Abstract: Mutations in calreticulin are discovered to be linked to myeloid malignancies. Disclosed are genomic sequences, cDNA sequences, mRNA sequences and protein sequences of mutant calreticulin that are linked to myeloid malignancies. Also disclosed are methods for diagnosing myeloid malignancy comprising determining the presence of a mutant allele of the calreticulin gene. Also disclosed are related compositions, kits and methods, including the medical use of inhibitors of mutant calreticulin.

Abstract: Provided herein are biomarkers for the treatment of pathological conditions, such as cancer, and method of using PD-1/PD-L1 pathway antagonists. In particular, provided are biomarkers for patient selection and prognosis in cancer, as well as methods of therapeutic treatment, articles of manufacture and methods for making them, diagnostic kits, methods of detection and methods of advertising related thereto.

Abstract: Described are biomarkers for neoplastic disease progression. Specifically, provided are methods of determining neoplastic disease progression by determining the presence of retrotransposon insertion.

Abstract: Novel methods of classifying subjects as candidates for treatment with agent that inhibits or kills cancer associated mesenchymal cells, tumor initiating cancer cells, or cancer stem cells treatment and subsequent administration of the agent that inhibits or kills cancer associated mesenchymal cells, tumor initiating cancer cells, or cancer stem cells are disclosed within.

Abstract: This invention provides novel erbB2-binding internalizing antibodies. The antibodies, designated F5 and C1, specifically bind to c-erbB2 antigen and, upon binding, are readily internalized into the cell bearing the c-erbB2 marker. Chimeric molecules comprising the F5 and/or C1 antibodies attached to one or more effector molecules are also provided.

Abstract: Provided herein are humanized forms of murine RP215 monoclonal antibodies and methods of using the same. These humanized RP215 monoclonal antibodies were characterized in terms of their respective affinity and specificity to the corresponding tumor-associated antigen, CA215, and shown to be comparable to those of murine RP215.

Abstract: According to the present invention, an anticancer agent is provided that has as an active ingredient thereof a human antibody light chain that demonstrates cytotoxicity against cancer cells and particularly lung cancer cells. The anticancer agent of the present invention primarily comprises: a human antibody ?-type light chain in the form of a dimer in which the variable region is composed of a polypeptide represented by the amino acid sequence of SEQ ID NO: 1, 9 or 13 or an amino acid sequence in which one or a plurality of amino acids have been added, deleted or substituted in these amino acid sequences; or, a human antibody ?-type light chain in the form of a monomer in which the variable region is composed of a polypeptide represented by the amino acid sequence of SEQ ID NO: 19 or an amino acid sequence in which one or a plurality of amino acids have been added, deleted or substituted in the amino acid sequence.

Abstract: Provided herein are compositions comprising a micelle having a hydrophobic superparmagnetic iron oxide nanoparticle (SPION) core, a first coating comprising a cationic polymer, and a second coating comprising a polynucleotide. Also provided are methods of using the compositions for transfection and/or transformation of a cell with the polynucleotide. Further provided are methods of detecting transfection of a cell with the polynucleotide.

Abstract: Antigen binding proteins that activate GITR are provided. Nucleic acids encoding the antigen binding proteins and vectors and cells containing such nucleic acids are also provided. The antigen binding proteins have value in therapeutic methods in which it is useful to to stimulate GITR signaling, thereby inducing or enhancing an immune response in a subject. Accordingly, the antigen binding proteins have utility in a varienty of immunotherapy treatments, including treatment of various cancers and infections.

Abstract: The invention provides a tumor cell genetically modified to express a nucleic acid encoding a secreted form of a heat shock protein (hsp) gp96 polypeptide. The invention also provides a method of stimulating an immune response to a tumor by administering a tumor cell genetically modified to express a nucleic acid encoding a secreted form of a gp96 polypeptide.

Abstract: In order to reduce the side effects of paclitaxel derivatives having excellent anti-cancer effects, an attempt was made to produce a liposome encapsulating paclitaxel derivatives such as paclitaxel monoglycosides and docetaxel monoglycosides. However, the introduction efficiency of paclitaxel derivatives, etc., into a liposome was poor, and this technique was not developed to a practical level. The present invention provides a method for producing a liposome encapsulating a paclitaxel monoglycoside and/or a docetaxel monoglycoside, and having an antibody specifically recognizing a cancer cell, the method comprising a step of bringing a liposome encapsulating a polyoxyethylene ester derivative, a lower alcohol, and a buffer or water into contact with a solution in which a paclitaxel monoglycoside and/or a docetaxel monoglycoside is dissolved in an alkylene glycol-containing buffer or water.

Abstract: The present invention comprises a humanized monoclonal antibody that binds to the chemokine receptor CCR4. This antibody is derived from Mab 1567 and recognizes the same epitope. Binding of the invented antibody to CCR4 inhibits ligand-mediated activities and is used to treat symptoms of cancer. Moreover, the antibody is used in combination with vaccines to suppress the activity of regulatory T cells.

Abstract: The present invention provides antibodies useful as therapeutics for treating and/or preventing diseases associated with cells expressing GT468, including tumor-related diseases such as breast cancer, lung cancer, gastric cancer, ovarian cancer, and hepatocellular cancer.

Abstract: The present invention relates to a method for diagnosing neuroendocrine cancers via detecting the presence of N-methyl D-asparate-associated (NMDA) glutamate receptors type 1 and/or type 2. Methods for preventing and treating neuroendocrine cancers are also disclosed.

Abstract: Methods and compositions are provided for diagnosing or inhibiting invasion or metastasis of a cancer in a subject based on MenaINV.

Abstract: Methods for determining the presence of cancer stem cells by detecting GD2 expression. Also provided are methods for reducing proliferation of cancer stem cells by contacting the cells with a GD2 targeting agent, such as an anti-GD2 antibody or a GD3 synthase inhibitor. GD3 synthase inhibitor compounds are also provided.

Abstract: The invention described herein relates to the detection, diagnosis, and treatment of intestinal metaplasias that develop to esophageal, gastric, and pancreatic adenocarcinoma. The stem cells and differentiated cells of these intestinal metaplasias show high expression of CDH17 as well as other proteins. The invention also includes a clonal population of Barrett's esophagus stem cells as well as the stem cells of the surrounding normal epithelia and methods of using them for the detection, diagnosis, and treatment of Barrett's esophagus.

Abstract: The present invention provides compositions and methods useful for promoting or reducing T-cell trafficking to a target tissue. Also provided are compositions and methods useful for promoting or inhibiting antigen-presenting cell (APC) activation. The invention is related to discovery of functional characteristics of TIM-3, a molecule that is preferentially expressed on the surface of Th1 cells. The methods are useful for treating disorders including cancer, infectious disease, allergy, asthma, and autoimmune disease.

Abstract: The present invention relates to means and methods of determining whether a tumor cell or a cancer cell is responsive to an anti-CD44 antibody or to an antigen binding fragment thereof. The method comprises the determination of the major CD44 isoform in a sample, wherein if the major CD44 isoform is CD44s, the tumor cell or cancer cell is responsive to said anti-CD44 antibody. Also means and methods of treating a cancer patient that has been determined to respond to an anti-CD44 antibody are subject of the present invention.

Abstract: The present invention relates to a pharmaceutical combination that comprises an IGF1R inhibitor and an mTOR inhibitor for the treatment of cancer in a subject; a pharmaceutical composition comprising such a combination; the use of such a combination for the preparation of medicament for the treatment of cancer; a kit comprising such a combination as a combined preparation for simultaneous, separate or sequential use; and a method of treating cancer in a subject, especially a human.

Abstract: The invention features methods of diagnosis by assessing B7-H1 expression in a tissue from a subject that has, or is suspected of having, cancer, methods of treatment with agents that interfere with B7-H1-receptor interaction, methods of selecting candidate subjects likely to benefit from cancer immunotherapy, and methods of inhibiting expression of B7-H1.

Abstract: The invention relates to the use of monoclonal antibodies that only recognise the O-acetylated form of the GD2 ganglioside, or fragments of said antibody, for the diagnosis and the treatment of cancers in which the cells express the O-acetylated GD2, said antibody or said fragment recognising the O-acetylated GD2 molecules expressed by the tumoral cells and not recognising the GD2 molecules expressed at the surface of the peripheral nerves, in order to increase the specificity of the diagnosis and reduce the toxicity of the treatments. The invention also relates to artificially modified antibodies advantageously used for treating and diagnosing cancers in which the cells express the O-acetylated GD2.

Abstract: The present invention relates to methods and compositions for use in inducing tumor-specific antibody mediated complement-dependent cytotoxic response in an animal having a tumor comprising administering to said animal a composition comprising a replication competent oncolytic virus wherein administration of the composition induces in the animal production of antibodies that mediate a CDC response specific to said tumor.

Abstract: Compositions and methods for detecting, prognosing, inhibiting, treating, and/or preventing cancer are provided.

Abstract: This disclosure relates to anti-Siglec-15 antibodies and uses thereof, in particular in the treatment of leukaemia, such as acute myeloid leukaemia.

Abstract: Methods, compositions and compounds that include a nucleic acid comprising a sequence consisting essentially of polyT/polyU and an agent that inhibits the production or activity of an immunosuppressive compound for treating tumors are described.

Abstract: Antibodies that specifically bind to an extracellular domain of human Jagged 1 or human Jagged2 and modulate Jagged activity, and methods of using said antibodies to inhibit tumor growth are disclosed. Also described are methods of treating cancer comprising administering a therapeutically effect amount of an anti-Jagged antibody to a patient having a tumor or cancer.

Abstract: The invention encompasses polypeptides, polynucleotides, and antibodies, for Artemin and related ligands, including Persephin (PSPN). The invention also encompasses expression vectors and host cells for producing these polypeptides, polynucleotides, or antibodies. The invention further encompasses diagnostics and therapeutics, especially for cancer, and particularly breast cancer, colon cancer, prostate cancer, endometrial cancer, lung cancer, stomach cancer, liver cancer, and others, comprising one or more of the disclosed polypeptides, polynucleotides, antibodies, expression vectors, host cells, or compositions thereof. Particularly encompasses are inhibitors of Artemin and/or related ligands, and uses for these inhibitors.

Abstract: Novel methods of classifying subjects as candidates for treatment with a cancer associated mesenchymal cell, tumor initiating cancer cell, or cancer stem cell inhibitor treatment and subsequent administration of the cancer associated mesenchymal cell, tumor initiating cancer cell, or cancer stem cell inhibitor are disclosed within.

Abstract: The present invention provides methods of treating cancer by administering an IL8-CXCR1 pathway inhibitor (e.g., an anti-CXCR1 antibody or Repertaxin) alone or in combination with an additional chemotherapeutic agent such that non-tumorigenic and tumorigenic cancer cells in a subject are killed. The present invention also provides compositions and methods for detecting the presence of and isolating solid tumor stem cells in a patient (e.g., based on the presence of CXCR1 or FBXO21).

Abstract: The present invention provides novel high affinity antibodies and fragments thereof that bind to the cancer antigen PSCA. The antibodies of the present invention may be used for cancer diagnosis, prognosis, treatment, visualization, and the like. The present invention also provides methods for the detection, visualization, and treatment of various cancers expressing PSCA.

Abstract: A method for inducing apoptosis of a neoplastic cell expressing C3aR or C5aR includes administering at least one complement antagonist to the cell so that the at least one complement antagonist substantially reduces or inhibits the activity of protein kinase B in the neoplastic cell.

Abstract: Methodologies and technologies for potentiating antibody-based cancer treatments by increasing complement-mediated cell cytotoxicity are disclosed. Further provided are methodologies and technologies for overcoming ineffective treatments correlated with and/or caused by sub-lytic levels of complement-activating monoclonal antibodies (“mAb”) against cancer antigens or cancer antigens with low tumor cell density. While detectable levels of passively administered or vaccine-induced mAb against some antigens are able to delay or prevent tumor growth, low levels of mAb induce sublytic levels of complement activation and accelerate tumor growth. This complement-mediated accelerated tumor growth initiated by low mAb levels results in activation of the PI3K/AKT survival pathway. Methodologies and technologies relating to administration of PI3K inhibitors to overcome low dose mAb-initiated, complement-mediated PI3K activation and accelerated tumor growth are disclosed.

Abstract: A genetic locus and corresponding family of proteins associated with regulation of immune function and cell survival are provided. These genes encode cell surface molecules with conserved IgV and mucin domains. The locus comprising the TIM family is genetically associated with immune dysfunction, including asthma. Furthermore, the TIM gene family is located within a region of human chromosome 5 that is commonly deleted in malignancies and myelodysplastic syndrome. Polymorphisms in the gene sequences are associated with the development of airway hyperreactivity and allergic inflammation, and T cell production of IL-4 and IL-13. The proteins include the human hepatitis A cellular receptor, hHAVcr-1.

Abstract: The present disclosure describes a pharmaceutical combination of an anti-CD38 antibody and lenalidomide and a pharmaceutical combination of an anti-CD38 antibody and bortezomib.

Abstract: The present invention relates to the ex vivo differentiation of NK cells from CD34+ hematopoietic stem cells. Such NK cells and their progenitor cells can be used in therapies of a broad range of malignancies. In the present invention it is shown that IL-12 modulates ex vivo NK cell differentiation. Specific, we achieved significantly higher expression of KIR, CD16 and CD62L in the presence of IL-12 in the cell culture system. The induction of receptor expression by IL-12 occurred predominantly on an augmented population of CD33+NKG2A+ NK cells early during NK cell differentiation. These cells further show enhanced cytolytic activity against MHC class I positive AML targets. In line with the enhanced CD16 expression, IL-12 modulated ex vivo generated NK cells exhibit an improved antibody-dependent-cytotoxicity, using anti CD20 antibody on various B cell targets. Additional to the enhanced expression of CD62L, we show that this cell population consists of a specific chemokine receptor profile.

Abstract: Provided herein are methods for identifying a subject with an increased likelihood of developing or having metastatic papillary thyroid cancer (PTC), or a subject with an increased likelihood of developing or having recurrent PTC, and the treatment of such a subject.

Abstract: The subject matter of the present invention relates to an in vitro method for the screening of anti-cancer compounds based on the capacity for these compound to interact with netrin-1 receptor and/or to inhibit the dimerization of the intracellular domain of the netrin-1 receptor expressed in tumor cells. The invention also relates to a method for predicting the presence of metastatic or aggressive cancer, or for determining the efficiency of an anti-cancer treatment based on the measuring of the expression level of netrin-1. The invention further comprises kits and compounds as a medicament for the treatment of cancer such as metastatic breast cancer, related to the overexpression of netrin-1 by the tumor cells.

Abstract: The invention provides Nrp2 antagonists, such as anti-Nrp2 antibodies, and their use in the prevention and treatment of tumor metastasis.

Abstract: Disclosed are novel inhibitors of the Axl receptor tyrosine kinase (RTK) and methods of using such inhibitors in a variety of therapeutic approaches in the areas of cancer therapy and anti-thrombosis (anti-clotting) therapy.

Abstract: The application provides methods of diagnosis, prognosis, prophylaxis and treatment of CD30+ cancers.

Abstract: The invention provides antibodies that specifically bind to human CD134. Anti-human CD134 antibodies specifically bind to the extracellular domain of human CD134, including non-OX40 ligand (OX40L) binding domains on human CD134, which is expressed on e.g. activated human conventional effector CD4 and/or CD8 T lymphocytes (Teffs) and on activated human suppressive regulatory CD4 T lymphocytes (Tregs). Humanized anti-human CD134 antibodies are useful (e.g. to empower Teffs anti-cancer effector function and/or to inhibit Tregs suppressive function) for cancer treatment.

Abstract: The present invention provides for methods and pharmaceutical compositions for treating disorders using treatment regimens involving multiple agents. In one aspect, a method of treatment is provided resulting in reduced toxicity and/or synergistic effect by administration according to a described dosing schedule.

Abstract: The present invention relates to methods to treat or prevent cancers in a subject, in particular the present invention relates to a method of treating and/or preventing cancer comprising targeting cancer stem cells by administering miRNAs which have reduced expression or are lacking in the cancer stem cells. In some embodiments, the miRNAs that are reduced or lacking in cancer stem cells are let-7 miRNAs. In alternative embodiments, the present invention relates to a method of treating and/or preventing cancer comprising targeting cancer stem cells by administering miRNAs which have increased expression levels in the cancer stem cells. Another aspect of the present invention relates to methods to enrich for a cancer stem cell population. Another aspect of the present invention relates to methods to identify miRNAs which contribute to the self-renewal capacity of cancer stem cells.

Abstract: The present invention provides novel IgE antibodies useful for inhibiting or preventing metastatic cancer. Also provided are methods to inhibit tumor metastasis by modulating the activity of at least one non-tumor cell, treating a patient to inhibit or prevent tumor metastases of a primary solid tumor, treating metastatic carcinoma, reducing metastasis of carcinoma cells, and reducing the growth kinetics of a primary solid tumor or a metastasized cell or tumor.

Abstract: The present invention provides methods of inhibiting angiogenesis in a malignant tumor, inhibiting metastasis of a malignant tumor and of inhibiting transformation of a benign tumor to a malignant tumor. The present invention also provides assays for identifying inhibitors of angiogenesis in a malignant tumor, inhibitors of metastasis of a malignant tumor and of inhibitors of transformation of a benign tumor to a malignant tumor.

Abstract: Methods are provided for treatment of hematologic cancers, particularly lymphomas and leukemias, including without limitation myelogenous and lymphocytic leukemias. A combination of antibodies specific for CD47; and specific for a cancer associated cell surface marker are administered to the patient, and provide for a synergistic decrease in cancer cell burden. The combination of antibodies may comprise a plurality of monospecific antibodies, or a bispecific or multispecific antibody. Markers of interest include without limitation, CD20, CD22, CD52, CD33; CD96; CD44; CD123; CD97; CD99; PTHR2; and HAVCR2.

Abstract: The present invention relates to a method for treating breast cancer in a subject having a hyperactivation of the Epidermal Growth Factor Receptor 1 and/or 2 (EGFR and/or ErbB2 HER2), as compared to the normal subject population, or expressing deltaHER2, which method comprises the step of administering to said subject a therapeutically effective amount of a modulator of the CUB domain-containing protein 1 (CDCP1).

Abstract: The present invention relates to antibodies and antigen binding fragments thereof that bind the extracellular domain of the HER3 receptor and inhibit various HER3 receptor related functions via ligand-dependent and/or ligand-independent mechanisms. Also provided are compositions with increased half-life. In addition, the invention provides compositions and methods for diagnosing and treating diseases associated with HER3 mediated signal transduction.

Abstract: The technology described herein is directed to methods, assays, and systems relating to determining the level of SAKT signaling activity in a sample obtained from a subject as well as methods relating to administering inhibitors and/or agonists of SAKT signaling.