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

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

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

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

Advances in breast cancer (BC) research have demonstrated differences between black and white women with regarding tumour behaviour, patient outcome and response to treatment which can be explained by underlying genetic changes. The tumour suppressor gene p53 has been speculated to be involved in tumour biology of triple negative and/or basal –like BC and more commonly observed in black than caucasian women. Materials and methods: In this study, the protein expression of p53 was investigated in tissue samples from a series of 308 Nigerian women, prepared as a tissue microarray (TMA), using immunohistochemistry. Clinicopathological parameters, biomarkers of functional significance in BC and patient outcome of tumours expressing p53 in Nigerian women were correlated with UK grade matched series. Results: A significantly large proportion of BC from Nigerian women showed high p53 expression compared with UK women (p<0.001). In those tumours showing positive p53 in the Nigerian series, a significant proportion were premenopausal, diagnosed before 50 years, larger in size, with evidence of metastasis into lymphatic vessels ( all p<0.001). In addition, p53 positive expression was also significantly correlated with negative expression of ER and PgR (p<0.001, p<0.03 respectively), BRCA1, MDM2 (all p<0.001), p21 (p=0.006) and E-cadherin (p=0.001) and positively associated with P-cadherin (p=0.001), triple negative phenotype, basal cytokeratin (CK) 5/6 expression (p<0.04) and basal phenotype compared with the UK series (p<0.001). Survival analyses showed Nigerian women with BC were significantly associated with poor BC specific survival (p<0.001, but no significant association with disease free interval was observed. Conclusion: In this study, protein expressions of p53 pathways are different between Nigerian and UK BC women and this may also contribute to differences in tumour biology. Therefore, targeting these p53 pathways for therapeutic usage might improve the poor outcome observed in Black Nigerian women.
Breast Neoplasms ; Genes, p53

Mutations in the p53 gene seem to be the most common genetic changes in human malignancies. Mutation or altered p53 expression is a common occurrence in many solid neoplasms, including head and neck carcinomas. Recent studies have also shown p53 alterations in several premalignant conditions of the colon, esophagus, lung, and brain. Preliminary data have suggested that p53 mutations may be involved in tumor progression. This study was performed to determine the incidence of p53 mutations in histologically 27 squamous cell carcinomas, 19 basal cell carcinomas, 18 Schneiderian papillomas, 3 Schneiderian papillomas with malignant transformation, and 15 pleomorphic adenomas of the head and neck region. The degree of p53 gene overexpression was also evaluated according to differentiation, histologic type of tumor, and tumor progression in the head and neck carcinomas. The results were as follows; 1) Eighteen of 27 squamous cell carcinomas, and 4 of 27 dysplasias adjacent to the squamous cell carcinoma of the head and neck expressed p53 protein, but none of the normal control specimens expressed detectable p53 protein. There was no relationship between differentiation of squamous cell carcinoma and p53 protein expression. 2) Twelve of 19 basal cell carcinomas expressed p53 protein; the adenoid type especially overexpressed p53 protein. 3) Nine of 15 pleomorphic adenomas expressed p53 protein especially in the epithelial components. 4) Thirteen of 18 Schneiderian papillomas and all Schneiderian papillomas with malignant transformation expressed p53 protein. The above results indicate that the p53 protein expression is a useful tool for the prediction of tumor progression in the head and neck tumor, but there was no relationship between the differentiation of the tumor and p53 protein expression.
Humans ; Incidence ; Adenoma ; Genes, p53

In Vietnam war, US army applied a great amount of herbicides (especially the agent orange) which was contaminated with a very poisonous chemical named dioxin. There were a high prevalence of some cancers among people who were exposed to dioxin. In oncology, the p53 gene plays an important role as a tumor suppression gene. This study was carried out to investigate the p53 gene in peripheral blood lymphocyte from a number of veterans who served in dioxin exposed regions in Vietnam. The 1st group (exposed group) include 25 veterans who served in the dioxin exposed regions in Vietnam for at least three years. The 2nd group (control group) include 15 veterans who served only in Northern Vietnam. DNA samples were extracted from peripheral blood lymphocyte. PCR was carried out for 35 cycles with the specific primers P18-M10. PCR products were checked by electrophoresis. The results showed that: exposed group: The frequency of the investigated p53 gene is 40% (10/25 samples). Control group: the frequency of the investigated p53 gene is 73.3% (11/15 samples). There is a significant difference between the frequency of the p53 gene in the group of dioxin exposed veterans and that of the control group (p<0.05).
Genes, p53 ; Veterans ; Lymphocytes ; Dioxins

No abstract available.
Carcinoma, Hepatocellular* ; Cell Line* ; Genes, p53* ; Humans

BACKGROUND: Gemcitabine is a new anti-cancer agent for treating non-small cell lung cancer. Functioning as an antimetabolite, it induces anti-cancer effects by suppressing DNA synthesis after being incorporated into the DNA as a cytosine arabinoside analogue. When Gemcitabine is incorporated into the DNA, the p53 gene may be activated by induction of the DNA defect. However, there are a few studies on the molecular mechanisms of Gemcitabine-induced cell death. This study examined the role of p53 in Gemcitabine-induced cell death. METHODS: A549 and NCl-H358 lung cancer cells were used in this study. The cell viability test was done using a MTT assay at Gemcitabine concentrations of 10nM, 100nM, 1uM, 10uM and 100uM. A FACScan analysis with propium iodide staining was used for the cell cycle analysis. Western blot analysis was done to investigate the extent of p53 activation. For the functional knock-out of p53, stable A549-E6 cells and H358-E6 cells were transfected pLXSN-16E6SD which is over expresses the human papilloma virus E6 protein that constantly degrades p53 protein. The functional knock out of p53 was confirmed by Western blot analysis after treatment with a DNA damaging agent, doxorubicine. RESULTS: Gemcitabine exhibited cell toxicity in dose-dependent fashion. The cell cycle analysis resulted in an S phase arrest. Western blot analysis significant p53 activation in time-dependent manner. Gemcitabine-induced cytotoxicity was reduced by 20-30% in the A549-E6 cells and the 30-40% in H358-E6 cells when compared with the A549-neo and H358-neo control cells. CONCLUSION: Gemcitabine induces an S phase arrest, as expected for the anti-metabolite, and activates the p53 gene. Furthermore, p53 might play an important role in Gemcitabine-induced cell death. Further investigation into the molecular mechanisms on how Gemcitabine activates the p53 gene and its signaling pathway are recommended.
Humans ; Lung Neoplasms ; Genes, p53 ; Antimetabolites

Transitional cell carcinoma of the urinary bladder is the most common cancer of the genitourinary tract in Korea and its prognosis is determined by the histologic grade and clinical stage present at initial diagnosis. Recently, an extensive search for a more objective and reproducible method to evaluate the proliferation activity of cancer cells has been done. The p53 gene is located on the short arm of the chromosome 17 and acts as a cancer suppressor gene. Mutant p53 gene induces malignant transformation. Recent studies reveal that the level of mutant p53 protein is elevated in some human tumor and many diverse transformed cell lines. Heat shock proteins(HSPs) are present constitutively in normal cells, where they play an important role in normal cell metabolism. In mammalian cells, they are induced by a variety of physical and chemical stimuli. A protein that belongs to the hsp70 family, called hsc70, is only slightly heat inducible and is found at a higher level in growing cells than in the resting cells. The mutant p53 protein binds with hsc70 and the p53-hsc70 complex has functional significance in the transforming capacity of the mutant p53. We investigated the correlation between the p53 and hsc70 by immunohistochemical methods and with better defined prognostic indicators such as histologic grade, clinical stage, and DNA ploidy pattern in 42 transitional cell carcinomas of the urinary bladder. The results are summarized as follows. p53 expression rate was higher in the DNA aneuploid group than in the DNA diploid group(p=0.061), but there was no significant difference in the histologic grade(p=0.861) or clinical stage(p=0.154). The higher the hsc70 expression rate was, the poorer the tumor differentiation(p=0.000) and the deeper the invasion(p=0.001). The aneuploid group showed a higher hsc70 expression rate than the diploid group(p=0.017). 27 of 42(64.3%) carcinomas showed positivity of both p53 and hsc70. Though statistically insignificant, their correlation showed a relatively low correlation coefficient (P=0.059). In conclusion, we suspect that p53 and hsc70 are closely correlated to each other by comparing the results of this immunohistochemical study, and hsc70 will be a useful prognostic marker in transitional cell carcinomas of the urinary bladder after sufficient follow up studies are performed.
Humans ; Follow-Up Studies ; Genes, p53