Abstract: Methods and compositions for treating cancer, particularly breast cancer, are disclosed.

Abstract: The present invention is based, in part, on the identification of novel antibodies that have binding affinity for both PD-L1 and PD-L2 and methods of using same. In one aspect, an isolated monoclonal antibody, or antigen-binding fragment thereof, which specifically binds both PD-L1 and PD-L2, is provided. In one embodiment, both PD-L1 and PD-L2 are human PD-L1 and human PD-L2.

Abstract: The invention includes the use of the HE/HE4a markers to assess ovarian cancer in a subject. Included also are compositions and methods of using HE/HE4a marker for diagnosis, grading and staging of ovarian cancers, determining prognosis and treatment effectiveness of a subject who has been diagnosed with ovarian cancer.

Abstract: Described herein are materials and methods for treating subjects having a HER-3 associated disease, by administering a first agent that binds to HER-3, in combination with a second agent that binds and/or inhibits another member of the HER family. The first and the second agent may be a biologic, such as an antigen-binding protein, or a small molecular tyrosine kinase inhibitor, for example.

Abstract: The present invention provides MT4-MMP inhibitor and EGFR inhibitor for use in the treatment of cancer, wherein said MT4-MMP inhibitor and EGFR inhibitor are different from each other. MT4-MMP (MMP-17) is a glycosylphosphatidyl inositol (GPI) anchored MMP produced by cancer cells that promotes tumor vascularization and metastases. The present invention found that MT4-MMP expression promotes cancer cell proliferation. These effects involve retinoblastoma protein (Rb) inactivation, cyclin dependent kinase CDK4 activation and Epidermal Growth Factor Receptor (EGFR) signaling. Co-immuno-precipitations indicate the existence of protein complexes harboring MT4-MMP and EGFR. The present invention further found a novel mechanism of MT4-MMP action through an outside-in signaling involving EGFR. An unexpected crosstalk between an MMP and EGFR was identified and recognized as a key driver of cancer cell biology.

Abstract: The invention relates to anti-HER3/HER4 antigen binding proteins, e.g. anti-HER3/HER4 antibodies, that bind to the beta-hairpin of HER3 and the beta-hairpin of HER4, methods for selecting these antigen binding proteins, their preparation and use as medicament.

Abstract: The invention relates to anti-HER3 antigen binding proteins, e.g. anti-HER3 antibodies, that bind to the beta-hairpin of HER3, methods for selecting these antigen binding proteins, their preparation and use as medicament.

Abstract: This invention relates to a composition of a non-labeled monoclonal antibody binding to a tumor antigen and a second monoclonal antibody labeled with a NIR fluorescence label, binding to the same tumor antigen, wherein the first and second antibody exhibit no cross reactivity. The composition can be used for the treatment of patients suffering of solid tumors which are associated with an overexpression of such a tumor antigen. The invention further relates to a the co-administration of said first and second antibody as wells as to a method of acquiring a NIR fluorescence images of such tumors or the patients suffering from such tumors during the treatment of said patient with such composition.

Abstract: The present invention describes methods and pharmaceutical compositions for the treatment of cancer in mammals, more particularly in human subjects. More specifically, the invention concerns anti-tumor vaccines based upon plasmid DNA and/or genetic vectors carrying a codon-usage optimized sequence and coding for a mutant form of the ErbB-3 receptor. Furthermore, the invention refers to monoclonal antibodies directed against the ErbB-3 receptor, obtained using these methods and capable to block its activity in cancer cells.

Abstract: The subject invention discloses a method for determining the prognosis and probable clinical course of a subject diagnosed with B-CLL. Specifically, the invention involves comparing CD38 expression in a biological sample from the subject containing B-CLL cells to a baseline level of CD38 expression, wherein an elevated level of CD38 expression in relation to the baseline level of CD38 expression may indicate poor prognosis or aggressive course of disease in the subject. Also disclosed is a method for determining whether the Ig V genes of the B-CLL cells of a B-CLL patient are mutated, comprising comparing CD38 expression in a biological sample from the subject containing B-CLL cells to a baseline level of CD38 expression, wherein a lower level of CD38 expression in relation to the baseline level indicates IG V gene mutation.

Abstract: Chimeric ErbB ligand binding molecules having detectable binding activity for more ErbB ligands than any one of native ErbB1, ErbB3 or ErbB4 are disclosed. Preferably, the binding molecules bind a broad spectrum and, more preferably, the full spectrum of ErbB ligands. The chimeric ErbB ligand binding molecules generally have a subunit LI derived from one of Erb-B1, 3, or 4 and a subunit LII derived from another distinct ErbB receptor type. The sub-domain, SI, which joins LI and LII can be from either one of the receptor types or can have portions from both. Pharmaceutical compositions that contain the molecules and methods for the treatment of ErbB sensitive diseases are also disclosed.

Abstract: This invention relates to novel monoclonal antibodies that specifically bind to the alpha-folate receptor. In some embodiments, the antibodies inhibit a biological activity of folate receptor-? (FR-?). The antibodies are useful in the treatment of certain cancers, particularly cancers that have increased cell surface expression of the alpha-folate receptor (“FR-?”), such as ovarian, breast, renal, colorectal, lung, endometrial, or brain cancer. The invention also relates to cells expressing the monoclonal antibodies, antibody derivatives, such as chimeric and humanized monoclonal antibodies, antibody fragments, and methods of detecting and treating cancer using the antibodies, derivatives, and fragments.

Abstract: This invention relates to novel monoclonal antibodies that specifically bind to the alpha-folate receptor. In some embodiments, the antibodies inhibit a biological activity of folate receptor-? (FR-?). The antibodies are useful in the treatment of certain cancers, particularly cancers that have increased cell surface expression of the alpha-folate receptor (“FR-?”), such as ovarian, breast, renal, colorectal, lung, endometrial, or brain cancer. The invention also relates to cells expressing the monoclonal antibodies, antibody derivatives, such as chimeric and humanized monoclonal antibodies, antibody fragments, and methods of detecting and treating cancer using the antibodies, derivatives, and fragments.

Abstract: Anti-human B7-H4 antibody “6H3”, antigen-binding fragments, derivatives, and humanized variants thereof that are capable of immunospecifically binding to B7-H4, and the uses of such molecules in the diagnosis and the treatment of cancer and other diseases are disclosed. In preferred embodiments, the molecules are used to retard or prevent tumor growth, inhibit tumor-mediated suppression, eliminate tumors and/or deplete or block the activity of tumor-associated macrophages (“TAMs”) so as to alter their activity and/or decrease TAM-mediated immune suppression.

Abstract: The invention relates to methods and related products for treatment and determining modes of treatment for cancer or prognosis of cancer. Preferably the methods are related to the induction of CD80 in p53 responsive cancer cells.

Abstract: Provided is a method for evaluating test agents as candidates for treating prostatic diseases, including benign prostatic hyperplasia and androgen dependent and androgen independent prostate cancer. The method comprises providing a mouse comprising a human prostate primary xenograft, where the xenograft contains blood vessels that include human endothelial cells, initiating androgen deprivation in the mouse, administering to the mouse a test agent within a period of 1-7 days after initiating the androgen deprivation, and determining a reduction in human epithelial cells in the xenografts and/or a reduction in number of the endothelial cells or blood vessels in the xenograft. Also provided is a method for treating an individual for human prostate cancer or benign prostatic hyperplasia.

Abstract: P-Selectin on platelets and endothelium binds cell surface chondroitin sulfate (CS) proteoglycans, which are abundantly and stably expressed on the surface many cancer cells. Binding of the cancer cells through the CS moieties may be blocked to inhibit the interaction of cancer cells with platelets and endothelium. The present inventors disclose compositions and methods for the inhibition of cancer metastasis.

Abstract: The invention provides neuregulin antagonists and methods of using the neuregulin antagonists in delaying the time to tumor recurrence or preventing resistance of cancer cells to treatment with a therapeutic agent.

Abstract: The present invention relates to methods of diagnosing and methods of treating hepatocellular carcinoma in a subject. The invention also relates to antagonists of PLVAP proteins, such as antibodies that specifically bind PLVAP proteins, as well as compositions and kits comprising antagonists of PLVAP proteins. The invention further relates to humanized antibodies that specifically bind PLVAP protein.

Abstract: An isolated truncated desmoglein 4 (DSG4) polypeptide splice variant of the invention is characterized by an amino acid sequence that lacks a region encoded before exon 9 or beyond exon 10 of the DSG4 gene having the polynucleotide sequence of SEQ ID NO: 75. Also disclosed is a method of diagnosing a cancer, or monitoring the course thereof, in a patient. The method comprises detecting in a tissue sample of a patient the expression of a tumor-associated antigen comprising the extracellular domain of a DSG4 polypeptide encoded by a DSG4 gene having the polynucleotide sequence of SEQ ID NO: 75, or a truncated DSG4 polypeptide splice variant characterized by an amino acid sequence that lacks a region encoded before exon 9 or beyond exon 10 of the DSG4 gene.