Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two H-ras oncogenes were detected by NIH/3T3 transfection assay out of 16 primary kidney tumors, 15 renal cell carcinomas (RCC), and one transitional cell carcinoma in 16 patients. Analysis of ras Mr 21,000 protein suggested single point mutations within codon 12 and 61 in each case. The restriction endonuclease analysis of H-ras gene at codon 12 confirmed this in one of them, and the remaining 15 tumors did not have a mutation at this site. DNAs from the noncancerous portions of the kidney with codon 12 mutated tumor, but not leukocytes from the same patient, showed an abnormal resistance to the endonucleases MspI and HpaII, suggesting a presence of codon 12 mutated H-ras gene in the noncancerous cells. No amplification of ras genes was detected in the 16 tumors analyzed. In one of eight tumors from patients heterozygous for H-ras related BamHI restriction fragments, one allele was lost in the tumor but not in the noncancerous portion of the same kidney. Although cytogenetic studies have previously suggested nonrandom involvement of c-raf-1 gene in RCC, no abnormality in the size nor amount of raf transcript was detected in the 15 RCCs. Our results thus indicated that the genetic lesions affecting ras genes do occur in human RCC, and probably serve as one of multisteps in the carcinogenic process.
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PMID:Activated H-ras oncogenes in human kidney tumors. 245 38

Length variation of a ribosomal DNA "spacer" region in four chromosomally characterized transitional cell carcinoma cultures was analyzed by restriction endonuclease cleavage and Southern blotting. Cell lines with relative karyotypic conservation, such as UM-UC-2 (modal chromosome number 48, four marker chromosomes) demonstrate little change in the genetically regulated pattern of rDNA spacer length polymorphisms (7.6, 6.7 and 6.0 kilobases) which may be found in normal cells. Cell lines with more aberrant karyotypes, such as UM-UC-3 (modal chromosome number 86, 12 marker chromosomes) and UM-UC-4 (modal number 51, ten marker chromosomes) show fewer ribosomal DNA length variants (7.6, 6.7 kilobases for the former, 7.6 kilobases for the latter), consistent with relaxed constraints on the drive for ribosomal gene homogeneity through inter and intrachromosomal exchange. Uncharacterized rDNA length variants of low copy number were observed in cell lines with many marker chromosomes. Analysis of repetitive DNA structure provides an additional criterion for tumor diagnosis and staging, and a characterized series of tumor cell lines may provide a useful system for understanding repetitive DNA evolution.
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PMID:Cell-specific ribosomal DNA spacer variability in human urothelial carcinoma cultures. 287 45

Urinary stone disease and bladder cancer are two of the most commonly seen urologic diseases in Taiwan. Tumor necrosis factor-alpha (TNF-alpha) is one of the cytokines secreted by macrophages and is related to a sequence of events in response to inflammation and cancer formation. We investigated the polymorphism of the TNF-alpha gene promoter -308 as a genetic marker in searching for the association between these two commonly seen urologic diseases. One hundred and fourteen patients with transitional cell carcinoma of the urinary bladder and 103 patients with calcium oxalate stone were compared with 150 healthy controls. The polymorphism was detected by polymerase chain reaction-based restriction analysis (Nco I endonuclease). The results revealed no significant differences between normal individuals and the patients with the two commonly seen urologic diseases (P > 0.05). We concluded that the polymorphism of the TNF-alpha promoter -308 is not a valid genetic marker for these two urologic diseases.
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PMID:Lack of evidence for the association of tumor necrosis factor-alpha gene promoter polymorphism with calcium oxalate stone and bladder cancer patients. 1182 95