作者: Jörg Reichrath , Knuth Rass , Paul Gutwein , Steven Dooley , Markus Seifert
DOI: 10.1007/978-1-4615-5051-8_39
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摘要: Microsatellite instability (MSI) secondary to replication errors can be detected in various malignant human epithelial and melanocytic skin tumors.1 is a recently recognized genetic mechanism important the development of cancers that characterized by length changes at repetitive loci scattered throughout genome.2,3 In most patients with hereditary nonpolyposis colon cancer (HNPCC), where almost every tumour reveals high incidence mutations microsatellite repeat sequences, it was shown predisposition attributable defects any one four genes, all which encode homologs microbial mismatch repair proteins mutS mutL.3,4 The hMSH-2 gene specifies homolog, whereas hMLH1, hPMS1, hPMS2 mutL.5 Analysis 16 exons hMSH2 34 unrelated HNPCC kindreds has revealed heterogeneous spectrum mutations.3,6 Tumour cells display are typically defective correction, thus providing direct link between DNA-mismatch enzymes stability afforded this DNA system.7 Recently, we have cloned promoter region site homology p53 consensus binding sequence.8 Using gel mobility shift assays were able show purified least vitro potential bind specifically motif.9