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AssigneeThe Trustees of Columbia University in the City of New York
InventorsArianna L. Kim, David Bickers, Mohammad Athar
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A mechanism whereby aberrant Shh signaling converges on the Akt1-mTOR pathway, conferring selective growth advantage and enhanced survival of tumor cells has been identified. Utilizing a mouse model of BCNS, a pivotal role has been discovered for Akt1 signaling in BCC tumorigenesis. Based on the results described here certain embodiments are directed to methods and pharmaceutical formulations for treating BCC/BCNS, other cancers that are Shh+ and Akt+, cancers that are Shh+ and mTOR plus and cancers that are Shh+ by administering therapeutically effective amounts of various combinations of Akt inhibitors, Shh pathway inhibitors such as SMO inhibitors, and mTOR inhibitors.
A method for treating basal cell carcinoma, basal cell nevus syndrome cancer, or XP BCC, comprising administering a therapeutically effective amount of an Akt inhibitor.
A method for treating a cancer that has activated sonic hedgehog and Akt, comprising administering a therapeutically effective amount of a sonic hedgehog pathway inhibitor and an Akt inhibitor, or a therapeutically effective amount of a sonic hedgehog pathway inhibitor and an mTOR inhibitor, a combination thereof.
A method for treating a cancer that has activated sonic hedgehog and mTOR cancer, comprising administering a therapeutically effective amount of a sonic hedgehog pathway inhibitor and an mTOR inhibitor, or sonic hedgehog inhibitor, an Akt inhibitor and an mTOR inhibitor.
A pharmaceutical composition, comprising a therapeutically effective amount of an Akt1 inhibitor together with a sonic hedgehog pathway inhibitor or a therapeutically effective amount of an Akt1 inhibitor, sonic hedgehog pathway inhibitor and an mTOR inhibitor.
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Dependencies are inferred from the claim text.