Abstract: Disclosed herein are antitumor compositions and methods of interfering with the biological activity of PC cell derived growth factor (PCDGF), anti-PCDGF receptor antibodies, fragments thereof, and methods of making anti-PCDGF receptor antibodies. The methods involve inhibiting the proliferation of tumor cells expressing the PCDGF receptor by contacting the surface of the cell with anti-PCDGF receptor antibodies. Anti-PCDGF receptor antibodies are capable of binding to the surface of a cell and interfering with the binding of PCDGF to its receptor. Also provided are compositions comprising anti-PCDGF receptor antibodies and cytotoxic molecules (e.g., toxins, oncotoxins, mitotoxins, immunotoxins, and antisense oligonucleotides).

Abstract: Embodiments of the invention provide methods and compositions for method for diagnosing and treating diseases including cancer. In one embodiment diagnosing tumorigenicity is accomplished by measuring the level of PCDGF receptor expression in a tissue sample suspected of being tumorigenic. In another embodiment, a determination of whether tumorigenic cells will be responsive to an anti-PCDGF therapy is accomplished by determining whether there is a measured level of PCDGF receptor in a tissue sample suspected of being tumorigenic. In yet another embodiment, a method for treating a subject having a disease related to the amplification or overexpression of PCDGF includes administering a PCDGF receptor or fragment thereof to a patient in amounts effective to inhibit the biological activity of PCDGF. The invention also provides isolated PCDGF receptor nucleic acid molecules and proteins encoded by the PCDGF receptor nucleic acid molecules.

Abstract: Methods and compositions for restoring sensitivity to the antitumorigenic effects of antiestrogen therapy and/or cytotoxic therapy and inducing cell apoptosis are provided. Contacting tumor cells to GP88 antagonists (e.g., anti-GP88 antibodies, anti-GP88 antisense nucleic acids, GP88 siRNA, and small molecules) induces apoptosis and restores sensitivity to the antitumorigenic effects of antiestrogen therapy and cytotoxic therapy.

Abstract: Methods and compositions for restoring sensitivity to the antitumorigenic effects of antiestrogen therapy and/or cytotoxic therapy and inducing cell apoptosis are provided. Contacting tumor cells to GP88 antagonists (e.g., anti-GP88 antibodies, anti-GP88 antisense nucleic acids, GP88 siRNA, and small molecules) induces apoptosis and restores sensitivity to the antitumorigenic effects of antiestrogen therapy and cytotoxic therapy.

Abstract: Novel monoclonal antibodies and binding fragments thereof specific to human breast cancer, lung cancer, colon cancer and other cancers. The monoclonal antibody does not bind to the cell surface of normal human tissues. The corresponding cancer-specific antigen with an apparent molecular weight of 150 kd and polynucleotides encoding the antigen and the CDR regions of the antibody are Also disclosed are methods for diagnosis, prognosis and treatment of human breast cancer. The antibodies have tumor specificity and are useful for therapy, diagnosis, monitoring, detecting and imaging of cancers. The antibody-recognized cancer-specific surface antigens can serve as targets for detecting, diagnosing, inhibiting or killing cancer cells.

Abstract: Novel monoclonal antibodies and binding fragments thereof specific to human breast cancer, lung cancer, colon cancer and other cancers. The monoclonal antibody does not bind to the cell surface of normal human tissues. The corresponding cancer-specific antigen or antigens with an apparent molecular weight of 40-52 130-200 kDa and polynucleotides encoding the antigen and the CDR regions of the antibody are also disclosed, as well as methods for diagnosis, prognosis and treatment of human breast cancer. The antibodies have tumor specificity and are useful for therapy, diagnosis, monitoring, detecting and imaging of cancers. The antibody-recognized cancer-specific surface antigens can serve as targets for detecting, diagnosing, inhibiting or killing cancer cells.

Abstract: Disclosed herein are methods of increasing the proliferation of non-tumorigenic B cells. The methods involve administering PCDGF and optionally other B cells stimulators (e.g., IgM, LPS) to B cells resulting in an increase in B cell proliferation. The methods of the invention can be used, for example, to establish B cells lines, to sort B cells from a mixed population of cells, or to activate resting B cells.

Abstract: Methods and compositions for breast cancer treatment and prevention by inducing overexpression of adipose differentiation related protein (ADRP) in the cancer cells. Over expression of ADRP causes breast cancer cells to re-differentiate, whereby cancer cell proliferation and tumorigenesis is inhibited and cancer cells are induced to undergo apoptosis. Also disclosed are pharmaceutical compositions comprising polynucleotides encoding ADRP, ADRP polypeptides or analogs or mimetics thereof, and methods for screening for ADRP agonists.

Abstract: Methods and kits for diagnosing tumorigenicity by measuring the concentration of GP88 in blood, plasma, serum, saliva, urine and other biological fluids. The methods and kits detect GP88 in biological fluids at a concentration as low as about 0.1 to 10 nanograms per milliliter and are useful for determining whether a patient has a tumorigenic condition, whether the patient is likely to be responsive to anti-tumorigenic therapies, and whether the treated patient is responding to anti-tumorigenic therapy by measuring the concentration of GP88 in the patient's serum or other biological fluid.

Abstract: Methods and compositions for restoring growth inhibition sensitivity to a tumor cell resistant to growth inhibition by HER2 antagonists. The methods involve administering a PCDGF antagonist to the cell in an amount effective to stimulate or restore growth inhibition sensitivity to HER2 antagonists. The invention also provides treatment regimens, and therapeutic compositions comprising an HER2 antagonist and a PCDGF antagonist.

Abstract: Methods and kits for diagnosing tumorigenicity and for determining whether a cancer patient is resistant to the pharmacological effects of antiestrogen therapy. Increased levels of the PCDGF (GP88) growth factor are indicative of tumorigenicity and resistance to the pharmacological effects of antiestrogen therapy. The methods and kits of the invention are useful for assessing the tumorigencity of a biological sample from a patient and determining whether the patient is a candidate for antiestrogen, including tamoxifen, therapy.

Abstract: Methods and compositions for restoring sensitivity to the antitumorigenic effects of antiestrogen therapy and/or cytotoxic therapy and inducing cell apoptosis are provided. Contacting tumor cells to GP88 antagonists (e.g., anti-GP88 antibodies, anti-GP88 antisense nucleic acids, GP88 siRNA, and small molecules) induces apoptosis and restores sensitivity to the antitumorigenic effects of antiestrogen therapy and cytotoxic therapy.

Abstract: Novel monoclonal antibodies and binding fragments thereof specific to human breast cancer, lung cancer, colon cancer and other cancers. The monoclonal antibody does not bind to the cell surface of normal human tissues. The corresponding cancer-specific antigen with an apparent molecular weight of 150 kd and polynucleotides encoding the antigen and the CDR regions of the antibody are Also disclosed are methods for diagnosis, prognosis and treatment of human breast cancer. The antibodies have tumor specificity and are useful for therapy, diagnosis, monitoring, detecting and imaging of cancers. The antibody-recognized cancer-specific surface antigens can serve as targets for detecting, diagnosing, inhibiting or killing cancer cells.

Abstract: This invention relates to products and methods for treating cancer and for diagnosing tumorigenicity and other diseases associated with alteration in GP88 expressing or action. Antagonists to an 88 KDa autocrine growth and tumorigenicity stimulator are provided which inhibit its expression or biological activity. The antagonists include antisense oligonucleotides and antibodies.

Abstract: This invention relates to products and methods for treating cancer and for diagnosing tumorigenicity and other diseases associated with alteration in GP88 expression or action. Antagonists to an 88 KDa autocrine growth and tumorigenicity stimulator are provided which inhibit its expression or biological activity. The antagonists include antisense oligonucleotides and antibodies.

Abstract: This invention relates to products and methods for treating cancer and for diagnosing tumorigenicity and other diseases associated with alteration in GP88 expression or action. Antagonists to an 88 KDa autocrine growth and tumorigenicity stimulator are provided which inhibit its expression or biological activity. The antagonists include antisense oligonucleotides and antibodies.

Abstract: This invention relates to products and methods for treating cancer and for diagnosing tumorigenicity and other diseases associated with alteration in GP88 expression or action. Antagonists to an 88 KDa autocrine growth and tumorigenicity stimulator are provided which inhibit its expression or biological activity. The antagonists include antisense oligonucleotides and antibodies.

Abstract: Disclosed herein are compositions and methods for reducing the growth of hematopoietic malignant cells (e.g., B-cell leukemia cells). The methods involve reducing the growth of hematopoietic malignant cells by contacting hematopoietic malignant cells with GP88 antagonists. GP88 is an 88 KDa autocrine growth factor that promotes the growth of hematopoictic malignant cells. Antagonists to GP88 are provided which inhibit its expression or biological activity. The antagonists include antisense oligonucleotides and antibodies. Also provided are methods for determining if a patient is responding or is responsive to anti-cancer therapy (e.g., glucocorticoid therapy). Increased levels of GP88 in hematopoietic cells indicates a patient is not responding or responsive to anti-cancer therapy.

Abstract: Methods and kits for diagnosing tumorigenicity by measuring the concentration of GP88 in blood, plasma, serum, saliva, urine and other biological fluids. The methods and kits detect GP88 in biological fluids at a concentration as low as about 0.1 to 10 nanograms per milliliter and are useful for determining whether a patient has a tumorigenic condition, whether the patient is likely to be responsive to anti-tumorigenic therapies, and whether the treated patient is responding to anti-tumorigenic therapy by measuring the concentration of GP88 in the patient's serum or other biological fluid.

Abstract: Disclosed herein are antitumor compositions and methods of interfering with the biological activity of PC cell derived growth factor (PCDGF), anti-PCDGF receptor antibodies, fragments thereof, and methods of making anti-PCDGF receptor antibodies. The methods involve inhibiting the proliferation of tumor cells expressing the PCDGF receptor by contacting the surface of the cell with anti-PCDGF receptor antibodies. Anti-PCDGF receptor antibodies are capable of binding to the surface of a cell and interfering with the binding of PCDGF to its receptor. Also provided are compositions comprising anti-PCDGF receptor antibodies and cytotoxic molecules (e.g., toxins, oncotoxins, mitotoxins, immunotoxins, and antisense oligonucleotides).