Heide Ford of the University of Colorado Cancer Center has done intensive research on the homeobox superfamily of genes, which encode transcription factors that are essential during normal development and are often dysregulated in cancer. Dr. Ford has demonstrated that the developmental regulator Six1 is overexpressed in a variety of carcinoma cell lines as compared to normal cell surface epithelium. Six1 overexpression leads to increased A-type cyclin expression and increased proliferation. In addition, Six1 overexpression renders tumors resistant to TNF-related apoptosis inducing ligand (TRAIL)-mediated apoptosis, and Six1 knockdown in the TRAIL-resistant SKOV3 ovarian carcinoma line dramatically sensitizes the cells to TRAIL.
There are currently clinical trials with TRAIL ongoing at CU. Dr. Ford’s technology would allow for accurate identification of patients who will most likely benefit from TRAIL, and potential use as a marker for tailoring patient therapy once these therapies are approved by the FDA (perhaps in conjunction with the FDA label for TRAIL).
Dr. Ford’s earlier results (available upon request) are focused on elucidating the mechanism through which Six1 confers resistance to TRAIL ligands and receptor antagonists. In particular, expression of Six1 seems to be linked with upregulation of certain decoy receptors for those molecules. More recently, Dr. Ford and her collaborators have found that expression
of Six1 is linked to resistance to other classes of cancer
therapeutics, including VEGF therapeutics (link).
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