44 results about "Neoplastic growth" patented technology

The present invention provides a fully human antibody that binds human EGFR with affinity comparable to or higher than IMC-C225, and that neutralizes activation of EGFR. Antibodies include whole immunoglobulins, monovalent Fabs and single chain antibodies, multivalent single chains antibodies, diabodies, triabodies, and single domain antibodies. The invention further provides nucleic acids and host cells and animals that encode and express these antibodies. The invention further provides a method for neutralizing activation of EGFR, treating in a mammal with neoplastic growth and non-cancerous hyperproliferative diseases using the antibodies alone or in combination with other agents.

A method of treating cancer by targeting two proteases, MMP-9 and cathepsin B is provided. Therapeutic compositions comprising one or more plant extracts that inhibit MMP-9 and / or cathepsin B, which are capable of inhibiting neoplastic and / or endothelial cell migration, tumor growth, tumor-induced angiogenesis and / or metastasis are also provided. The therapeutic compositions of the invention can be used in the treatment of cancer, and methods of inhibiting tumor growth, tumor metastasis, and / or tumor-induced angiogenesis using the therapeutic compositions alone or in combination with an anti-cancer agent are, therefore, also provided.

The invention relates to a high frequency bipolar unrecoverable electroporation system. The high frequency bipolar unrecoverable electroporation system comprises an upper layer information managementmodule, a lower computer control module and a bipolar high voltage pulse discharging circuit, wherein the upper layer information management module is used for receiving set working parameters, and transmitting the received working parameters to the lower computer control module, and then a control signal is generated and transmitted to the bipolar high voltage pulse discharging circuit to producebipolar high voltage pulse. Compared with a conventional unipolar irreversible electroporation pulse sequence, the high frequency bipolar unrecoverable electroporation system can better and more uniformly increase the induced transmembrane potential of cells which are tightly arrayed to a simulation electroporation threshold, so that an ablation region is more uniform; and through the adoption ofthe high frequency bipolar unrecoverable electroporation system disclosed by the invention, favorable tumor ablation effects and the purpose of restraining the growth of tumor can be achieved, and the high frequency bipolar unrecoverable electroporation system has favorable safety and favorable validity.

Neoplastic tissue, viral and bacterial infections, and other physiological disorders and conditions are treated by irradiation of the host with electromagnetic radiation at a wavelength that is differentially absorbed by the offending tissue or cells. Radiation with differential absorption is also used in the sterilization of articles and packing made from synthetic polymers and for the treatment of food stuffs.

The present application relates to conjugates comprising interleukin 2 (IL2), and a tumour necrosis factor, such as tumour necrosis factor alpha (TNFα), and an antibody molecule. The antibody molecule preferably binds to an antigen associated with neoplastic growth and / or angiogenesis, such as the Extra-Domain A (EDA) of fibronectin. The conjugate may be used in the treatment of cancer.

Neoplastic tissue, viral and bacterial infections, and other physiological disorders and conditions are treated by irradiation of the host with electromagnetic radiation at a wavelength that is differentially absorbed by the offending tissue or cells. Radiation with differential absorption is also used in the sterilization of articles and packing made from synthetic polymers and for the treatment of food stuffs.

A neoplastic stem cell population enriched for expression of the OCT4 transcription factor as well as methods for their identification, isolation and enrichment are described. The OCT4-enriched neoplastic stem cell population is further utilized for the induction and analysis of cancer in an animal. In addition, methods of preventing, abrogating, or inhibiting cancer, tumor growth, and metastasis via OCT4 inhibition are further provided.

The invention discloses a polypeptide specifically combined with beta-catenin protein with high affinity, and application and a synthesis method of the polypeptide. The amino acid sequence of the polypeptide is LEHRERSLQT(X1)RDIQRML(X2)P, wherein X1 is leucine, norleucine or homoleucine, and X2 is phenylalanine, 1-naphthyl alanine, 2-naphthyl alanine, 2-anthryl alanine or 9-anthryl alanine. The polypeptide is used for inhibiting growth of cancer cells. By the polypeptide, various tumor treatment targets can be achieved. The polypeptide inhibits opening of a beta-catenin protein-mediated Wnt signal pathway by inhibiting mutual combination of the beta-catenin protein and BCL9 in the cancer cells, so that growth of tumors is inhibited, self-apoptosis of the cells is induced, and the tumor disease treatment targets are achieved. The synthesis method of the polypeptide is simple and easy to implement, and the final product has high yield efficiency, has mass production potential, and has great drug clinical transformation potential.

Compounds comprising two human GlxI inhibitors covalently linked via a chemical linker are provided, wherein each of said two human GlxI inhibitors, which may be the same or different, is an S-substituted glutathione or an S-substituted glutathione prodrug, wherein said GlxI inhibitors each have a γ-glutamyl amino group, wherein said chemical linker is covalently bound to each GlxI inhibitor via said γ-glutamyl amino group, and wherein said chemical linker has a length of at least 50 Angstroms. Monovalent irreversible inactivators of human GlxI are also provided. An antineoplastic composition is provided, which comprises a compound described above and a pharmaceutically acceptable carrier. In vitro and in vivo methods of preventing or inhibiting the growth and proliferation of neoplastic cells and / or tumors are also provided.

The present invention relates to an isoxazole derivative, the compound of formula (I)herein after referred to as GIT27-NO, which is the NO-donating structurally modified form of (S,R)-3-phenyl-4,5-dihydro-5-isoxazole acetic acid, herein after referred to as VGX-1027. Treatment of three tumor cell lines, rat astrocytoma C6, mouse fibrosarcoma L929, and mouse melanoma B16 cells with GIT27-NO resulted in a significant reduction of cell respiration and of number of viable cells, while VGX-1027 was completely ineffective. Hemoglobin, which act as NO-scavenger, restored cell viability, thus indicating the NO-mediated tumoricidal effect of compound (I). GIT27-NO triggered apoptotic cell death in L929 cell cultures, while autophagic cell death is mainly responsible for the diminished viability of C6 and B16 cells. Moreover, GIT27-NO induced the production of reactive oxygen species which can be neutralized by antioxidant N-acetyl cysteine (NAC), indicating that reactive oxygen species (ROS) are at least partly involved in the reduction of cell viability. The anti-tumor activity of GIT27-NO is mediated through activation of MAP kinases (ERK1 / 2, p38 and JNK) in cell-specific manner. The role of MAP kinases was further confirmed by specific inhibitors of these molecules, PD98059, SB202190, and SP600125. Finally, in vivo treatment with GIT27-NO significantly reduced tumor growth in syngeneic C57BL / 6 mice implanted with B16 melanoma.

This invention provides a nucleus-permeable small-molecule inhibitor, L2P4 (where L2 is 4-(4-(Diethylamino)styryl)-N-carboxymethylpyridinium chloride and P4 is an amino acid sequence comprising CAhxYFMVFGGRrRK and they were coupled through amide bond) and synthesis thereof, which effectively targets the dimerization interface of EBNA1, a critical process for the growth of EBVs and the associated tumors. The present invention also provides method of treating and imaging EBV-associated cancers.

The invention discloses a type 2 diabetes mellitus mouse pancreatic cancer model construction method based on a living body imaging technology. The method comprises the following steps: culturing human-derived pancreatic cancer tumor cells, and then carrying out cell transfection to construct a pancreatic cancer cell strain capable of stably expressing luciferase genes; establishing a type 2 diabetes mellitus mouse model, then establishing a type 2 diabetes mellitus mouse pancreatic cancer model, finally carrying out living body bioluminescence imaging observation, dynamically observing tumorgrowth and metastasis conditions in a model mouse by using an animal living body imaging system, then placing the model mouse in the living body imaging system for exposure imaging, and collecting photon numerical values of the model mouse; and drawing a growth curve of the tumor cells in the model mouse. The method disclosed by the invention provides an ideal experimental animal model for researching a molecular mechanism from blood glucose regulation of pancreatic cancer to early metastasis in vivo, and opens up a new field for preparing animal models for clinically treating chronic diseasescomplicated with malignant tumors.

The present invention relates to methods of inducing expression of a polynucleotide encoding a therapeutic polypeptide, e.g., TNF-α, in a cell comprising contacting the cell with a construct comprising an Egr-1 promoter operably linked to a polynucleotide encoding the polypeptide, and at least one chemotherapeutic agent, wherein the chemotherapeutic agent induces expression of the polypeptide. The invention also relates to methods of inhibiting a neoplastic cell, comprising contacting the cell with a construct comprising an Egr-1 promoter operably linked to a polynucleotide encoding TNF-α and a chemotherapeutic agent. The present invention further relates to methods of inhibiting or reducing the growth of a tumor in a subject, comprising co-administering to the subject a construct comprising an Egr-1 promoter operably linked to a polynucleotide encoding TNF-α and a chemotherapeutic agent, wherein the co-administration inhibits or reduces the ability of the tumor to grow.

The present invention is directed to nucleic acids encoding a secreted polypeptide that inhibits neoplastic growth in tumor cells. Also provided herein are vectors and host cells comprising those nucleic acid sequences, chimeric polypeptide molecules comprising the polypeptides of the present invention fused to heterologous polypeptide sequences, antibodies which bind to the polypeptides of the present invention and to methods for producing the polypeptides of the present invention.

The inventors have identified a novel cell-penetrating sequence, termed hAP10, from the C-terminus of the human protein Acinus. hAP10 was able to efficiently enter various normal and cancerous cells, likely through an endocytosis pathway, and to deliver an EGFP cargo to the cell interior. Cell penetration of a peptide, hAP10DR, derived from hAP10 by mutation of an aspartic acid residue to an arginine was dramatically increased. Interestingly, a peptide containing a portion of the heptad leucine repeat region domain of the survival protein AAC-11 (residues 377-399) fused to either hAP10 or hAP10DR was able to induce tumor cells death in vitro and to inhibit tumor growth in vivo in a sub-cutaneous xenograft mouse model for the Sézary syndrome. Combined, the results indicate that hAP10 and hAP10DR may represent promising vehicles for in vitro or in vivo delivery of bioactive cargos, with potential use in clinical settings. Thus the present invention relates to cell penetrating peptides and uses thereof for intracellularly delivery of molecules.

The invention relates to a breast-cancer-treating genetic drug hdm2-siRNA design, synthesizing, cytosis detecting, target mRNA and target protein level silence action detection, induced cell apoptosis and cycle retardation detection and in vivo antineoplastic action detection, wherein the short interference RNA (siRNA) designed aiming hdm2 gene can inhibit the accretion or MCF-cell after cell transfection, specifically lower the mRNA level and HDM2 protein expression level of the hdm2 genes, and induce MCF-7 cytogenesis apoptosis and G1 period retardation simultaneously.

The invention discloses a PADI4 (Protein-arginine Deiminase type IV) stimulated DC-CIK (Dendritic Cell-Cytokine-Induced Killer) cell composition and application and belongs to the technical field of immunotherapy of tumors. The invention provides the PADI4 stimulated DC-CIK cell composition and application thereof to tumor therapy through researching a potential effect of PADI4 used as a tumor marker to DC-CIK cell immunotherapy. PADI4 protein can be used for remarkably promoting DC maturation, CIK cell proliferation and cell toxicity; PADI4 stimulated DC-CIK cells are used for remarkably inhibiting the growth of the tumors and the PADI4 has influences on the growth of the tumors through promoting the DC maturation, the CIK cell proliferation and the cell toxicity. The PADI4 possibly becomes a target antigen with strong attraction, which is used for enhancing the cell immunotherapy.