| http://purl.uniprot.org/citations/21668377 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21668377 | http://www.w3.org/2000/01/rdf-schema#comment | "Dysregulation of apoptosis plays a crucial role in carcinogenesis. Thus, genetic alterations within caspase genes would be expected to provoke a deficient apoptotic signaling thereby facilitating the development of prostate cancer (PCa). In the present study we investigated whether three different polymorphisms in the caspase-5 and -3 genes are differentially expressed in PCa. In a hospital-based case control study in northern India, we genotyped 192 PCa patients and 225 unrelated healthy controls for caspase-5 (G>C) (T>C) and caspase-3 (G>A) polymorphisms using amplification refractory mutation system and polymerase chain restriction fragment length polymorphism methods. Data were statistically analyzed and variant genotype GG of caspase-3 demonstrated increased risk for PCa (odds ratio [OR]=2.72, p=0.005). Similarly variant allele carrier (AG+GG) (OR=1.53, p=0.034) and G allele (OR=1.54, p=0.005) were also statistically associated with PCa risk. High risk for PCa was also observed with respect to caspase-5 (CC) diplotypes (OR=21.67, p=0.012, Pc=0.048). We observed significantly enhanced risk for PCa due to interaction between caspase-3 and -5 gene polymorphisms. In association of genotypes with clinical characteristics, heterozygous TC genotype of caspase-5 (T>C) conferred risk with high Gleason grade tumor (OR=2.35, p=0.042). In case-only analysis, interaction of environmental risk factors and genotypes did not further modulate the risk for PCa. Our observations suggested positive association of caspase-3 and diplotype analysis of caspase-5 to be associated with PCa risk. Interaction of caspase-3 and -5 genotypes also modulated the PCa risk."xsd:string |
| http://purl.uniprot.org/citations/21668377 | http://purl.org/dc/terms/identifier | "doi:10.1089/dna.2011.1285"xsd:string |
| http://purl.uniprot.org/citations/21668377 | http://purl.uniprot.org/core/author | "Singh A.K."xsd:string |
| http://purl.uniprot.org/citations/21668377 | http://purl.uniprot.org/core/author | "Mandal R.K."xsd:string |
| http://purl.uniprot.org/citations/21668377 | http://purl.uniprot.org/core/author | "Mittal R.D."xsd:string |
| http://purl.uniprot.org/citations/21668377 | http://purl.uniprot.org/core/author | "Mittal T."xsd:string |
| http://purl.uniprot.org/citations/21668377 | http://purl.uniprot.org/core/date | "2012"xsd:gYear |
| http://purl.uniprot.org/citations/21668377 | http://purl.uniprot.org/core/name | "DNA Cell Biol"xsd:string |
| http://purl.uniprot.org/citations/21668377 | http://purl.uniprot.org/core/pages | "67-73"xsd:string |
| http://purl.uniprot.org/citations/21668377 | http://purl.uniprot.org/core/title | "Association of caspases with an increased prostate cancer risk in north Indian population."xsd:string |
| http://purl.uniprot.org/citations/21668377 | http://purl.uniprot.org/core/volume | "31"xsd:string |
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