Abstract: Peptides that stimulate subcutaneous adipogenesis in mammals and uses thereof are provided.

Abstract: Peptides of 5 to 14 amino acids in length that stimulate subcutaneous adipogenesis and uses thereof are provided.

Abstract: Peptides of 5 to 14 amino acids in length that stimulate subcutaneous adipogenesis in mammals and uses thereof are provided.

Abstract: Peptides that stimulate subcutaneous adipogenesis in mammals and uses thereof are provided.

Abstract: Herein are described synthetic organotypic microvascular niches formed by self-assembly of stromal cells cultured endothelial cells seeded with cells of interest to model and determine dormancy state of these cells of interest in these tissues. These models demonstrated that endothelial-derived thrombospondin-1 induces sustained cancer cell quiescence. We further describe dormancy models, and identified active tumor-promoting, endothelial tip cell-derived factors. Our work reveals that stable microvasculature constitutes a ‘dormant niche,’ whereas sprouting neovasculature sparks micrometastatic outgrowth.

Abstract: CD44 is an integral hyaluronan receptor that can either promote or inhibit motogenic signaling in tumor cells. Rhamm is a non-integral cell surface (CD168) and intracellular hyaluronan binding protein that promotes cell motility in vitro and whose expression is strongly upregulated in aggressive tumors. The present invention describes compositions and methods for the prognosis and diagnosis of cancer by the detection of CD44/Rhamm complexes. The use of labeled Rhamm-binding agents in culture and in vivo to identify tumorigenic progenitor cells that exhibit an aggressive phenotype characterized by high Rhamm and CD44 expression is further described. Specific methods include using hyaluronan to target imaging or therapeutic agents to these progenitor tumor subsets in breast and likely other cancers.

Abstract: The application describes therapeutic compositions and methods for treating cancer. For example, therapeutic compositions and methods related to inhibition of FAM83A (family with sequence similarity 83) are provided. The application also describes methods for diagnosing cancer resistance to EGFR inhibitors. For example, a method of diagnosing cancer resistance to EGFR inhibitors by detecting increased FAM83A levels is described.

Abstract: Peptides of 5 to 14 amino acids in length that stimulate subcutaneous adipogenesis in mammals and uses thereof are provided.

Abstract: The present invention provides compositions and methods for inhibiting MMPs, especially MMP-3, MMP-9 and MMP-14. The invention relates to the field of diagnostic and prognostic methods of human cancers, especially breast cancer and the field of matrix metalloproteases, as targets for diagnostics and therapeutics.

Abstract: Peptides of 5 to 14 amino acids in length that stimulate subcutaneous adipogenesis and uses thereof are provided.

Abstract: Herein is described the methods and compositions for modulation of Rhamm, also known as CD 186, and its effects on wound repair, muscle differentiation, bone density and adipogeneisis through its ability to regulate mesenchymal stem cell differentiation. Compositions and methods are provided for blocking Rhamm function for selectively increasing subcutaneous, but not, visceral fat. Compositions and methods for modulating Rhamm in wound repair are also described.

Abstract: Methods are provided for the rapid and robust screening test agents for adipogenic activity. Agents testing positive in the assays are good candidate agents for wrinkle reduction, normalizing skin appearance after reconstructive or cosmetic surgery, e.g., grafted tissue on burn victims, normalizing skin appearance during and after wound healing, and the like. In certain embodiments the methods involve providing mammalian test cells with adipogenic potential wherein said cells are primed for, but withheld from differentiation into adipocytes; contacting the cells with the test agent(s); and screening said test cells for an adipocyte phenotype wherein the presence of a feature characteristic of an adipocyte is an indicator that said test agent is adipogenic.

Abstract: The present invention provides methods, kits, and compositions for treating cancer with cytotoxic agents. Preferably, the cytotoxic agents are selected from: IL-25, BMP1O, FGF1 1, VDBP, ATIII and IL1-F7, and any combination thereof. In other preferred embodiments, the cancer is breast cancer. These agents can be supplied, for example, as proteins or as part of nucleic acid expression vector.

Abstract: Methods and compositions for using 14-3-3sigma gene and protein as a highly sensitive and specific basal breast cancer biomarker, which when present, correlates with metastasis and poor outcome in independent patient cohorts. Methods and compositions for targeting 14-3-3sigma-regulated actin cytoskeletal interactions, activity and function may benefit patients having the basal-like breast cancer subtype.

Abstract: A method for increasing or monitoring apoptosis in tumor cells by the co-administration of ionizing radiation and an anti-integrin antibody. Increasing apoptosis reduces tumor growth in vivo and in a cell culture model. The antibody is directed against the beta-1 integrin subunit and is inhibitory of beta-1 integrin signaling. Other molecules having an inhibitory effect on beta-1 integrin, either in signaling or in binding to its cognate extracellular receptors may also be used. The present method is particularly of interest in treatment of tumor cells associated with breast cancer, wherein radiation is currently used alone. The present method further contemplates a monoclonal antibody suitable for human administration that may further comprise a radioisotope attached thereto.

Abstract: The application describes therapeutic compositions and methods for treating cancer. For example, therapeutic compositions and methods related to inhibition of FAM83A (family with sequence similarity 83) are provided. The application also describes methods for diagnosing cancer resistance to EGFR inhibitors. For example, a method of diagnosing cancer resistance to EGFR inhibitors by detecting increased FAM83A levels is described.

Abstract: Herein is described the methods and compositions for modulation of Rhamm, also known as CD 186, and its effects on wound repair, muscle differentiation, bone density and adipogeneisis through its ability to regulate mesenchymal stem cell differentiation. Compositions and methods are provided for blocking Rhamm function for selectively increasing subcutaneous, but not, visceral fat. Compositions and methods for modulating Rhamm in wound repair are also described.

Abstract: CD44 is an integral hyaluronan receptor that can either promote or inhibit motogenic signaling in tumor cells. Rhamm is a non-integral cell surface (CD168) and intracellular hyaluronan binding protein that promotes cell motility in vitro and whose expression is strongly upregulated in aggressive tumors. The present invention describes compositions and methods for the prognosis and diagnosis of cancer by the detection of CD44/Rhamm complexes. The use of labeled Rhamm-binding agents in culture and in vivo to identify tumorigenic progenitor cells that exhibit an aggressive phenotype characterized by high Rhamm and CD44 expression is further described. Specific methods include using hyaluronan to target imaging or therapeutic agents to these progenitor tumor subsets in breast and likely other cancers.

Abstract: The present invention provides methods and compositions for the diagnosis and treatment of cells lacking normal growth arresting characteristic. The present invention demonstrates that many tumor cells lack normal cell surface ?-dystroglycan and thereby lack dystroglycan function. Dystroglycan can be lost from the cell surface by proteolytic shedding of a fragment of ?-dystroglycan into the surrounding medium. Upon restoration of dystroglycan function and over-expression of the dystroglycan gene, the once tumorigenic cells revert to non-tumorigenic cells which polarize and arrest cell growth in the presence of basement membrane proteins, demonstrating that dystroglycan functions as a tumor marker and suppressor.

Abstract: A method for increasing or monitoring apoptosis in tumor cells by the co-administration of ionizing radiation and an anti-integrin antibody. Increasing apoptosis reduces tumor growth in vivo and in a cell culture model. The antibody is directed against the beta-1 integrin subunit and is inhibitory of beta-1 integrin signaling. Other molecules having an inhibitory effect on beta-1 integrin, either in signaling or in binding to its cognate extracellular receptors may also be used. The present method is particularly of interest in treatment of tumor cells associated with breast cancer, wherein radiation is currently used alone. The present method further contemplates a monoclonal antibody suitable for human administration that may further comprise a radioisotope attached thereto.