Abstract: The present invention is directed to a method of inhibiting tumor formation in a cancer patient at a site remote from sites of prior tumor formation and to a method of preventing metastases. These methods involve administering to the cancer patient an inhibitor of vascular endothelial growth factor receptor 1+ bone marrow-derived cells under conditions effective either to inhibit tumor formation in the cancer patient at a site remote from sites of prior tumor formation or to prevent metastases. Candidate compounds useful for such purposes can be screened depending on whether they bind to vascular endothelial growth factor receptor 1+ bone marrow-derived cells. Metastases in a cancer patient can be monitored by evaluating a patient sample for detection and quantification of vascular endothelial growth factor receptor 1+ bone marrow-derived cells and comparing the level of vascular endothelial growth factor receptor 1+ bone marrow-derived cells to prior levels.

Abstract: The present invention relates to adenovirus E4ORF 1 gene and to endothelial cells engineered to express the E40RF 1 gene. The present invention also relates to uses of the E40RF 1 gene, and cells expressing the E40RF1 gene, and to compositions comprising the E4ORF 1 gene, or comprising cells expressing the E4ORF 1 gene.

Abstract: The present invention relates to slitrk proteins as markers of stem and progenitor cells, including embryonic stem cells and hematopoietic stem and progenitor cells, and also as a marker of leukemia and lymphoma cells, and of endothelial cells. The invention provides, inter alia, methods for purifying slitrk-positive cells, methods for detecting slitrk-positive cells, purified preparations of slitrk-positive cells, therapeutic compositions containing purified slitrk-positive cells, methods for targeting therapeutic agents to slitrk-positive cells, and methods of treatment, including but not limited to, methods of administering slitrk-positive cells to subjects in need thereof.

Abstract: The present invention relates to GPR1 25 as a marker of stem and progenitor cells, including multipotent adult spermatogonial-derived stem cells (MASCs), spermatogonial stem and progenitor cells, skin stem or progenitor cells, intestinal stem or progenitor cells, neural stem or progenitor cells, and cancer stem cells. The invention provides, inter alia, methods for enriching or isolating GPR125-positive stem or progenitor cells, methods for detecting GPR125-positive stem or progenitor cells, methods for culturing GPR125-positive stem or progenitor cells, purified GPR125-positive stem or progenitor cells, therapeutic compositions containing purified GPR125-positive stem or progenitor cells, methods for targeting therapeutic agents to GPR125-positive stem and progenitor cells, and methods of treatment comprising administering GPR125-positive stem and progenitor cells, or differentiated cells derived therefrom, to subjects in need thereof.

Abstract: The present invention relates to methods of inducing or inhibiting the angiogenic process and promoting vessel growth or stabilization in an organ by modulating the trk receptor pathway. The present invention also relates to a method for treating a pathological disorder in a patient which includes administering a trk receptor ligand or an inhibitor or expression or activity of a trk receptor ligand. The present invention also relates to a method of screening for a modulator of angiogenesis, vessel growth, or vessel stabilization. Another aspect of the present invention is a method of diagnosing or monitoring a pathological disorder in a patient which includes determining the presence or amount of a trk receptor ligand or activation of a trk receptor ligand in a biological sample.

Abstract: The present invention is directed to a method of inhibiting tumor formation in a cancer patient at a site remote from sites of prior tumor formation and to a method of preventing metastases. These methods involve administering to the cancer patient an inhibitor of vascular endothelial growth factor receptor 1+ bone marrow-derived cells under conditions effective either to inhibit tumor formation in the cancer patient at a site remote from sites of prior tumor formation or to prevent metastases. Candidate compounds useful for such purposes can be screened depending on whether they bind to vascular endothelial growth factor receptor 1+ bone marrow-derived cells. Metastases in a cancer patient can be monitored by evaluating a patient sample for detection and quantification of vascular endothelial growth factor receptor 1+ bone marrow-derived cells and comparing the level of vascular endothelial growth factor receptor 1+ bone marrow-derived cells to prior levels.

Abstract: The present invention relates to methods of inducing or inhibiting the angiogenic process and promoting vessel growth or stabilization in an organ by modulating the trk receptor pathway. The present invention also relates to a method for treating a pathological disorder in a patient which includes administering a trk receptor ligand or an inhibitor or expression or activity of a trk receptor ligand. The present invention also relates to a method of screening for a modulator of angiogenesis, vessel growth, or vessel stabilization. Another aspect of the present invention is a method of diagnosing or monitoring a pathological disorder in a patient which includes determining the presence or amount of a trk receptor ligand or activation of a trk receptor ligand in a biological sample.

Abstract: This invention relates to methods for treating, preventing and/or managing hematopoietic neoplasm in a subject by administering to the subject combretastatin A-4 phosphate, or a pharmaceutically acceptable salt thereof. The method may further comprise co-administering a chemotherapeutic agent.

Abstract: The present invention is directed to a method of inhibiting tumor formation in a cancer patient at a site remote from sites of prior tumor formation and to a method of preventing metastases. These methods involve administering to the cancer patient an inhibitor of vascular endothelial growth factor receptor 1+ bone marrow-derived cells under conditions effective either to inhibit tumor formation in the cancer patient at a site remote from sites of prior tumor formation or to prevent metastases. Candidate compounds useful for such purposes can be screened depending on whether they bind to vascular endothelial growth factor receptor 1+ bone marrow-derived cells. Metastases in a cancer patient can be monitored by evaluating a patient sample for detection and quantification of vascular endothelial growth factor receptor 1+ bone marrow-derived cells and comparing the level of vascular endothelial growth factor receptor 1+ bone marrow-derived cells to prior levels.

Abstract: The invention provides methods of treating and preventing loss of tissue vascularization that can occur, for example, upon aging.

Abstract: The present invention relates to slitrk proteins as markers of stem and progenitor cells, including embryonic stem cells and hematopoietic stem and progenitor cells, and also as a marker of leukemia and lymphoma cells, and of endothelial cells. The invention provides, inter alia, methods for purifying slitrk-positive cells, methods for detecting slitrk-positive cells, purified preparations of slitrk-positive cells, therapeutic compositions containing purified slitrk-positive cells, methods for targeting therapeutic agents to slitrk-positive cells, and methods of treatment, including but not limited to, methods of administering slitrk-positive cells to subjects in need thereof.

Abstract: The present invention relates to a method of isolating stem cells from a mixed population of different cell types. This method involves selecting a promoter which functions only in said stem cells and not in the other cell types. The promoter can have a nucleotide sequence selected from the group consisting of SEQ ID NO: 4, SEQ ID NO: 5, SEQ ID NO: 6, SEQ ID NO: 7, and SEQ ID NO: 8. A nucleic acid molecule encoding a marker protein under control of said promoter is introduced into all cell types of said mixed population and only the stem cells, but not the other cell types, within said mixed population are allowed to express said marker protein. The cells of said mixed population of cell types that are expressing the marker protein, which are restricted to the stem cells are identified and separated from the mixed population, where the separated cells are restricted to the stem cells. The promoter, nucleic acid constructs comprising it, and the resulting stem cells are also disclosed.

Abstract: The present invention relates to methods of inducing or inhibiting the angiogenic process and promoting vessel growth or stabilization in an organ by modulating the trk receptor pathway. The present invention also relates to a method for treating a pathological disorder in a patient which includes administering a trk receptor ligand or an inhibitor or expression or activity of a trk receptor ligand. The present invention also relates to a method of screening for a modulator of angiogenesis, vessel growth, or vessel stabilization. Another aspect of the present invention is a method of diagnosing or monitoring a pathological disorder in a patient which includes determining the presence or amount of a trk receptor ligand or activation of a trk receptor ligand in a biological sample.

Abstract: The invention provides methods of treating and preventing loss of tissue vascularization that can occur, for example, upon aging.

Abstract: The present invention is directed to a method of inhibiting tumor formation in a cancer patient at a site remote from sites of prior tumor formation and to a method of preventing metastases. These methods involve administering to the cancer patient an inhibitor of vascular endothelial growth factor receptor 1+ bone marrow-derived cells under conditions effective either to inhibit tumor formation in the cancer patient at a site remote from sites of prior tumor formation or to prevent metastases. Candidate compounds useful for such purposes can be screened depending on whether they bind to vascular endothelial growth factor receptor 1+ bone marrow-derived cells. Metastases in a cancer patient can be monitored by evaluating a patient sample for detection and quantification of vascular endothelial growth factor receptor 1+ bone marrow-derived cells and comparing the level of vascular endothelial growth factor receptor 1+ bone marrow-derived cells to prior levels.

Abstract: The invention is directed to a purified population of mammalian endothelial, muscle, or neural stem cells. The invention further provides methods for isolating such populations of cells; methods for using such populations of cells for treating mammals; methods for making vectors for gene therapy; and methods for carrying out gene therapy with such vectors.

Abstract: The present invention relates to a method of isolating stem cells from a mixed population of different cell types. This method involves selecting a promoter which functions only in said stem cells and not in the other cell types. The promoter can have a nucleotide sequence selected from the group consisting of SEQ ID NO: 4, SEQ ID NO: 5, SEQ ID NO: 6, SEQ ID NO: 7, and SEQ ID NO: 8. A nucleic acid molecule encoding a marker protein under control of said promoter is introduced into all cell types of said mixed population and only the stem cells, but not the other cell types, within said mixed population are allowed to express said marker protein. The cells of said mixed population of cell types that are expressing the marker protein, which are restricted to the stem cells are identified and separated from the mixed population, where the separated cells are restricted to the stem cells. The promoter, nucleic acid constructs comprising it, and the resulting stem cells are also disclosed.

Abstract: The invention is directed to a purified population of mammalian endothelial, muscle, or neural stem cells. The invention further provides methods for isolating such populations of cells; methods for using such populations of cells for treating mammals; methods for making vectors for gene therapy; and methods for carrying out gene therapy with such vectors.

Abstract: The present invention is directed to methods of isolating mammalian stem cells expressing the VEGF receptor VEGFR-1 and compositions thereof. The present invention is also directed to methods of using such isolated mammalian stem cells expressing VEGFR-1 to treat various conditions, which can involve inducing hematopoiesis, vasculogenesis and/or angiogenesis, myogenesis, and neurogenesis to treat the various condition. Finally, the present invention is directed to therapeutic methods using a molecule that binds and activates or stimulates VEGFR-1, for example, P1GF, to stimulate proliferation and/or differentiation and mobilization, i.e., motogenesis, of stem cells.

Abstract: The present invention is directed to methods of inhibiting tumor cells by administering an antagonist which inhibits the VEGF/VEGFR-1 autocrine loop of tumor cells. Additional antagonists can be added to inhibit endothelial paracrine loop by inhibiting other VEGFRs expressed on endothelial cells, particularly VEGFR-2. Examples of antagonists include antibodies and small molecules. A preferred cancer for treatment is breast cancer.