Abstract: Methods are provided for increasing stem cells, hematopoietic progenitor/stem cells, mesenchymal progenitor/stem cells, mesodermal progenitor/stem cells, muscle progenitor/stem cells, or neural progenitor/stem cells in vivo in a mammalian subject. Methods are also provided for treating an immune related disease, a mesenchymal/mesoderm degenerative disease, or a neurodegenerative disease in a mammalian subject in need thereof.

Abstract: The present invention is directed toward a method of treating a subject for a condition mediated by aberrant Wnt/?-catenin signaling by selecting a subject with a condition mediated by aberrant Wnt/?-catenin signaling and administering to the selected subject a compound selected from the group consisting of those set forth in Table 1, Table 2, and a pharmaceutically acceptable salt thereof. A method of similarly modulating the Wnt/?-catenin pathway in a subject is also discussed.

Abstract: The present invention is directed toward a method of treating a subject for a condition mediated by aberrant Wnt/?-catenin signaling by selecting a subject with a condition mediated by aberrant Wnt/?-catenin signaling and administering to the selected subject a compound selected from the group consisting of those set forth in Table 1, Table 2, and a pharmaceutically acceptable salt thereof. A method of similarly modulating the Wnt/?-catenin pathway in a subject is also discussed.

Abstract: The present invention is directed toward a method of treating a subject for a condition mediated by aberrant Wnt/?-catenin signaling by selecting a subject with a condition mediated by aberrant Wnt/?-catenin signaling and administering to the selected subject at least one compound selected from the group consisting of those set forth in Table 1, Table 2, Table 3, and a pharmaceutically acceptable salt thereof. A method of similarly modulating the Wnt/?-catenin pathway in a subject is also discussed.

Abstract: The present invention is directed to a composition comprising a modulator of the Wnt/?-catenin pathway, such as a GSK-3 inhibitor, or a pharmaceutically acceptable salt thereof either with a benzamide derivative or a pharmaceutically acceptable salt thereof or with a hydroxamic acid or a pharmaceutically acceptable salt thereof. The present invention is also directed to a method of treating bipolar disorder in a subject by administering either a benzamide derivative or a hydroxamic acid to the subject under conditions effective to treat a bipolar disorder. A modulator of the Wnt/?-catenin pathway, such as a GSK-3 inhibitor, or a pharmaceutically acceptable salt thereof may also be administered to a subject.

Abstract: Methods are provided for increasing stem cells, hematopoietic progenitor/stem cells, mesenchymal progenitor/stem cells, mesodermal progenitor/stem cells, muscle progenitor/stem cells, or neural progenitor/stem cells in vivo in a mammalian subject. Methods are also provided for treating an immune related disease, a mesenchymal/mesoderm degenerative disease, or a neurodegenerative disease in a mammalian subject in need thereof.

Abstract: The present invention provides two novel polypeptides, referred to as the “N” and “C” fragments of hedgehog, or N-terminal and C-terminal fragments, respectively, which are derived after specific cleavage at a G?CF site recognized by the autoproteolytic domain in the native protein. Also included are sterol-modified hedgehog polypeptides and functional fragments thereof. Methods of identifying compositions which affect hedgehog activity based on inhibition of cholesterol modification of hedgehog protein are described.

Abstract: The present invention provides two novel polypeptides, referred to as the “N” and “C” fragments of hedgehog, or N-terminal and C-terminal fragments, respectively, which are derived after specific cleavage at a G? CF site recognized by the autoproteolytic domain in the native protein. Also included are sterol-modified hedgehog polypeptides and functional fragments thereof. Methods of identifying compositions which affect hedgehog activity based on inhibition of cholesterol modification of hedgehog protein are described.

Abstract: The present disclosure relates to the regulation and function of the Wnt/?-catenin signaling pathway and the ERK signaling pathway. The disclosure provides methods of treatment for melanoma by administering both an inhibitor of ERK signaling and an activator of Wnt/?-catenin signaling. These methods may be used alone or in combination with other strategies targeting melanoma cell survival. The disclosure also provides diagnostic methods for predicting a patient's clinical response to inhibitors of ERK signaling.

Abstract: The present invention is directed toward a method of treating a subject for a condition mediated by aberrant Wnt/?-catenin signaling by selecting a subject with a condition mediated by aberrant Wnt/?-catenin signaling and administering to the selected subject a compound selected from the group consisting of those set forth in Table 1, Table 2, and a pharmaceutically acceptable salt thereof. A method of similarly modulating the Wnt/?-catenin pathway in a subject is also discussed.

Abstract: The present invention is directed toward a method of treating a subject for a condition mediated by the Wnt/?-catenin pathway by selecting a subject with a condition mediated by the Wnt/?-catenin pathway and administering to the selected subject a compound selected from the group consisting of those set forth in Table 1, Table 2, and a pharmaceutically acceptable salt thereof. A method of similarly inhibiting the Wnt/?-catenin pathway in a subject is also disclosed.

Abstract: The present invention provides two novel polypeptides, referred to as the “N” and “C” fragments of hedgehog, or N-terminal and C-terminal fragments, respectively, which are derived after specific cleavage at a G?CF site recognized by the autoproteolytic domain in the native protein. Also included are sterol-modified hedgehog polypeptides and functional fragments thereof. Methods of identifying compositions which affect hedgehog activity based on inhibition of cholesterol modification of hedgehog protein are described.

Abstract: The present invention is directed to a method of determining the prospects for survival of a melanoma patient. This method involves providing a biological sample from a patient diagnosed with melanoma, determining the level of an indicator of Wnt/?-catenin activation in the sample, comparing the level of the indicator of Wnt/?-catenin activation in the sample against a standard level of the indicator of Wnt/?-catenin activation correlated to survival of melanoma, and determining a patient's prospects for survival of melanoma based on the comparison. The present invention also relates to a method of improving survival of melanoma patients, decreasing metastases in melanoma patients, decreasing proliferation of cancer cells in melanoma patients, decreasing melanoma recurrence in melanoma patients, and/or decreasing tumor size in melanoma patients. This involves selecting melanoma patients and subsequently determining and monitoring therapy based on their level of Wnt/?-catenin activation.

Abstract: The present invention is directed toward a method of treating a subject for a condition mediated by aberrant Wnt/?-catenin signaling by selecting a subject with a condition mediated by aberrant Wnt/?-catenin signaling and administering to the selected subject at least one compound selected from the group consisting of those set forth in Table 1, Table 2, Table 3, and a pharmaceutically acceptable salt thereof. A method of similarly modulating the Wnt/?-catenin pathway in a subject is also discussed.

Abstract: The present invention is directed to a composition comprising a modulator of the Wnt/?-catenin pathway or a pharmaceutically acceptable salt thereof and an N-cinnamyl-N?-benzhydryl piperazine or a pharmaceutically acceptable salt thereof. The present invention is also directed to a method of treating a neoplastic condition in a subject by administering the modulator of the Wnt/?catenin pathway or a pharmaceutically acceptable salt thereof and an N-cinnamyl-N?-benzhydryl piperazine or a pharmaceutically acceptable salt thereof to the subject under conditions effective to treat a neoplastic disorder.

Abstract: Methods are provided for increasing stem cells, hematopoietic progenitor/stem cells, mesenchymal progenitor/stem cells, mesodermal progenitor/stem cells, muscle progenitor/stem cells, or neural progenitor/stem cells in vivo in a mammalian subject. Methods are also provided for treating an immune related disease, a mesenchymal/mesoderm degenerative disease, or a neurodegenerative disease in a mammalian subject in need thereof.

Abstract: Methods are provided for increasing stem cells, hematopoietic progenitor/stem cells, mesenchymal progenitor/stem cells, mesodermal progenitor/stem cells, muscle progenitor/stem cells, or neural progenitor/stem cells in vivo in a mammalian subject. Methods are also provided for treating an immune related disease, a mesenchymal/mesoderm degenerative disease, or a neurodegenerative disease in a mammalian subject in need thereof.

Abstract: A method is provided for increasing the activity of adult and embryonic stem cells, progenitor cells and/or differentiated cells in vivo in a vertebrate subject. Methods are provided for increasing cell or tissue regeneration in a vertebrate subject by administering one or more Wnt/?-catenin signal-promoting agents and/or one or more inhibitors of ?-catenin-independent signaling to the vertebrate subject in need thereof.

Abstract: The present invention is directed a Lef1/?-catenin-dependent reporter and to transgenic fish containing this reporter. The present invention is also directed to the use of the reporter and the transgenic fish as a model for the ?-catenin signaling pathway. The model is useful for identifying genes in the ?-catenin signaling pathway and for identifying drugs that can modulate the ?-catenin signaling pathway. Such drugs are useful for treating or preventing melanoma, colorectal cancer and osteoporosis, among other disease conditions.

Abstract: The present invention is directed a Lef1/&bgr;-catenin-dependent reporter and to transgenic fish containing this reporter. The present invention is also directed to the use of the reporter and the transgenic fish as a model for the &bgr;-catenin signaling pathway. The model is useful for identifying genes in the &bgr;-catenin signaling pathway and for identifying drugs that can modulate the &bgr;-catenin signaling pathway. Such drugs are useful for treating or preventing melanoma, colorectal cancer and osteoporosis, among other disease conditions.