The activity of �-catenin (�-cat), a key component of the Wnt signaling pathway, is deregulated in about 40 % of ovarian endometrioid adenocarcinomas (OEAs), usually as a result of CTNNB1 gene mutations. The function of �-cat in neoplastic transformation is dependent on T-cell factor (TCF) transcription factors, but specific genes activated by the interaction of �-cat with TCFs in OEAs and other cancers with Wnt pathway defects are largely unclear. As a strategy to identify �-cat/TCF transcriptional targets likely to contribute to OEA pathogenesis, we used oligonucleotide microarrays to compare gene expression in primary OEAs with mutational defects in �-cat regulation (n � 11) to OEAs with intact regulation of �-cat activity (n � 17). Both hierarchical clustering and principal component analysis based on global gene expression distinguished �-cat-defective tumors from those with intact �-cat regulation. We identified 81 potential �-cat/TCF targets by selecting genes with a
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