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Brizape
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amia_tokenized_split_0404_dev

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9841584
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## RESULTS
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18345036
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We previously reported that actin damage by treatment with an actin-depolymerizing agent including pectenotoxin-2 induces Bim-mediated apoptosis in p53-deficient human tumors. In this study, we investigated a molecular mechanism underlying Bim-mediated apoptosis of p53-deficient tumor cells following actin damage. We found that actin inhibitors increased the protein levels of p53 and p21 and thereby inactivated both Cdk2 and Cdc2 kinases. However, p53- or p21-knockout cells fail to induce p21 and hence kept both Cdk2 and Cdc2 kinases active even after treatment with actin inhibitor. The p53- or p21-knockout cells became multinucleate and polyploidy in association with induction of apoptosis. Expression of Bcl-x(L) resulted in accumulation of polyploid cells in association with inhibition of apoptosis. However, expression of a dominant negative mutant (Cdk2dn) and treatment with chemical inhibitors for Cdk2 suppressed not only accumulation of multinucleated cells, but also induction of Bim expression and apoptosis. Therefore, these results suggest that Bim-mediated apoptosis following actin damage due to deregulation of Cdk2 actin damage. We found that actin inhibitors increased the protein levels of p53 and p21 and thereby inactivated both Cdk2 and Cdc2 kinases. However, p53- or p21-knockout cells fail to induce p21 and hence kept both Cdk2 and Cdc2 kinases active even after treatment with actin inhibitor. The p53- or p21-knockout cells became multinucleate and polyploidy in association with induction of apoptosis. Expression of Bcl-x(L) resulted in accumulation of polyploid cells in association with inhibition of apoptosis. However, expression of a dominant negative mutant (Cdk2dn) and treatment with chemical inhibitors for Cdk2 suppressed not only accumulation of multinucleated cells, but also induction of Bim expression and apoptosis. Therefore, these results suggest that Bim-mediated apoptosis following actin damage due to deregulation of Cdk2 and the cell cycle by the absence of functional p53 Cdc2 p53 and p21 and thereby inactivated both Cdk2 and Cdc2 kinases. However, p53- or p21 Cdk2 and Cdc2 kinases. However, p53- or p21-knockout cells fail to induce p21 and hence kept both Cdk2 and Cdc2 Cdk2 and Cdc2 kinases active even after treatment with actin inhibitor. The p53 actin inhibitor. The p53- or p21-knockout cells became multinucleate and polyploidy in association with induction of apoptosis. Expression of Bcl-x(L) p21 -knockout cells became multinucleate and polyploidy in association with induction of apoptosis. Expression of Bcl-x(L) resulted in accumulation of polyploid cells in association with inhibition of apoptosis. However, expression of a dominant negative mutant (Cdk2dn) and treatment with chemical inhibitors for Cdk2 suppressed not only accumulation of multinucleated cells, but also induction of Bim Cdk2 Cdk2 causes Bim-mediated apoptosis in p53-deficient tumors following actin damage.
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14645426
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9841584
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## SETTING
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19706845
[ "A", "hospital-based", "case-control", "study", "of", "440", "CRC", "patients", "and", "800", "cancer-free", "controls", "was", "conducted.", "Personal", "information", "was", "collected", "by", "a", "Semi-Quantitative", "Food", "Frequency", "Questionnaire.", "The", "tagSNPs", "were", "screened", "in", "the", "HapMap", "with", "Haploview", "by", "setting", "the", "minor", "allele", "frequency", "at", "0.03", "with", "the", "highest", "score", "of", "r(2)", "form", "each", "block.", "Genotypes", "were", "identified", "by", "using", "the", "SNPLex", "System.", "Both", "crude", "and", "adjusted", "odds", "ratio", "(OR)", "and", "95%", "confidence", "interval", "(CI)", "were", "used", "to", "evaluate", "the", "risk", "of", "each", "SNP." ]
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A hospital-based case-control study of 440 CRC patients and 800 cancer-free controls was conducted. Personal information was collected by a Semi-Quantitative Food Frequency Questionnaire. The tagSNPs were screened in the HapMap with Haploview by setting the minor allele frequency at 0.03 with the highest score of r(2) form each block. Genotypes were identified by using the SNPLex System. Both crude and adjusted odds ratio (OR) and 95% confidence interval (CI) were used to evaluate the risk of each SNP.
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14645426
[ "##", "RESULTS" ]
[ 0, 0 ]
## RESULTS
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22899730
[ "##", "IMPACT" ]
[ 0, 0 ]
## IMPACT
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12534642
[ "(i)", "CYP1A2", "cytochrome", "P450", "enzyme", "1A2", " ", "gene", "(CYP1A2)", "have", "been", "reported.", "Here,", "frequencies,", "linkage", "disequilibrium", "and", "phenotypic", "consequences", "of", "six", "SNPs", "are", "described." ]
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(i) CYP1A2 cytochrome P450 enzyme 1A2 gene (CYP1A2) have been reported. Here, frequencies, linkage disequilibrium and phenotypic consequences of six SNPs are described.
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8709782
[ "##", "FINDINGS" ]
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## FINDINGS
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25374237
[ "Individuals", "with", "-31C", "allele", "and", "CC", "genotype", "were", "found", "to", "have", "a", "higher", "risk", "of", "developing", "colon", "cancer", "(OR=13.4,", "p=0.01).", "The", "-241", "CT", "genotype", "considerably", "increased", "the", "risk", "of", "colon", "cancer", "(OR=12.0,", "p=0.0001).", "However,", "there", "was", "no", "significant", "varaition", "of", "the", "survivin", "-625", "C/G", "polymorphism", "survivin", " ", "-31", "G/C", "(", "rs9904341", "),", "-241", "C/T", "(", "rs17878467", ")", "and", "-625", "C/G", "(", "rs8073069", ")", "polymorphism", "in", "promotor", "site", "of", "survivin", " ", "gene", "associated", "with", "apoptosis", "was", "investigated", "using", "the", "polymerase", "chain", "reaction-restriction", "fragment", "length", "polymorphism", "(PCR-RFLP)", "method." ]
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Individuals with -31C allele and CC genotype were found to have a higher risk of developing colon cancer (OR=13.4, p=0.01). The -241 CT genotype considerably increased the risk of colon cancer (OR=12.0, p=0.0001). However, there was no significant varaition of the survivin -625 C/G polymorphism survivin -31 G/C ( rs9904341 ), -241 C/T ( rs17878467 ) and -625 C/G ( rs8073069 ) polymorphism in promotor site of survivin gene associated with apoptosis was investigated using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method.
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22545919
[ "Currently,", "the", "TNM", "classification", "of", "malignant", "tumours", "based", "on", "clinicopathological", "staging", "remains", "the", "standard", "for", "colorectal", "cancer", "(CRC)", "prognostication.", "Recently,", "we", "identified", "the", "mitochondrial", "oxidative", "phosphorylation", "chain", "as", "a", "consistently", "overrepresented", "category", "in", "the", "published", "gene", "expression", "profiling", "(GEP)", "studies", "on", "CRC", "prognosis." ]
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Currently, the TNM classification of malignant tumours based on clinicopathological staging remains the standard for colorectal cancer (CRC) prognostication. Recently, we identified the mitochondrial oxidative phosphorylation chain as a consistently overrepresented category in the published gene expression profiling (GEP) studies on CRC prognosis.
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17938238
[ "The", "genetics", "of", "hereditary", "colon", "cancer." ]
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The genetics of hereditary colon cancer.
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14734469
[ "##", "RESULTS" ]
[ 0, 0 ]
## RESULTS
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[ 1, 1, 1, 1, 1 ]
[ -100, 0, 0, 0, -100 ]