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

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

No abstract available.
Genes, ras* ; Humans*

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.
Genes, erbB-1

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