No abstract available.
Genes, Neoplasm*

No abstract available.
Genes, Neoplasm*

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

Grammatical inference methods are expected to find grammatical structures hidden in biological sequences. One hopes that studies of grammar serve as an appropriate tool for theory formation. Thus, we have developed JSequitur for automatically generating the grammatical structure of biological sequences in an inference framework of string compression algorithms. Our original motivation was to find any grammatical traits of several cancer genes that can be detected by string compression algorithms. Through this research, we could not find any meaningful unique traits of the cancer genes yet, but we could observe some interesting traits in regards to the relationship among gene length, similarity of sequences, the patterns of the generated grammar, and compression rate.
Genes, Neoplasm ; Motivation ; Natural Language Processing

BACKGROUND: Two tumor suppressor genes, p53 and p16, which have different roles in controlling the cell cycle and inducing apoptosis, are frequently inactivated during carcinogenesis including lung cancer. Single tumor suppressor gene therapies using tither with p53 or p16 have been studied extensively. However, there is a paucity of reports regarding a combined gene therapy using these two genes. METHODS: The combined effect of p53 and p16 gene transfer by the adenoviral vector on the growth of lung cancer cell lines and its interactive mechanism was investigated. RESULTS: An isobologram showed that the co-transduction of p53 and p16 exhibited a synergistic growth inhibitory effect on NCI H358 and an additive effect on NCI H23. Cell cycle analysis demonstrated the induction of a synergistic G1/S arrest by a combined p53 and p16 transfer. This synergistic interaction was again confirmed in a soft agar clonogenic assay. CONCLUSION: These observations suggest the potential of a p53 and p16 combination gene therapy as another potent strategy in cancer gene therapy.
Adenoviridae ; Agar ; Apoptosis ; Carcinogenesis ; Cell Cycle ; Cell Line* ; Genes, Neoplasm ; Genes, p16 ; Genes, Tumor Suppressor ; Genetic Therapy ; Lung Neoplasms* ; Lung*

OBJECTIVE: The aim of this study is to evaluate the role of tumor suppressor genes, p53 and Rb gene, as well as apoptosis in the carcinogenesis of ovarian epithelial tumors. And the value of these factors as prognostic markers to tell the transformation of borderline tumors to overt carcinomas is also studied. METHOD: Thirty cases of ovarian epithelial benign and borderline tumors and invasive carcinoma were used and the expression of the p53 protein and Rb gene protein were evaluated by immunohistochemical method. The apoptosis was evaluated by TUNNEL method. RESULTS: Positive rate of p53 expression in benign, borderline and invasive tumors were 0, 28, and 94 %, respectively. And also, p53 was highly expressed in chemoresistant cases (2/3), in residual tumor (4/5) and in recurred cancer (2/2). Rb protein was partly lost in the borderline tumors, but the rate of Rb protein loss in both borderline tumors and invasive carcinomas were similar. Apoptosis were more active in overt carcinomas than in borderline and benign tumors. In borderline tumors, p53 protein was expressed as 28.6% positivity, and apoptosis was expressed as 28.6% negativity, which showed indirectly that there was apoptosis induction effect of p53. In ten cases of invasive carcinomas showing highly expressed p53, apoptosis revealed all positive reaction except 2 cases, and Rb protein revealed variously. This result supported the apoptosis imduction effect of p53, but it was difficult to find the association of expression degree between the two tumor supressor genes CONCLUSION: In conclusion, the values of p53 is a discriminating factor of malignancy from benign and the expression of p53 is related with clinical aggressivity such as recurrence and residual cancers. Apoptosis are more active in overt carcinoma than in benign & borderline tumor, and in borderline tumor the expression of p53 is related to apoptosis induction which results to carcinomatous change.
Apoptosis* ; Carcinogenesis ; Genes, Retinoblastoma* ; Genes, Tumor Suppressor ; Neoplasm, Residual ; Recurrence ; Retinoblastoma Protein

The p53 gene, which resides on the short arm of chromosome 17, has been described as a tumor suppressor gene playing a role of G1 checkpoint monitering DNA damage, but mutation of this gene has been shown in numerous types of human cancers. The nm23-H1 gene encodes human NDP(nucleotide diphosphate) kinase. The expression of nm23-H1 gene was postulated to inversely correlate with metastatic potential of malignant tumors. We examined immunohistochemical expression in 30 cases of stomach cancers including 10 cases each of early gastric cancers(EGC), advanced gastric cancers without lymph node involvement, and advanced gastric cancers with lymph node involvement, which were stained with mouse monoclonal antibody of p53(PB53-12) and nm23-H1. Positive nuclear staining of p53 was frequently found in advanced gastric cancers with lymph node involvement (80%). The lymph node positive group showed high expression of p53(80%), and low expression of nm23-Hl(30%) than lymph node negative group. There was no significant correlation of p53 and nm23-H1 expression with tumor size, invasion depth, TNM stages, distant metastasis and histologic differentiation. Based on the present study, the expression of p53 and down regulation of nm23-H1 are thought to be correlated with tumor progression and lymph node involvement, and may be a useful prognostic factor in gastric cancers.
Humans ; Mice ; Animals ; Neoplasm Metastasis ; Genes, Tumor Suppressor ; Stomach Neoplasms ; Genes, p53

PURPOSE: Cancer gene therapeutic strategy using p53 tumor suppresser gene have been suggested to be effective in many solid tumors including non-small cell lung cancer (NSCLC). To test generalized applicability, we tested a number of non-small cell lung cancer cell lines for their sensitivity to adenoviral-mediated wild-type p53 gene transfer. MATERIALS AND METHOD: Replication-incompetent recombinant adenovirus encoding wild- type p53 (Avp53) under the control of the human cytomegalovirus (CMV) promoter was constructed and the cytotoxic effectiveness was evaluated in various NSCLC cell lines. Because 20 moi (multiplicity of infection; number of active virus particle/cell number) of Avp53 showed highly-effective cytotoxicity in p53-deleted cell lines (NCI-H1299, and NCI-H358), same amount was used for other cell lines. RESULTS: Variable degree of cytotoxicity were observed in cell line with p53 mutation, but almost no effect were observed in those with will-type p53. Neither the infectivity of adenovirus, which was observed by x-gal stain after adenoviral mediated lac Z gene, nor the expression of p53 protein in infected cell, which was observed by western blot, was not the useful marker to expect the cytotoxic effect of Avp53. However, in responsive cell lines with Avp53, prominent expression of p21 protein, which was observed by western blot, was noticed. CONCLUSION: In conclusion, adenoviral-mediated wild-type p53 transfer may not be applicable to every patient with non-small cell lung cancer, especially when the tumor has wild-type p53 gene. Better method to predict the effectiveness before application and strategy to widen the applicable extent is needed.
Adenoviridae ; Blotting, Western ; Carcinoma, Non-Small-Cell Lung* ; Cell Line* ; Cytomegalovirus ; Genes, Neoplasm ; Genes, p53* ; Humans

PURPOSE: This study was carried out to evaluate the expression of p53 and bcl-2 protein in the adenocarcinoma of gallbladder. MATERIALS AND METHODS: Thirty three cases of adenocarcinoma of gallbladder were immunohistochemically stained for p53 and bcl-2 protein. RESULTS: p53 protein was expressed in 51.5%(17/33) of adenocarcinoma. p53 protein expression was not significantly correlated with histologic grade of adenocarcinoma, depth of invasion, lymph node metastasis, distant metastasis and TNM stage, respectively(p>0.05). bcl-2 protein was expressed in 12.1%(4/33) of adenocarcinoma. bcl-2 protein expression was not significantly correlated with tumor size, histologic grade, depth of invasion, lymph node metastasis, distant metastasis and TNM stage, respectively(p>0.05). There is no correlation between expression of p53 and bcl-2 in gallbladder adenocarcioma(p > 0.05). CONCLUSION: This study suggest that p53 gene mutation plays an important role in carcinogenesis of gallbladder adenocarcinoma. The role of bcl-2 protein in gallbladder adenocarcinoma may be not significant.
Adenocarcinoma* ; Apoptosis ; Carcinogenesis ; Gallbladder* ; Genes, p53 ; Lymph Nodes ; Neoplasm Metastasis

PURPOSE: Telomerase is known to play a role of adding repetitive parts to chromosomal ending and to be involved in carcinogenic process through cell immortalization. The purpose of this study is to evaluate that restraining of telomerase activation can have killing effect on cancer cell and enhance susceptibility of cancer cells to anticancer substance. METHODS: The killing effect on melanoma cells was studied by using recombinant adenovirus that makes it possible to inhibit telomerase from getting activated, with such targets as two types of melanoma cell lines. This recombinant adenovirus was used combined with cisplatin, one of the most representative anticancer medicine to evaluate enhancement in susceptibility of cancer cells to anticancer substance. RESULTS: From the result of cytotoxic assay, it is found that melanoma cells have much resistance to cisplatin on the whole. In the case of using Ad-OA of recombinant virus alone, killing effect on melanoma cells was insignificant. On the other hand, when Ad-OA was used in combination with cisplatin, susceptibility of melanoma cell lines to cisplatin was enhanced. CONCLUSIONS: Ad-OA, recombinant adenovirus, could be used as a supplementary medicine in the targeted cancer gene therapy against cancer cell lines resistant to cisplatin.
Adenoviridae* ; Cell Line* ; Cisplatin* ; Genes, Neoplasm ; Hand ; Homicide ; Melanoma* ; Telomerase