99 results about "Tumor proteins" patented technology

The present invention provides antigen binding proteins that specifically bind to Wilms' tumor protein (WT1), including humanized, chimeric and fully human antibodies against WT1, antibody fragments, chimeric antigen receptors (CARs), fusion proteins, and conjugates thereof. The antigen binding proteins and antibodies bind to HLA-A0201-restricted WT1 peptide. Such antibodies, fragments, fusion proteins and conjugates thereof are useful for the treatment of WT1 associated cancers, including for example, breast cancer, ovarian cancer, prostate cancer, chronic myelocytic leukemia, multiple myeloma, acute lymphoblastic leukemia (ALL), acute myeloid/myelogenous leukemia (AML) and myelodysplastic syndrome (MDS). In more particular embodiments, the anti-WT1/A antibodies may comprise one or more framework region amino acid substitutions designed to improve protein stability, antibody binding and/or expression levels.

The present application generally discloses delivery of an agent which can be therapeutic or prophylactic and, more particularly, the preparation and use of attenuated bacteria, such as Salmonella, containing a bacteriophage in which the genome of the bacteriophage has been modified to encode for a gene product of interest, e.g., an antigen or an anti-tumor protein. The bacteria functions as a vector for delivering the bacteriophage encoded gene product of interest to an appropriate site of action, e.g., the site of a solid tumor.

We teach a strategy to obtain large quantities of desired APCs, activated B cells, which are superior in their capacity to present tumor protein antigen in a multiadministration protocol. Human B cells can be obtained from peripheral blood in large numbers. These cells can be activated in vitro by coculture with CD40L (CD40-B cells) and an immunosuppressive agent such as cyclosporin A. They can expanded up to 1x103 to 1x104 fold in 2 weeks or 1x105 to 1x106 fold in 2 months. We demonstrate these cells are most efficient APCs comparable to DCs in stimulating allogeneic CD4+ CD45RA+, CD4+ CD45RO+, and CD8+ T cells. In contrast to DCs, CD40-B cells are fully functional even in the presence of immunosuppressive cytokines such as IL-10 and TGFbeta.

In an attempt to improve primary disease responsiveness and/or to overcome resistant disease, the present disclosure provides a method for treating or inhibiting the proliferation of a WT-1-dependent cancer comprising providing to a subject in need thereof a therapeutically effective amount of a tyrosine kinase inhibitor along with an anti-WT-1/HLA antibody, that is, an antibody that specifically binds to a peptide of Wilms' tumor protein (WT-1) presented on the surface of the cancer cells in an HLA-restricted fashion.

The present invention provides erythrocytes or nucleated erythrocyte precursors from animals or patients with SS or SA hemoglobin or erythroleukemia cells stably transfected with BCAM/Lu which are capable of selectively localizing in tumor vasculature promoting ischemia and occlusion and carrying oncolytic viruses, antitumor proteins, plasmids, toxins and chemotherapy into the tumor milieu. Nucleated erythroid precursors containing SS or SA hemoglobin and transfected with nucleic acids encoding a hypoxia-responsive element and containing nucleic acids encoding expression of oncolytic viruses, superantigens, toxins, viruses, antitumor proteins and chemotherapy are also useful in inducing a potent and specific tumoricidal response. An especially favored carrier is an SS nucleated erythroid precursor transfected with a replication competent oncolytic adenovirus or self-replicating alphavirus expressing a fusogenic membrane glycoprotein or a tumoricidal polypeptide.

Specific modifying agent is coupled to an anti-tumor protein on a certain site. It conquers the disadvantages which include high antigenicity, short circulating half-life, nonuniform modified sites, inhomogeneous component, reduced activity and uncontrollable quality of the products prepared by non-specific modifying method. The anti-tumor protein coupled with specific modifying agent can be used for the treatment of tumor and for manufacturing an anti-tumor medicament.

The invention discloses an SERS sensor for integrated detection of tumor protein and nucleic acid markers and a preparation method thereof. The SERS sensor comprises a silver nanorod array substrate and an SERS probe, wherein the surface of the silver nanorod array substrate is modified with a tetrahedral DNA structure; the tetrahedral DNA structure is formed by self-assembling six DNA single chains, and three DNA single chains are arranged on three edges of the tetrahedral DNA structure, are respectively connected with three capture chains and are used for respectively and specifically binding nucleic acid and a protein marker. The detection limits of the SERS sensor for detecting nucleic acid and protein respectively reach the Amol/L magnitude and the fg/mL magnitude; the integrated detection of various nucleic acid and protein biomarkers in complex environments such as serum can be realized. The sensor disclosed by the invention is simple to prepare, high in detection sensitivity and good in reliability, can realize high-sensitivity detection of biomarkers with extremely low abundance in the early stage of lung cancer, and has good universality for various tumor biomarkers.

The present invention relates to an attenuated mutant strain of Salmonella comprising a recombinant DNA molecule encoding Wilms' tumor Protein 1. In particular, the present invention relates to the use of said attenuated mutant strain of Salmonella in cancer immunotherapy.

Efficient sequence specific gene silencing is possible through the use of siRNA technology. By selecting particular siRNAs by rational design, one can maximize the generation of an effective gene silencing reagent, as well as methods for silencing genes. Methods, compositions, and kits generated through rational design of siRNAs are disclosed.

Compositions and methods for the therapy and diagnosis of cancer, such as lung cancer, are disclosed. Compositions may comprise one or more lung tumor proteins, immunogenic portions thereof, or polynucleotides that encode such portions. Alternatively, a therapeutic composition may comprise an antigen presenting cell that expresses a lung tumor protein, or a T cell that is specific for cells expressing such a protein. Such compositions may be used, for example, for the prevention and treatment of diseases such as lung cancer. Diagnostic methods based on detecting a lung tumor protein, or mRNA encoding such a protein, in a sample are also provided.

The present invention relates to a p53-activating agent capable of transferring wild-type tumor protein p53 (p53) from an inactive conformation into an active conformation capable of inducing apoptosis, for use in the treatment of melanoma, wherein said p53-activating agent is administered simultaneously or sequentially with a BRAF-inhibiting agent capable of inhibiting activity of serine/threonine-protein kinase B-Raf (BRAF) comprising an activating mutation.

The invention discloses a protein peptide fragment sourced from FOXM1 protein and containing 1-138-position amino acid residue sequences at a nitrogen end of the FOXM1 protein, and provides a candidate capable of inhibiting functions of FOXM1 and used for developing protein peptide type anti-tumor drugs. The protein peptide fragment contains protein with one of the following amino acid residue sequences: 1) a protein shown in SEQ ID NO:1 in a sequence table; 2) a protein peptide capable of inhibiting or reducing activity and functions of FOXM1 by replacing, deleting, inserting and/or adding one, two or more amino acid residues to the protein shown in SEQ ID NO:1 in the sequence table. The recombinant protein prepared on the basis of the amino acid sequence shown in SEQ ID NO:1 in the sequence table and having membrane penetrating capacity shows an inhibition action on various tumor cells.

The invention relates to COnditional Bispecific Redirected Activation constructs, or COBRAs, that are administered in an active pro-drug format. Upon exposure to tumor proteases, the constructs are cleaved and activated, such that they can bind both tumor target antigens (TTAs) as well as CD3, thus recruiting T cells expressing CD3 to the tumor, resulting in treatment. In some embodiments, the tumor target antigen is B7H3.

The present invention provides application of crosslinked polyethylenimine as an oncoprotein antigen vaccine vector, and overcomes the problem that protein antigen after penetration into the body can be degraded easily by enzyme, leading to weak immunogenicity of the vaccine. In an aqueous solution, the polymer material is capable of forming a complex antigen nanoparticle with antigen, in order to achieve loading of tumor protein antigen. The present invention uses RF33.70 as a target cell model, OVA as a model antigen, and C57BL / 6 mice bone marrow-derived dendritic cells as antigen cross presenting cells, and detects the antigen cross-presentation, cytotoxicity and in vivo anti-tumor effect of the complex nanoparticles formed by biodegradable PEI as the antigen vector and the OVA.

A method for identifying T-cell epitopes which can be used to elicit T cells targeting cells capable of regenerating cancers is disclosed. The method identifies T-cell epitopes with a high curative potential, high potency and high probability of T cell recognition (HP). The method includes: (i) identifying high curative potential tumor protein target i.e., identifying HP-TP; (ii) identifying peptide sequences within the protein sequence of an HP-TP that have a high probability of eliciting T cell killing; and (iii) qualifying the sequence specificity based on the fold difference between the specific target and non-targets. The identified T-cell epitopes include a core sequence of 9 amino acids homologous to a sequence expressed within a qualified HP-TP. The T-cell epitopes can be used in a method for reprogramming T cells to selectively attack tumor cells capable of perpetuating a tumor and treating patients, for example, cancer patients.

The invention provides a method for determining a sample source. The method comprises the following steps: (1) carrying out protein content determination treatment on a sample so as to obtain the tumor protein marker content of the sample; (2) standardizing the sample data, wherein the data comprises the tumor protein marker content obtained in the step (1) and the dummy variable conversion data of clinical data; and (3) based on the standardized sample data obtained in the step (2) and a prediction model, determining the probability that the to-be-detected sample comes from a cancer patient.According to the method provided by an embodiment of the invention, whether the to-be-detected sample comes from a cancer patient or not can be accurately and conveniently determined through the prediction model based on the protein content and clinical data of the to-be-detected sample, so a foundation is laid for further research of cancer-related pathogenic mechanisms or early screening of cancer.

The invention provides a method for screening tumor protein markers on the basis of a multilayer complex network. According to the method, node betweennesses of a random forest mode and of a complex network are combined to provide a new visual angle to discover the tumor pathogenic factors and diagnosis markers. Through bioinformatics and mathematic statistical analysis, the correlation of multilayer protein network data is established and a screening method which is more convenient and higher in correctness is disclosed, so that more valuable reference is provided or the cancer diagnosis and drug discovery.

The invention provides an anti-tumor protein RE26, which has a molecular weight of 26 kD and an isoelectric point of 4.3. The preparation method comprises the steps of: obtaining an RE25 crude extract through crude separation, and further separating and purifying through three times of ion-exchange column chromatography to obtain an RE26 pure protein which is for preparing medicines or reagents for treating, diagnosing and researching tumor especially lymphoma diseases. The anti-tumor proteins RE26 of the invention has the special activity of recognizing lymphoma cells and inducing the apoptosis of the lymphoma cells , thereby providing a new way for treating, diagnosing and researching tumor diseases and especially lymphoma diseases.

The invention discloses a recombinant influenza virus rescue method and an application of the same in tumor therapy. The method for preparing recombinant viruses that express antibodies to anti-tumorprotein or contain coding genes of fusion protein includes that single-stranded coding genes, heavy-strained coding genes an/or light-stranded coding genes of anti-tumor protein antibodies are savedby viruses to obtain recombinant viruses with single-stranded, heavy-stranded and/or light-stranded coding genes of anti-tumor protein antibodies and other transforming growth factor receptor or extracellular domain coding genes of the receptor. The recombinant viruses expressing immune checkpoint suppress antibodies are designed; the heavy and light chains encoding immune checkpoint suppress antibodies are constructed in the HA region and NA region of PR8 viruses respectively, and the recombinant oncolytic influenza viruses are constructed to express anti-pd1 anti-pd-L1 antibodies. The oncolytic recombinant influenza viruses provided can target and kill tumor cells without obvious impact on normal host cells and can be used for targeted tumor therapy.