Microsatellite instability in colorectal adenocarcinoma cell lines that have full-length adenomatous polyposis coli protein.
Almost 20% of colon cancers are characterized by genomic instability at simple repeated sequences. This instability is the result of a deficient DNA mismatch repair system. Sporadic, as well as hereditary carcinomas of the proximal colon display this effect. In this study, we examined colorectal adenocarcinoma cell lines, with or without wild-type adenomatous polyposis coli (APC) protein, for the presence of microsatellite instability. The three cell lines that maintained full-length APC protein also displayed the highest level of instability, suggesting a negative correlation between APC mutations and microsatellite instability. This data, in addition to other studies that show a negative correlation between microsatellite instability and mutations in p53 and K-ras, support the idea of a second pathway for colorectal cancer development.
Heinen
C D
CD
Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Ohio 45267-0524, USA.
Richardson
D
D
White
R
R
Groden
J
J
D000230:Adenocarcinoma / Q000235:genetics* / Q000378:metabolism; D025601:Adenomatous Polyposis Coli Protein; D015153:Blotting, Western; D003062:Codon; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000378:metabolism; D003598:Cytoskeletal Proteins / Q000096:biosynthesis / Q000235:genetics*; D004273:DNA, Neoplasm / Q000235:genetics*; D004276:DNA, Satellite / Q000235:genetics*; D016368:Frameshift Mutation; D017491:Genes, APC; D018095:Germ-Line Mutation; D006801:Humans; D012091:Repetitive Sequences, Nucleic Acid; D014407:Tumor Cells, Cultured
D025601:Adenomatous Polyposis Coli Protein; D003062:Codon; D003598:Cytoskeletal Proteins; D004273:DNA, Neoplasm; D004276:DNA, Satellite