-2 activation are not a critical step in the development of lymphomatoid papulosis. Further studies are needed to elucidate the role of p53 gene mutation and bcl-2 activation in the development and progression of lymphomatoid papulosis.
Male ; Humans ; Genes, p53

No abstract available.
DNA* ; Genes, Retinoblastoma* ; Ploidies*