Abstract: The present invention relates to the identification of a novel role of CXCR-4 in cell transformation and aberrant cellular proliferation. In particular, the present invention relates to the altered gene expression of CXCR-4 in a number of primary tumors and cell lines derived from tumors, in addition to, the altered gene expression of ligands for CXCR-4. Further, the present invention relates, in part, to the Applicants' surprising discovery that the inhibition of CXCR-4 gene expression or the inhibition of CXCR-4 activity in transformed cells reverses the transformed phenotype.

Abstract: The present invention provides tangential flow filtration devices and methods for enriching a heterogenous mixture of blood constituents for leukocytes by removal of non-leukocyte blood constituents. In one particular embodiment the device can provide a composition enriched in monocytes.

Abstract: The present invention relates to the identification of a novel role of CXCR-4 in cell transformation and aberrant cellular proliferation. In particular, the present invention relates to the altered gene expression of CXCR-4 in a number of primary tumors and cell lines derived from tumors, in addition to, the altered gene expression of ligands for CXCR-4. Further, the present invention relates, in part, to the Applicant's surprising discovery that the inhibition of CXCR-4 gene expression or the inhibition of CXCR-4 activity in transformed cells reverses the transformed phenotype.

Abstract: Methods and compositions for use of human dendritic cells to activate T cells for immunotherapeutic responses against primary and metastatic prostate cancer are disclosed. In one embodiment, human dendritic cells, after exposure to a prostate cancer antigen or specific antigenic peptide, are administered to a prostate cancer patient to activate the relevant T cell responses in vivo. In an alternate embodiment, human dendritic cells are exposed to a prostate cancer antigen or specific antigenic peptide in vitro and incubated or cultured with primed or unprimed T cells to activate the relevant T cell responses in vitro. The activated T cells are then administered to a prostate cancer patient. Methods and compositions for human dendritic cells with extended life span and cryopreserved dendritic cells are disclosed.

Abstract: The present invention provides methods for inducing the maturation of immature dendritic cells (DC) and for activating those cells without the use of a dendritic cell maturation agent. The activated DC can be used for inducing an antigen specific T cell response. Methods of the invention can also comprise the addition of a directional maturation agent, such as interferon gamma, to induce a Th-1 and/or Th-2 bias in the response obtained. The present invention also provides dendritic cell populations useful for activating and for inducing antigen specific T cells. Similarly, activated antigen specific T cell populations, and methods of making the same are provided.

Abstract: The present invention provides methods and compositions for the inhibition of proliferation rate of target cells, for example tumor cells. In particular, a nucleic acid encoding a connexin protein, fragment, derivative or analog thereof can be incorporated into a target cell. Expression of the nucleic acid sequence encoding the connexin protein, fragment, derivative or analog thereof, particularly connexin 43 and non-phosphorylated connexin 43, reduces the level of bc1-2 expression in the cells thereby inducing the cells to enter apoptosis. Connexin protein, fragments, derivatives, or analogs thereof can also be administered to the cell population to reduce bc1-2 expression inducing apoptosis in the cell population. It has further been found that the addition of an antagonist of MCP-1 activity can enhance the effects of connexin on tumor cell proliferation. Also, the prognosis of a subject undergoing standard chemotherapy can be assessed by correlating the expression levels of connexin and bc1-2.

Abstract: The present invention provides tangential flow filtration devices and methods for enriching a heterogenous mixture of blood constituents for leukocytes by removal of non-leukocyte blood constituents. In one particular embodiment the device can provide a composition enriched in monocytes.

Abstract: The present invention provides methods for enriching a heterogenous mixture of bone marrow or blood constituents for stem cells by removal of non-stem cell constituents comprising separation of the non-stem cell constituents using a tangential flow filtration device.

Abstract: The present invention provides tangential flow filtration devices and methods for enriching a heterogeneous mixture of blood constituents for leukocytes by removal of non-leukocyte blood constituents. In one particular embodiment the device can provide a composition enriched in monocytes. One embodiment includes a remover unit (1) having a crossflow chamber (3) separated by a microporous filter (5) from a filtrate chamber (4), the remover unit (1) also having a tangential flow inlet (6), a fluid outlet (7) for a fluid enriched in leukocytes and a filtrate outlet (8).

Abstract: The present invention relates to the identification of a novel role of CXCR-4 in cell transformation and aberrant cellular proliferation. In particular, the present invention relates to the altered gene expression of CXCR-4 in a number of primary tumors and cell lines derived from tumors, in addition to, the altered gene expression of ligands for CXCR-4. Further, the present invention relates, in part, to the Applicant's surprising discovery that the inhibition of CXCR-4 gene expression or the inhibition of CXCR-4 activity in transformed cells reverses the transformed phenotype.

Abstract: The present invention relates to monoclonal antibodies that bind to the extracellular domain of prostate-specific membrane antigen (PSMA), hybridoma cell lines producing the antibodies, and methods of using such antibodies for diagnosis and treatment of cancer. In particular, thirty-five monoclonal antibodies reactive with PSMA expressed on the cell surface are exemplified. Additionally, the present invention relates to a novel protein variant (PSM?) of PSMA detected by a number of the antibodies of the invention. The hydrolase activity of PSMA and PSM? allows the use of an immunoenzymatic assay for their detection.

Abstract: The present invention provides methods for inducing the maturation of immature dendritic cells (DC) and for activating those cells without the use of a dendritic cell maturation agent. The activated DC can be used for inducing an antigen specific T cell response. Methods of the invention can also comprise the addition of a directional maturation agent, such as interferon gamma, to induce a Th-I and/or Th-2 bias in the response obtained. The present invention also provides dendritic cell populations useful for activating and for inducing antigen specific T cells. Similarly, activated antigen specific T cell populations, and methods of making the same are provided.

Abstract: The present invention provides methods and compositions for the inhibition of proliferation rate of target cells, for example tumor cells. In particular, a nucleic acid encoding a connexin protein, fragment, derivative or analog thereof can be incorporated into a target cell. Expression of the nucleic acid sequence encoding the connexin protein, fragment, derivative or analog thereof, particularly connexin 43 and non-phosphorylated connexin 43, reduces the level of bcl-2 expression in the cells thereby inducing the cells to enter apoptosis. Connexin protein, fragments, derivatives, or analogs thereof can also be administered to the cell population to reduce bcl-2 expression inducing apoptosis in the cell population. It has further been found that the addition of an antagonist of MCP-1 activity can enhance the effects of connexin on tumor cell proliferation. Also, the prognosis of a subject undergoing standard chemotherapy can be assessed by correlating the expression levels of connexin and bcl-2.

Abstract: The present invention relates to monoclonal antibodies that bind to the extracellular domain of prostate-specific membrane antigen (PSMA), hybridoma cell lines producing the antibodies, and methods of using such antibodies for diagnosis and treatment of cancer. In particular, thirty-five monoclonal antibodies reactive with PSMA expressed on the cell surface are exemplified. Additionally, the present invention relates to a novel protein variant (PSM?) of PSMA detected by a number of the antibodies of the invention. The hydrolase activity of PSMA and PSM? allows the use of an immunoenzymatic assay for their detection.

Abstract: The present invention relates to monoclonal antibodies that bind to the extracellular domain of prostate-specific membrane antigen (PSMA), hybridoma cell lines producing the antibodies, and methods of using such antibodies for diagnosis and treatment of cancer. In. particular, thirty-five monoclonal antibodies reactive with PSMA expressed on the cell surface are exemplified. Additionally, the present invention relates to a novel protein variant (PSM?) of PSMA detected by a number of the antibodies of the invention. The hydrolase activity of PSMA and PSM? allows the use of an immunoenzymatic assay for their detection.

Abstract: The present invention relates to the identification of a novel role of Nr-CAM in cell transformation and aberrant cellular proliferation. In particular, the present invention relates to the altered gene expression of Nr-CAM in a number of primary tumors and cell lines derived from tumors, in addition to, the altered gene expression of ligands for Nr-CAM. Further, the present invention relates, in part, to the Applicants' surprising discovery that the inhibition of Nr-CAM gene expression or the inhibition of Nr-CAM activity in transformed cells reverses the transformed phenotype.

Abstract: The present invention relates to monoclonal antibodies that bind to the extracellular domain of prostate-specific membrane antigen (PSMA), hybridoma cell lines producing the antibodies, and methods of using such antibodies for diagnosis and treatment of cancer. In particular, thirty-five monoclonal antibodies reactive with PSMA expressed on the cell surface are exemplified. Additionally, the present invention relates to a novel protein variant (PSM?) of the PSMA detected by a number of the antibodies of the invention. The hydrolase activity of PSMA and PSM? allows the use of an immunoenzymatic assay for their detection.

Abstract: The present invention relates to the identification of a novel role of CXCR-4 in cell transformation and aberrant cellular proliferation. In particular, the present invention relates to the altered gene expression of CXCR-4 in a number of primary tumors and cell lines derived from tumors, in addition to, the altered gene expression of ligands for CXCR-4. Further, the present invention relates, in part, to the Applicants' surprising discovery that the inhibition of CXCR-4 gene expression or the inhibition of CXCR-4 activity in transformed cells reverses the transformed phenotype.

Abstract: The present invention relates to the identification of a novel role of Nr-CAM in cell transformation and aberrant cellular proliferation. In particular, the present invention relates to the altered gene expression of Nr-CAM in a number of primary tumors and cell lines derived from tumors, in addition to, the altered gene expression of ligands for Nr-CAM. Further, the present invention relates, in part, to the Applicants' surprising discovery that the inhibition of Nr-CAM gene expression or the inhibition of Nr-CAM activity in transformed cells reverses the transformed phenotype.

Abstract: The present invention provides methods and compositions for the inhibition of proliferation rate of target cells, for example tumor cells. In particular, a nucleic acid encoding a connexin protein, fragment, derivative or analog thereof can be incorporated into a target cell. Expression of the nucleic acid sequence encoding the connexin protein, fragment, derivative or analog thereof, particularly connexin 43 and non-phosphorylated connexin 43, reduces the level of bcl-2 expression in the cells thereby inducing the cells to enter apoptosis. Connexin protein, fragments, derivatives, or analogs thereof can also be administered to the cell population to reduce bcl-2 expression inducing apoptosis in the cell population. It has further been found that the addition of an antagonist of MCP-1 activity can enhance the effects of connexin on tumor cell proliferation. Also, the prognosis of a subject undergoing standard chemotherapy can be assessed by correlating the expression levels of connexin and bcl-2.