568 results about "Wilm's tumor" patented technology

Methods for the treatment of lymphoma by administration of a B cell-specific antibody are described. The invention encompasses providing to a patient both unlabeled antibodies and antibodies labeled with a radioisotope. A principal advantage of the method is that tumor responses can be obtained in a radiometric dose range that does not require hematopoietic stem cell replacement as an adjunct therapy also described is a composition useful in the treatment of lymphoma.

Anti-TNF antibodies, fragments and regions thereof which are specific for human tumor necrosis factor-alpha (TNFalpha) and are useful in vivo diagnosis and therapy of a number of TNFalpha-mediated pathologies and conditions, as well as polynucleotides coding for murine and chimeric antibodies, methods of producing the antibody, methods of use of the anti-TNF antibody, or fragment, region or derivative thereof, in immunoassays and immunotherapeutic approaches are provided.

This invention provides monoclonal antibody-producing hybridomas designated 27.F7 and 27.B1. The invention also provides methods for detecting TIP-2 antigen-bearing cancer cells in a sample, detecting the presence of TIP-2 antigen, optionally on the surface of cancer cells, immunohistochemical screening of a tissue section for the presence of TIP-2 antigen bearing cancer cells, diagnosing cancer in a subject, monitoring progression of cancer wherein the cancer cells are TIP-2 antigen-bearing cells, delivering exogenous material to TIP-2 antigen-bearing cancer cells of a human subject, and treating cancer in a human subject. This invention further provides a kit for detecting the presence of TIP-2 antigen-bearing cancer cells. This invention also provides isolated peptides having the amino acid sequences Lys Leu Leu Gly Gly Gln Ile Gly Leu (SEQ ID No:3) and Ser Leu Leu Gly Cys Arg His Tyr Glu Val (SEQ ID NO:4).

A small percentage of cells within an established solid tumor have the properties of stem cells. These solid tumor stem cells give rise both to more tumor stem cells and to the majority of cells in the tumor that have lost the capacity for extensive proliferation and the ability to give rise to new tumors. The solid tumor heterogeneity reflects the presence of tumor cell progeny arising from a solid tumor stem cell. This discovery is the basis for solid tumor stem cell compositions, methods for distinguishing functionally different populations of tumor cells, methods for using these tumor cell populations for studying the effects of therapeutic agents on tumor growth, and methods for identifying and testing novel anti-cancer therapies directed to solid tumor stem cells.

The present invention relates to immunotherapeutic methods, and molecules and cells for use in immunotherapeutic methods. In particular, the present invention relates to the immunotherapy of cancer. The present invention furthermore relates to tumour-associated T-helper cell peptide epitopes, alone or in combination with other tumour-associated peptides, that serve as active pharmaceutical ingredients of vaccine compositions which stimulate anti-tumour immune responses. In particular, the present invention relates to two novel peptide sequences derived from HLA class II molecules of human tumour cell lines, which can be used in vaccine compositions for eliciting anti-tumour immune responses.

The field of the present invention relates to genetically engineered fusion molecules, methods of making said fusion molecules, and uses thereof in anti-tumor immunotherapies. More specifically, the present invention relates to engineered fusion molecules consisting of a tumor targeting moiety fused with one or more costimulatory molecules / chemokines / cytokines.

The present invention relates to immunotherapeutic methods, and molecules and cells for use in immunotherapeutic methods. In particular, the present invention relates to the immunotherapy of cancer. The present invention furthermore relates to tumour-associated T-helper cell peptide epitopes, alone or in combination with other tumour-associated peptides, that serve as active pharmaceutical ingredients of vaccine compositions which stimulate anti-tumour immune responses. In particular, the present invention relates to 49 novel peptide sequences derived from HLA class II molecules of human tumour cell lines which can be used in vaccine compositions for eliciting anti-tumour immune responses.

The subject disclosure presents systems and computer-implemented methods for providing reliable risk stratification for early-stage cancer patients by predicting a recurrence risk of the patient and to categorize the patient into a high or low risk group. A series of slides depicting serial sections of cancerous tissue are automatically analyzed by a digital pathology system, a score for the sections is calculated, and a Cox proportional hazards regression model is used to stratify the patient into a low or high risk group. The Cox proportional hazards regression model may be used to determine a whole-slide scoring algorithm based on training data comprising survival data for a plurality of patients and their respective tissue sections. The coefficients may differ based on different types of image analysis operations applied to either whole-tumor regions or specified regions within a slide.

The present invention relates to compositions and methods for the treatment of tumor and / or malignant and / or cancerous cells. The present invention provides VSV vectors comprising nucleic acid encoding a cytokine, such as interleukin or interferon, or a suicide gene, such as thymidine kinase, or other biological protein, such as heat shock protein gp96, or endostatin or angiostatin, wherein said VSV vectors exhibit greater oncolytic activity against the tumor and / or malignant and / or cancerous cell than a wild-type VSV vector. The present invention also provides methods of making such vectors, host cells, expression systems, and compositions comprising such VSV vectors, and viral particles comprising such VSV vectors. The present invention also provides methods for producing oncolytic activity in a tumor and / or malignant and / or cancerous cell comprising contacting said cell with a VSV vector of the present invention. The present invention also provides methods for suppressing tumor growth comprising contacting said tumor with a VSV vector of the present invention. The present invention also provides methods for eliciting an immune response to a tumor cell in an individual.

The present invention relates to a method of diagnosing, classifying and grading of tumor growths and to determine whether the use of chimeric polioviruses is a proper course for the treatment of the tumors. More particularly, the method is directed to the use of antibodies to a poliovirus receptor (PVR), CD155, to detect the presence of CD155 on tumor cells in various organs, such as: breast, colon, bronchial passage, epithelial lining of the gastrointestinal, upper respiratory and genito-urinary tracts, liver, prostate and the brain.

The invention provides a method for more effective treatment of patients susceptible to or diagnosed with tumors overexpressing ErbB, as determined by a gene amplification assay, with an ErbB antagonist. Such method comprises administering a cancer-treating dose of the ErbB antagonist, preferably in addition to chemotherapeutic agents, to a subject in whose tumor cells ErbB has been found to be amplified e.g., by fluorescent in situ hybridization. ErbB antagonists described include an anti-HER2 antibody. Pharmaceutical packaging for providing the components for such treatment is also provided.

Provided are methods of generating an immune response to an antigen specifically associated with tumor vascular endothelial cells (TVECA). The method comprises administering to an individual an expression vector encoding the TVECA. The vector comprises a transcription unit encoding a secretable fusion protein, the fusion protein containing a TVECA and CD40 ligand. In other methods, administration of a fusion protein containing the TVECA and CD40 ligand is used to enhance the immune response above that obtained by vector administration alone. Further methods comprise the combination therapy using an expression vector encoding a secretable TVECA fusion protein and a tumor antigen vaccine.

The present invention relates to peptides, proteins, nucleic acids and cells for use in immunotherapeutic methods. In particular, the present invention relates to the immunotherapy of cancer. The present invention furthermore relates to tumor-associated T-cell peptide epitopes, alone or in combination with other tumor-associated peptides that can for example serve as active pharmaceutical ingredients of vaccine compositions that stimulate anti-tumor immune responses, or to stimulate T cells ex vivo and transfer into patients. Peptides bound to molecules of the major histocompatibility complex (MHC), or peptides as such, can also be targets of antibodies, soluble T-cell receptors, and other binding molecules.

Disclosed are a novel prostatic acid phosphatase and corresponding coding region derived from mouse. Also disclosed is a method of producing an immune response against an autologous polypeptide tumor antigen by immunizing a subject with a xenogeneic polypeptide antigen, either alone, as part of a viral antigen construct, or as part of a pulsed dendritic cell preparation.

The invention provides methods and compositions for the modulation of systemic immune responses by transplantation of hematopoietic stem cells transduced with genes encoding antigens and antigen presenting cell regulatory molecules. The invention includes bi-cistronic lentiviral expression vectors adapted for antigen expression in antigen presenting cells for use in DNA vaccines directed against pathogens and tumor antigens as well as for the treatment of autoimmune disease and for the establishment of antigen tolerance.

The invention discloses an anti-human CLDN18.2 antibody as well as an antigen binding fragment and a medical application thereof. Specifically, the present invention relates to a murine antibody comprising a CDR region of the anti-human CLDN18.2 antibody, a chimeric antibody and a humanized antibody, a fully humanized antibody, an antibody-dependent cytotoxicity (ADCC) comprising the antibody andthe antigen binding fragment thereof, complement dependent cytotoxicity (CDC), the killing effect on CLDN18.2 positive cells, the effect of inhibiting the growth of CLDN18.2 positive tumors, the in-vivo drug effect, a medicine containing the anti-human CLDN18.2 antibody and the antigen binding fragment thereof, a composition of the medicine thereof, and an application of the medicine in tumor treatment, in particular to treatment of CLDN18.2 positive tumor patients..

Methods of enhancing the efficacy of antibody-directed cellular cytotoxicity (ADCC) for therapy directed to killing of tumor cells are disclosed. Cancer specific cell surface antigens are bound by monoclonal antibodies, thereby stimulating a cytotoxic T cell response characterized by an upregulation of cell surface expression of costimulatory molecules on the T cell. The ADCC response is augmented by the subsequent administration of a second antibody that is an agonist of the costimulatory molecule.

The present invention discloses an anti-tumor compound and its preparation method,application, and pharmaceutical compositions. The anti-tumor compound is a 4 - nitro-substituted benzyl group ifosfamide ester prodrug thereof, or pharmaceuticallysalt, or solvate thereof of the structure of formula I. The structure of formula I. The present invention has the following advantage of being used for the treatment or prevention of mammalian tumor-related diseases, such as leukemia, hemangioma, glioma, Kaposi's sarcoma, ovarian cancer, breast cancer, lung cancer, pancreatic cancer, lymphoma, prostate, colon and skin tumors and their complications.

The present invention features compositions and methods for detecting, selecting a treatment method for, monitoring, and treating a neoplasia associated with a viral infection.

The present invention relates to chimeric immune receptor molecules for reducing or eliminating tumors. The chimeric receptors are composed a C-type lectin-like natural killer cell receptor, or a protein associated therewith, fused to an immune signaling receptor containing an immunoreceptor tyrosine-based activation motif. Methods for using the chimeric receptors are further provided.

To gain a better understanding of tumor angiogenesis, new techniques for isolating endothelial cells (ECs) and evaluating gene expression patterns were developed. When transcripts from ECs derived from normal and malignant colorectal tissues were compared with transcripts from non-endothelial cells, over 170 genes predominantly expressed in the endothelium were identified. Comparison between normal- and tumor-derived endothelium revealed 79 differentially expressed genes, including 46 that were specifically elevated in tumor-associated endothelium. Experiments with representative genes from this group demonstrated that most were similarly expressed in the endothelium of primary lung, breast, brain, and pancreatic cancers as well as in metastatic lesions of the liver. These results demonstrate that neoplastic and normal endothelium in humans are distinct at the molecular level, and have significant implications for the development of anti-angiogenic therapies in the future.

The present invention relates to chimeric immune receptor molecules for reducing or eliminating tumors. The chimeric receptors are composed a C-type lectin-like natural killer cell receptor, or a protein associated therewith, fused to an immune signaling receptor containing an immunoreceptor tyrosine-based activation motif. Methods for using the chimeric receptors are further provided.

This invention relates to the identification and treatment of aggressive lung cancer tumors in patients. More particularly, it provides a method of identifying patients with non-small cell lung carcinoma (NSCLC) who have an aggressive node-negative (N0) tumor and a likelihood of a poor overall survival. The method comprises the step of determining if one or more of certain identified proteins are activated in tumor cells obtained from the patient's tumor, wherein the activation of one or more of the proteins indicates that the patient has an aggressive N0 tumor and is likely to have a poor overall-survival. The invention also provides a method for selecting a treatment for an NSCLC patient with an N0 tumor and a method for treating such patients. It further provides a kit for identifying an NSCLC patient with an aggressive N0 tumor and a likelihood of a poor overall survival and a pharmaceutical composition for treating such patients.

This invention provides tumor metastasis-inhibiting monoclonal antibodies, mAb 41-2, mAb 50-6 and mAb 1A-5. The antigen recognized by mAb 50-6 and mAb 1A-5 has been identified as the PETA-3 antigen. The antigen recognized by mAb 41-2 has been identified as a novel tumor metastasis-associated antigen. Compositions and methods are provided that are useful for treating and diagnosing metastatic tumors.

Novel monoclonal antibodies that specifically bind to KAAG1 are described. In some embodiments, the antibodies block the biological activity of KAAG1 and are useful in composition in certain cancers, more particularly in cancers that have increased cell surface expression of KAAG1, such as ovarian, renal, lung, colorectal, breast, brain, and prostate cancer, as well as melanoma. The invention also relates to cells expressing the monoclonal antibodies and antigen binding fragments such as humanized and chimeric antibodies. Additionally, methods of detecting and treating cancer using the antibodies and fragments are also disclosed.

The present invention describes a method of prevention and / or treatment of a cancer or a tumor, and in particular a combination therapy, methods, compositions and pharmaceutical packages comprising a taxane and certain platinum-based chemotherapeutic agents.

Disclosed are compositions and methods related to rendering ineffective Th1 T cells resistant to the inhibitory cytokine milieu present in a cancer microenvironment. Tumor-specific T cells are modified to employ a chimeric receptor that binds inhibitory / suppressive cytokines and converts their intracellular consequences to a Th1 immunostimulatory / activating signal. The T cells employ a chimeric antigen receptor having exodomains for IL10, IL13 and / or IL4 fused with the signal transducing endodomains for IL2 and / or IL7.