Abstract: Epithelial cell cancers and precancerous conditions are detected by assaying for LRAT expression. Failure to detect LRAT expression indicates presence of cancer, and detection of lower than normal level of LRAT expression indicates a precancerous condition.

Abstract: Apoptosis-related antigenic compounds comprising an exposed antigenic site having the amino acid sequence SEQ ID NO: 1: Glu Asp Phe Asn Leu Gly Asp Ala Leu Asp 1               5                    10 or a functionally equivalent sequence comprising at least the sequence Ala Leu Asp are disclosed.

Abstract: Disclosed are antibodies that specifically inhibit VEGF binding to only one (VEGFR2) of the two VEGF receptors. The antibodies effectively inhibit angiogenesis and induce tumor regression, and yet have improved safety due to their specificity. The present invention thus provides new antibody-based compositions, methods and combined protocols for treating cancer and other angiogenic diseases. Advantageous immunoconjugate and prodrug compositions.

Abstract: The present invention provides a family of BAG-1 related proteins from humans (BAG-1L, BAG-1, BAG-2, BAG-3, BAG-4 and BAG-5), the invertebrate C. elegans (BAG-1, BAG-2) and the fission yeast S. pombe (BAG-1A, BAG-1B) and the nucleic acid molecules that encode them.

Abstract: Tubedown-1 (tbdn-1), a protein associated with acetyltransferase activity has been characterized and its cDNA isolated. Tbdn-1 regulates endothelial differentiation through protein acetylation, DNA-binding or by interacting with and/or acetylating other protein targets important for endothelial differentiation. In normal adult eyes, tbdn-1 is expressed highly in the corneal endothelium proper and in the vascular endothelium of the limbus and retina. Tbdn-1 is absent or downregulated in the vascular endothelia of diseased and injured eyes, including eyes from patients with proliferative retinopathies involving neovascularization. Inhibition of tbdn-1 expression in endothelial cells in vitro indicates tbdn-1 acts as an inhibitor of angiogenesis. Thus, high levels of tbdn-1 expression present in normal ocular endothelial cells is associated with suppression of abnormal neovascularization in the eye demonstrating the therapeutic usefulness of tbdn-1 as a regulator of retinal angiogenesis.

Abstract: Antibodies that bind to a 40 kDa protein which is expressed on tumors, but is not expressed on normal adult hemopoietic cells are disclosed. Also disclosed are methods for production and the use of such antibodies.

Abstract: The invention relates to a novel process for preparation of a biomarker specific for O-acetylated sialic acid and useful for the diagnosis, monitoring outcome of treatment and prediction of relapse of acute lymphoblastic leukemia, said process comprising the steps of (I) separating serum from the blood of patients of acute lymphoblastic leukemia; (ii) separation of low molecular weight fractions and galactose binding proteins from the serum on affinity matrix; (iii) passing the galactose free protein fraction obtained in step (ii) over another affinity matrix to capture O-acetyl sialic acid specific protein fraction; (iv) eluting specific protein fraction with a buffer at alkaline pH in the range of 8.0-11.

Abstract: Although the mechanism of induction of apoptosis through antibody dependent cellular cytotoxicity (ADCC) mediated by NK cells is well understood, little is known about the fate of the reactive NK cells. Nevertheless, it has been shown that NK cells previously activated by IL-2, but not naive NK cells, died by apoptosis after Fc&ggr;RIIIa crosslinking, or after engagement in cytolytic functions. It is demonstrated that apoptosis of naive NK cells is also observed after stimulation with a rat IgG2b anti CD2 mAb (LO-CD2a/BTI-322) or anti HLAI (LO-HLA-1)mAb. The NK apoptosis is rapid (within minutes), Fas-ligand and mRNA synthesis independent and does not require a cell contact. The intracellular mechanism of NK cell apoptosis is calcium, PKC and PLA2 dependent but calcineurin and P13 kinase independent. We suggest that NK cell apoptosis results from the crosslinking on the same cell surface of CD2 or HLA-I molecules and Fc&ggr;RIIIa that exhibits a high affinity for the rat IgG2b isotype.

Abstract: The present invention relates to the use of 1-deamino-8-D-arginine vasopressin (desmopressin), or a pharmaceutically acceptable salt thereof or a pharmaceutical composition containing any of them, in the preparation of a medication which minimizes metastatic dissemination during cancer surgery. Additionally, the invention also relates to pharmaceutical compositions comprising the same and to a method of treating a mammal in order to inhibit metastatic spread during surgical extirpation of a cancer mass.

Abstract: The present invention is directed to a protein isolated from S. aureus that is the target of RAP, called TRAP, which is characterized by a molecular weight of about 21 KDa, is capable of being phosphorylated by RAP, and comprises an amino acid sequence of SEQ ID NO:2. In addition, the present invention is directed towards an antibody immunoreactive with TRAP that is preferably a monoclonal antibody or a humanized antibody but may be a polyclonal antibody. The invention provides a method of treating S. aureus infection by administering such a TRAP-inhibiting agent. The invention also features methods for identifying compounds that inhibit TRAP activity and/or inhibit TRAP-RAP interaction.

Abstract: The present invention relates to novel members of the Tumor Necrosis Factor family of receptors. The invention provides isolated nucleic acid molecules encoding human TR11, TR11SV1, and TR11SV2 receptors. TR11, TR11SV1, and TR11SV2 polypeptides are also provided, as are vectors, host cells and recombinant methods for producing the same. The invention further relates to screening methods for identifying agonists and antagonists of TR11, TR11SV1, and TR11SV2 receptor activity. The present invention further relates to antibodies that specifically bind TR11, TR11SV1, and/or TR11SV2. Also provided are diagnostic methods for detecting disease states related to the aberrant expression of TR11, TR11SV1, and TR11SV2 receptors. Further provided are therapeutic methods for treating disease states related to aberrant proliferation and differentiation of cells which express the TR11, TR11SV1, and TR11SV2 receptors.

Abstract: The present invention encompasses methods for determining the likelihood that benign hyperplastic breast tissue or normal breast tissue adjacent to carcinoma tissue will become malignant. The methods comprise substantially isolating the tissue; and determining loss of heterozygosity (LOH) at chromosome 3p24 in the tissue. LOH at chromosome 3p24 is a prognostic indicator that the tissue may become malignant.

Abstract: This invention generally relates to the nucleic acid sequences of a novel gene FAIM that encodes an apoptosis inhibiting protein. Furthermore, this invention relates to methods of identifying and testing antagonists of FAIM activity and screening for inter- and intra-specific homologs and mutants of FAIM.

Abstract: The invention provides isolated nucleic acid and amino acid sequences of HsKip3, antibodies to HsKip3, methods of screening for HsKip3a modulators using biologically active HsKip3, and kits for screening for HsKip3a modulators.

Abstract: The present invention provides a novel MHRII-associated protein designated MHRII-AP62 and antibodies immunoreactive with the MHRII-AP62 protein. Also provided are kits containing these antibodies and methods of using the antibodies for the detection of the MHRII-AP62 protein. The present invention also provides for a nucleic acid encoding the MHRII-AP62 protein and nucleic acid probes for use in the detection of the MHRII-AP62 protein. Further provided by the present invention are agents that mimic the activity of the MHRII-AP62 protein by binding to the MHRII, agents that inhibit the activity of the MHRII-AP62 protein by binding to the MHRII-AP62 protein, or by binding to the nucleic acid encoding the MHRII-AP62 protein, and methods of using these agents to treat cancer and cancer causing diseases.

Abstract: The present invention provides for isolated DNA and protein corresponding to novel melanoma tumor-associated antigens, antibodies directed towards the novel antigens of the present invention as well as methods of using the antigens for inhibiting the growth of a melanoma tumor and methods of screening compounds that inhibit the novel antigens of the present invention.

Abstract: The present invention features a method of producing a multimeric protein from a hybrid cell formed from the fusion of two or more cells, each of which cell is engineered to express one component of the multimeric protein, as well as a method for screening for successful fusion of the cells to produce a desired hybrid cell. The methods of the invention are widely applicable to the production of proteins having two or more components.

Abstract: Disclosed are methods of inhibiting proliferative diseases characterized by TGF-&bgr;-mediated angiogenesis.

Abstract: The invention relates to a peptide with the sequence of RLLEFYLAM, methods for the use of the peptide, and antisera and monoclonal antibodies against the peptide. The peptide is derived from the NY-ESO-1 molecule, which form complexes with HLA molecules, leading to lysis of cells presenting these complexes, by cytolytic T lymphocytes.

Abstract: A panel of biomarkers for the diagnosis and treatment of breast cancer was examined in the saliva of a cohort of 1) healthy women, 2) women with benign lesions of the breast and 3) women with diagnosed breast cancer. Recognized tumor markers c-erbB-2 (erb), cancer antigen 15-3 (CA 15-3), and tumor suppresser oncogene protein 53 (p53) were found in the saliva of all three groups of women. The levels of erb and CA 15-3 in the cancer patients evaluated, however, were significantly higher than the salivary levels of healthy controls and benign tumor patients. Conversely, pantropic p53 levels were higher in controls as compared to those women with breast cancer and those with benign tumors.