Abstract: The invention demonstrates that canonical Wnt signaling is activated in certain primary tumors and tumor cell lines in the absence of ?-catenin or APC mutations and that inhibition of such activated canonical Wnt signaling in such tumor cells inhibits tumor growth and, at least in some cases, induces death of tumor cells. As further demonstrated herein, the activation of canonical Wnt signaling is associated with a higher rate of cancer recurrence in patients with Stage I Non-Small Cell Lung Cancer (NSCLC), which provides a new method for cancer prognosis, wherein activation of canonical Wnt signaling reflects a more aggressive tumor phenotype suggesting the need for a more aggressive therapy.

Abstract: The invention demonstrates that canonical Wnt signaling is activated in certain primary tumors and tumor cell lines in the absence of ?-catenin or APC mutations and that inhibition of such activated canonical Wnt signaling in such tumor cells inhibits tumor growth and, at least in some cases, induces death of tumor cells. As further demonstrated herein, the activation of canonical Wnt signaling is associated with a higher rate of cancer recurrence in patients with Stage I Non-Small Cell Lung Cancer (NSCLC), which provides a new method for cancer prognosis, wherein activation of canonical Wnt signaling reflects a more aggressive tumor phenotype suggesting the need for a more aggressive therapy.