| 摘要 |
Transcriptional changes mediated by high nuclear concentrations of beta-catenin are known to be involved in the early stages of tumourigenesis. The present invention relates to the discovery that truncations of the tumour suppressor Adenomatous polyposis coli (APC) which are found in cancer cells cause high levels of nuclear beta-catenin to accumulate by "trapping' beta-catenin within the nucleus. The high levels of "trapped' nuclear beta-catenin then affect transcription within the cell, Assays, methods and means are provided for modulating the interaction between modified APC and beta-catenin, thereby lowering the nuclear concentration of beta-catenin.
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