Abstract: This invention relates to the use of monoclonal and polyclonal antibodies that specifically bind to and have the ability in the alternative to become internalized by cells expressing endosialin and to induce an immune effector activity such as antibody-dependent cellular cytotoxicity. The antibodies are useful in specific delivery of pharmacologic agents to endosialin-expressing cells as well as in eliciting an immune-effector activity particularly on tumor and neovascular cells and precursors. The invention is also related to nucleotides encoding the antibodies of the invention, cells expressing the antibodies; methods of detecting cancer and neovascular cells; and methods of treating cancer and neovascular disease using the antibodies, derivatives and fragments.

Abstract: This invention relates to the staging, diagnosis, and treatment of cancerous diseases, particularly to the use of monoclonal antibodies, antigen binding fragments thereof, and/or cancerous disease modifying antibodies (CDMAB), optionally in combination with one or more CDMAB, chemotherapeutic agents, and conjugates thereof, as a means for initiating a cytotoxic response to human head and neck squamous cell carcinomas. The invention further relates to binding assays, which utilize the monoclonal antibodies, antigen binding fragments thereof, and/or CDMAB of the instant invention. The cancerous disease modifying antibodies can be conjugated to toxins, enzymes, radioactive compounds, cytokines, interferons, target or reporter moieties and hematogenous cells. In particular aspects, the CDMAB used in the methods of the invention is an anti-CD44 antibody, which may be the antibody produced by the hybridoma deposited with the ATCC having accession number PTA-4621 and/or a chimeric or humanized version thereof.

Abstract: This invention relates generally to monoclonal antibodies that recognize CD47, more specifically to CD47 antibodies that do not cause a significant level of agglutination of cells, to methods of generating these antibodies, and to methods of using these monoclonal antibodies as therapeutics.

Abstract: A composite polypeptide, said composite polypeptide comprising a desired polypeptide and an expression enhancing domain (“EED”), said EED comprising first and second cysteine amino acid residues Cys1 and Cys2, respectively, Cys1 being located closer to the N-terminus of the composite polypeptide molecule than Cys2, wherein Cys1 and Cys2 are separated by a polypeptide linker, said linker—being free of cysteine and proline;—defining a length sufficient to allow Cys1 and Cys2 to engage in an intramolecular disulfide bond with one another; and—having a flexible polypeptide conformation essentially free of secondary polypeptide structure in aqueous solution, wherein at least one of Cys1 and Cys2 is derivatized with a derivatization moiety.

Abstract: The present invention relates to articles of manufacture and methods for co-administration of antibodies and/or antibody-like molecules, and further concerns methods for intravenous administration of more than one antibody and/or antibody-like molecule to a subject in need from a stable mixture contained in the same article of manufacture, such as an intravenous infusion bag (IV bag).

Abstract: A method of modulating the plasma half-life of anti-glypican 3 antibody, a pharmaceutical composition comprising as an active ingredient the anti-glypican 3 antibody that has a plasma half-life that has been modulated, a method of preparing the anti-glypican 3 antibody and a pharmaceutical composition comprising the anti-glypican 3 antibody as an active ingredient are provided. Disclosed is a method of modulating the plasma half-life of anti-glypican 3 antibody by modifying an amino acid residue that is exposed on the surface of the anti-glypican 3 antibody; and anti-glypican 3 antibody that has a plasma half-life that has been modulated by amino acid residue modification, a pharmaceutical composition comprising as an active ingredient the anti-glypican 3 antibody, and a method of preparing the anti-glypican 3 antibody and producing a pharmaceutical composition comprising the anti-glypican 3 antibody as an active ingredient.

Abstract: Embodiments of the invention are directed to a method of inhibiting proliferation of a cell induced by asTF that includes exposing the proliferating cell to an inhibitor of asTF at a concentration sufficient to attenuate asTF induced proliferation. In an embodiment, the proliferating cell is a cancer cell such as a breast cancer cell. The inhibitor of asTF may be an anti-asTF antibody, such as a monoclonal antibody or an antibody fragment, a small molecule, a peptide, nucleic acid, and combinations thereof.

Abstract: The invention relates to the treatment and/or prevention of tumor diseases associated with cells expressing CLD-N6, in particular cancer and cancer metastasis using antibodies which bind to CLDN6. The present application demonstrates that the binding of antibodies to CLDN6 on the surface of tumor cells is sufficient to inhibit growth of the tumor and to prolong survival and extend the lifespan of tumor patients. Furthermore, binding of antibodies to CLDN6 is efficient in inhibiting growth of CLDN6 positive germ cell tumors such as teratocarcinomas or embryonal carcinomas, in particular germ cell tumors of the testis.

Abstract: The present invention discloses alpha particle emitting, radioactive constructs capable of killing large tumors (>1 mm in diameter), or other cells involved in human or animal diseases such as virus infected cells, autoimmune cells, or other pathological cells, including normal cells, that are targets for destruction, to achieve a therapeutic result. The alpha-emitting constructs have high specific activity.

Abstract: The present invention provides novel antibodies and functional fragments thereof specific for CD38, and methods of using the same for the treatment of diseases associated with CD38 expression, including hematological malignancies such as multiple myeloma.

Abstract: The present disclosure provides isolated monoclonal antibodies that specifically bind to CD22 with high affinity, particularly human monoclonal antibodies. Nucleic acid molecules encoding the antibodies of this disclosure, expression vectors, host cells and methods for expressing the antibodies of this disclosure are also provided. Antibody-partner molecule conjugates, bispecific molecules and pharmaceutical compositions comprising the antibodies of this disclosure are also provided. This disclosure also provides methods for detecting CD22, as well as methods for treating various cancers and inflammatory and autoimmune disorders using an anti-CD22 antibody of this disclosure.

Abstract: The present invention relates to the use of binding equivalents of monoclonal antibody 31.1, including chimerized and/or humanized versions thereof, antibody fragments as well as competitively binding and co-specific antibodies and antibody fragments, in the treatment of pancreatic cancer.

Abstract: The present disclosure provides isolated monoclonal antibodies, particularly human monoclonal antibodies, more particularly engineered antibodies resulting in increased binding to Fc receptors and/or increased potency for ADCC or immunoconjugates, which specifically bind to CADM1 with high affinity. Nucleic acid molecules encoding CADM1 antibodies, expression vectors, host cells and methods for expressing the CADM1 antibodies are also provided. Bispecific molecules and pharmaceutical compositions comprising the CADM1 antibodies are also provided. Methods for detecting CADM1, as well as methods for treating various cancers, including lung cancer and pancreatic cancer, are disclosed.

Abstract: The present invention provides a composition comprising naked humanized, chimeric, and human anti-CEA antibodies and a therapeutic agent, which is useful for treatment of CEA expressing cancers and other diseases, and methods of use in treatment using this composition.

Abstract: The present invention provides antibodies which bind to an epitope in the extracellular domain of human CC chemokine receptor 4 (CCR4) and which are capable of inhibiting the binding of macrophage-derived chemokine (MDC) and/or thymus and activation regulated chemokine (TARC) to CCR4. Also provided are inter alia immunoconjugates and compositions comprising such antibodies and methods and uses involving such antibodies, particularly in the medical and diagnostic fields.

Abstract: The present invention provides methods for reducing or inhibiting angiogenesis in a tissue, by contacting ?5?1 integrin in the tissue with an agent that interferes with specific binding of the ?5?1 integrin to a ligand expressed in the tissue. The invention further provides methods of reducing or inhibiting angiogenesis in a tissue in an individual, by administering to the individual an agent that interferes with the specific binding of ?5?1 integrin to a ligand expressed in the tissue; and methods of reducing the severity of a pathological condition associated with angiogenesis in an individual, by administering to the individual an agent that interferes with specific binding of ?5?1 integrin to a ligand in a tissue associated with the pathological condition.

Abstract: The present invention relates to the identification of membrane proteins associated with B-cell non-Hodgkin's lymphoma, breast cancer, cervical cancer, colorectal cancer, gastric cancer, glioblastoma, hepatocellular carcinoma, lung cancer, lymphoid leukaemia (particularly acute T-cell leukaemia and chronic lymphocytic leukaemia), melanoma, neuroblastoma, osteosarcoma, ovarian cancer, pancreatic cancer, prostate cancer, renal cell cancer and retinoblastoma which have utility as markers and for treatment of said cancers and which also form biological targets against which antibodies such as therapeutic antibodies (or other affinity reagents) or other pharmaceutical agents can be made.

Abstract: The present invention is related to the field of wound healing or tissue regeneration due to disease (i.e., for example, cardiovascular diseases, osetoarthritic diseases, or diabetes). In particular, the present invention provides compositions and methods comprising molecules with linked ?-gal epitopes for induction of an inflammatory response localized within or surrounding damaged tissue. In some embodiments, the present invention provides treatments for tissue repair in normal subjects and in subjects having impaired healing capabilities, such as diabetic and aged subjects.

Abstract: The invention relates to therapeutic conjugates with improved ability to target various cancer cells containing a targeting moiety and a therapeutic moiety. The targeting and therapeutic moieties are linked via an acid cleavable linkage that increases therapeutic efficacy of the immunoconjugate.

Abstract: An Fc variant of a parent Fc polypeptide, wherein said Fc variant exhibits altered binding to one or more Fc?Rs, wherein said Fc variant comprises at least one amino acid insertion in the Fc region of said parent Fc polypeptide.

Abstract: The present invention provides fully human monoclonal antibodies that specifically bind to GPNMB, and uses thereof. Nucleotide sequences encoding, and amino acid sequences comprising, heavy and light chain immunoglobulin molecules, particularly sequences corresponding to contiguous heavy and light chain sequences spanning the framework regions and/or complementarity determining regions (CDRs) are provided. The present invention also provides immunoconjugates comprising anti-GPNMB antibodies and methods of using such immunoconjugates. The present invention further provides methods of treating breast cancer using antibodies that bind to GPNMB, immunoconjugates and other derivatives thereof.

Abstract: The present invention relates to Fc variants having increased affinity for Fc?RIIb, methods for their generation, Fc polypeptides comprising optimized Fc variants, and methods for using optimized Fc variants.

Abstract: The present invention provides diagnostic and prognostic methods for predicting the effectiveness of treatment of a cancer patient with an IGF-1R kinase inhibitor. Methods are provided for predicting the sensitivity of tumor cell growth to inhibition by an IGF-1R kinase inhibitor, comprising assessing whether the tumor cell has undergone an epithelial to mesenchymal transition (EMT), by determining the expression level of epithelial and/or mesenchymal biomarkers, wherein tumor cells that have undergone an EMT are substantially less sensitive to inhibition by IGF-1R kinase inhibitors. Improved methods for treating cancer patients with IGF-1R kinase inhibitors that incorporate the above methodology are also provided.

Abstract: The present invention relates to optimized Fc variants, methods for their generation, and antibodies and Fc fusions comprising optimized Fc variants.

Abstract: The present invention relates to an in vitro method for assessing the risk that a subject suffers from a cancer, comprising measuring the expression level of Proline/arginine-rich end leucine repeat protein (PRELP) in cells from said subject, wherein an increased expression level of PRELP, as compared to healthy donors, indicates an increased probability of said subject suffering from cancer. It further relates to antibodies specific for PRELP and their use in diagnosis and therapy as well as a method for indicating a cell as a cancer cell.

Abstract: The present application relates to a variant Fc region comprising at least one modification relative to a wild-type human Fc region, where the modification selected from the group consisting of 434S, 252Y/428L, 252Y/434S, and 428L/434S, and the numbering is according to the EU index.

Abstract: Compositions and methods are provided for depletion of pluripotent cells. In one embodiment of the invention, methods are provided for depletion of pluripotent cells from a mixed population of differentiated cells and stem cells, to provide a population of cells substantially free of pluripotent stem cells. Monoclonal antibodies useful in depletion and in identification of pluripotent stem cells are also provided.

Abstract: The present invention relates to novel Fc variants that comprise at least one novel amino acid residue which may provide for enhanced effector function. More specifically, this invention provides Fc variants that have modified binding affinity to one or more Fc receptor or ligand (e.g., Fc gamma R, C1q). Additionally, the Fc variants have altered complement dependent cytotoxicity (CDC) activity and/or antibody-dependent cell-mediated cytotoxicity (ADCC). The invention further provides methods and protocols for the application of said Fc variants, particularly for therapeutic purposes.

Abstract: The present invention relates to trans-capsularly administering into a diseased joint a high specificity antagonist selected from the group consisting of: i) an inhibitor of a pro-inflammatory interleukin; ii) an inhibitor of TNF-? synthesis; iii) an inhibitor of membrane-bound TNF-?; iv) an inhibitor of a natural receptor of TNF-?; v) an inhibitor of NO synthase, vi) an inhibitor of PLA2 enzyme; vii) an anti-proliferative agent; viii) an anti-oxidant; ix) an apoptosis inhibitor selected from the group consisting of EPO mimetic peptides, EPO mimetibodies, IGF-I, IGF-II, and caspase inhibitors, and x) an inhibitor of MMPs; and xi) an inhibitor of p38 kinase.

Abstract: The present invention provides the TWEAK receptor and methods for identifying and using agonists and antagonists of the TWEAK receptor. In particular, the invention provides methods of screening for agonists and antagonists and for treating diseases or conditions mediated by angiogenesis, such as solid tumors and vascular deficiencies of cardiac or peripheral tissue.

Abstract: The present invention provides monoclonal IgE antibodies comprising Fc epsilon (?) constant regions and variable regions comprising at least one antigen binding region specific for binding a single epitope of a circulating, tumor-associated antigen (TAA) that is not a cell surface antigen wherein the epitope of the targeted antigen is not highly repetitive or is a non-repetitive epitope. The IgE antibodies of the invention are useful in the treatment of cancer associated with the tumor antigen. In one embodiment the TAA is prostate-specific antigen (PSA).

Abstract: Disclosed herein are isolated human monoclonal antibodies that specifically bind human mesothelin with a binding affinity of about 25 nM or less. Nucleic acids encoding these antibodies, expression vectors including these nucleic acid molecules, and isolated host cells that express the nucleic acid molecules are also disclosed. The antibodies can be used to detect human mesothelin in a sample. Methods of diagnosing cancer, or confirming a diagnosis of cancer, are disclosed herein that utilize these antibodies. Methods of treating a subject with cancer are also disclosed.

Abstract: The present invention is based, in part, on the discovery that galectin-1 (Gal1) plays a role in viral-associated PTLD, e.g., EBV-associated PTLD and hypoxia associated angiogenesis disorders. Accordingly, the invention relates to compositions, kits, and methods for diagnosing, prognosing, monitoring, treating and modulating viral-associated PTLD, e.g., EBV-associated PTLD and hypoxia associated angiogenesis disorders.

Abstract: A method of treating an autoimmune disease comprising administering to a patient a therapeutically effective amount of a CD20-binding polypeptide composition comprising a combination of a modified heavy chain variable region polypeptide and a modified light chain variable region polypeptide. The combination can be (a) a modified 2B8 antibody heavy chain variable region polypeptide of SEQ ID NO: 48; and a modified 2B8 antibody light chain variable region polypeptide of SEQ ID NO: 49; or (b) a modified Leu16 antibody heavy chain variable region polypeptide of SEQ ID NO: 50; and a modified Leu16 antibody light chain variable region polypeptide of SEQ ID NO: 51.

Abstract: The present application relates to a variant Fc region comprising at least one modification relative to a wild-type human Fc region, where the modification selected from the group consisting of 434S, 252Y/428L, 252Y/434S, and 428L/434S, and the numbering is according to the EU index.

Abstract: The present invention provides methods for treating a B-cell lymphoma in a human subject. The methods of the invention comprise administering to a subject in need thereof an antibody or antigen-binding fragment thereof that specifically binds human CD20. In certain embodiments, the methods of the invention are useful for treating non-Hodgkin's B-cell lymphoma.

Abstract: New combined therapeutic regimens for treatment of B-cell lymphomas are disclosed which comprise in particular administration of anti-CD20 antibodies to patients having low-, intermediate- or high-grade non-Hodgkins lymphomas.

Abstract: The present invention relates to IL-17 Receptor A (IL-17RA or IL-17R) antigen binding proteins, such as antibodies, polynucleotide sequences encoding said antigen binding proteins, and compositions and methods for treating diseases, such as various forms of cancer.

Abstract: Regulatory B cells (tBreg) are disclosed herein. These regulatory B cells express CD25 (CD25+) a pan B cell marker such as B220 (B220+), and also express CD19 (CD19+). These regulatory B cells suppress resting and activated T cells in cell contact-dependent manner. Methods for generating these regulatory B cells are also disclosed herein, as are methods for using these regulatory B cells to produce regulatory T cells (Treg). In some embodiments, methods for treating an immune-mediated disorder, such as an autoimmune disease, transplant rejection, graft-versus-host disease or inflammation, are disclosed. These methods include increasing regulatory B cell number or activity and/or by administering autologous regulatory B cells. Methods for treating cancer are also disclosed herein. These methods include decreasing regulatory B cell activity and/or number.

Abstract: The present application relates to a variant Fc region comprising at least one modification relative to a wild-type human Fc region, where the modification selected from the group consisting of 434S, 252Y/428L, 252Y/434S, and 428L/434S, and the numbering is according to the EU index.

Abstract: The present invention provides chimeric and humanized versions of anti-CD19 mouse monoclonal antibodies. The invention further relates to pharmaceutical compositions, immunotherapeutic compositions, and methods using therapeutic antibodies that bind to the human CD19 antigen and that may mediate ADCC, CDC, and/or apoptosis for the treatment of B cell diseases and disorders, such as, but not limited to, B cell malignancies, for the treatment and prevention of autoimmune disease, and for the treatment and prevention of graft-versus-host disease (GVHD), humoral rejection, and post-transplantation lymphoproliferative disorder in human transplant recipients.

Abstract: A therapeutic composition for treatment of cancer in a mammal is disclosed. The composition comprises an effective amount of a yeast beta-glucan composition which is suitable for oral administration and for absorption through the gastrointestinal tract of the mammal. The above therapeutic composition may further comprise antitumor antibodies or cancer vaccine composition, wherein the antitumor activities of the antitumor antibodies or the cancer vaccine composition are enhanced by the yeast glucan.

Abstract: We describe examples using aptamers for capturing and reporting the presence of a target, such as a pathogen. Examples described here include a set of aptamers that are specific to F. tularensisis. Other examples described here include an Aptamer-Linked Immobilized Sorbent Assay (ALISA) and dot blot assay. An example of a method provided here comprises: providing a set of DNA sequences that exhibit high binding affinity to target antigen, placing the DNA sequences in a sandwich aptamer-linked immobilized sorbent assay (ALISA), contacting the DNA sequences with a sample, and detecting whether the target is present in the sample. Some alternative implementations may include dot blots and different reporters. Quantum dot sandwich assays and quantum dot de-quenching reporters can be used.

Abstract: The present application relates to a variant Fc region comprising at least one modification relative to a wild-type human Fc region, where the modification selected from the group consisting of 434S, 252Y/428L, 252Y/434S, and 428L/434S, and the numbering is according to the EU index.

Abstract: The present invention relates to Notch-binding agents and Notch antagonists and methods of using the agents and/or antagonists for treating diseases such as cancer. The present invention provides antibodies that specifically bind to a non-ligand binding region of the extracellular domain of one or more human Notch receptor, such as Notch2 and/or Notch3, and inhibit tumor growth. The present invention further provides methods of treating cancer, the methods comprising administering a therapeutically effective amount of an antibody that specifically binds to a non-ligand binding region of the extracellular domain of a human Notch receptor protein and inhibits tumor growth.

Abstract: A method of inhibiting tumour angiogenesis in an individual, the method comprising administering to the individual an inhibitor of CLEC14A. The inhibitor may be an antibody, an siRNA molecule, an antisense molecule, or a ribozyme.

Abstract: The present invention provides vascular endothelial cell growth factor (VEGF) antagonists and methods of using VEGF antagonists. VEGF antagonists contemplated by the invention include VEGF antibodies and VEGF receptor fusion proteins. Methods of treating edema and stroke using VEGF antagonists are also provided.

Abstract: The present invention relates to diagnostic and therapeutic methods in the field of malignant disorders. Most particularly, the invention provides methods of determining the invasivity of malignant disorders and methods for reducing the invasivity of malignant disorders including the prevention or treatment of cancer cell invasion.

Abstract: The present invention relates to isolated antibodies and antigen-binding fragments thereof that bind naturally occurring human MAdCAM, wherein said naturally occurring human MAdCAM comprises a polypeptide with at least 90% sequence identity to SEQ ID NO:2 or SEQ ID NO:4, said naturally occurring human MAdCAM binds ?4?7, and wherein said isolated antibodies and antigen-binding fragments thereof inhibit binding of said naturally occurring human MAdCAM to human ?4?7, and wherein said antibody inhibits adhesion of RPMI 8866 cells to cells that express said human MAdCAM.

Abstract: The invention relates to the use of a binding member which binds to LewisY and Lewisb haptens in the treatment of tumours and leukaemia. The binding member may be an antibody which binds to LewisY and Lewisb haptens and cancer cells and induces cells death.