47 results about "Neoplastic growth" patented technology

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 relates to a pyridine chemical shown as the following general formula and having c-Met and / or ALK inhibitory activity and its pharmaceutically-acceptable salt or pharmaceutically-acceptable solvate, a preparation method thereof, a pharmaceutical composition containing the chemicals, and applications of the chemicals in preparation of medicines for preventing and treating abnormal proliferation and morphological change of cells and related diseases, such as hyperkiesis, related to hepatocyte growth factor receptor (HGFR) and / or anaplastic lymphoma kinase (ALK) in organism and diseases related to vascularization or cancerometastasis, especially application in preparation of medicines for treating and preventing growth and metastasis of tumor.

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.

Leptin was previously demonstrated to exert potent immune modulatory properties in several immune mediated disorders. The aim of the study was to determine leptin's anti-tumor effect in a murine model of human hepatocellular carcinoma (HCC). In vivo, Athymic T cell deficient (nude) mice transplanted with 1×106 human Hep3B cells, followed by administration of two daily intraperitoneal doses of 0.5 mg / gram leptin for 6 weeks. Leptin administration induced a significant reduction in tumor size and improved survival in nude mice. Histologically, tumors of leptin-administered mice featured increased inflammatory exudate in interphase areas. Leptin-induced tumor suppression was associated with a significant increase in peripheral natural killer (NK) cell number. Splenocytes from leptin-treated mice featured decreased expression of CIS mRNA. To determine which lymphocyte subset is a prerequisite for the anti tumor effect of leptin, T&B cell deficient (Scid) mice and T,B& NK deficient (Scid-Beige) mice were subcutaneously implanted with Hep3B tumor cells, with and without the daily intraperitoneal administration of 0.5 mg / gram leptin for 6 weeks. SCID mice featured leptin-associated tumor suppression similar to those of nude mice. In contrast, NK-deficient SCID-Beige mice developed larger tumors. To further establish natural killer cell's central role in mediation of leptin's anti-tumor effect, NK cells were incubated in vitro with increasing doses of leptin, demonstrating a dose-dependent increase in cytotoxic activity. Incubation of leptin with hepatoma cell line was found to induce a dose-dependent reduction in hepatoma cell proliferation, suggesting an additive direct anti-tumor effect. Further synergism in inhibition of hepatoma cell proliferation in vitro was achieved following addition of natural killer cells. HCC cells expressed leptin receptor mRNA, while addition of leptin induced increased mRMA expression of STAT2 and SOCS1 on tumor cell lines. Leptin administration induces a significant suppression of human HCC. This effect is mediated by induction of natural killer cell proliferation and activation, and by direct inhibition of tumor growth. Decreased natural killer cell expression of inhibitory CIS protein and over expression of the anti-proliferative STAT2 and SOCS1 proteins in HCC lines may underline both anti cancerous effects of leptin.

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.

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.

The present invention relates to a composition for preventing or treating cancer, which contains, as an active ingredient, a Panax ginseng cambium-derived cell line including wild ginseng or ginseng; a lysate thereof; an extract thereof; or a culture medium thereof.The cell line according to the present invention, a lysate thereof, an extract thereof and a culture medium thereof are derived from a natural and have minimized side effects compared to the conventional therapeutic drugs, and thus are safe for the human body. Also, they are involved directly in the growth of cancer to induce cancer cell death effectively, and show anticancer activity of inhibiting or reducing the formation of tumor or the growth of tumor, Accordingly, the cell line, the lysate thereof, the extract thereof and the culture medium thereof are useful for the prevention, treatment and alleviation 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.

The invention provides novel application of parthenolide, luteolin, chrysoeriol and ginsenoside Rg3, and specifically relates to preparation of the compounds or derivatives of the compounds in preparation of drugs for preventing and / or treating drug-resistant BRAF (V600E) mutant-type tumors. It is found that proliferation of tumor cells resistant to BRAF (V600E)-targeted drugs can be inhibited through parthenolide, luteolin, chrysoeriol and ginsenoside Rg3, the tumor cells include inherent and acquired tolerant tumor cells, and growth of tumors is inhibited. It is shown through results that parthenolide, luteolin, chrysoeriol and ginsenoside Rg3 have the potential to be developed as the safe and effective drugs for treating the drug-resistant BRAF (V600E) mutant-type tumors.

The invention provides an application of a combination of a sulfhydryl oxidase 1 agonist and sorafenib in preparation of liver cancer treatment cells. The sulfhydryl oxidase 1 agonist comprises lentivirus for overexpression of sulfhydryl oxidase 1 and recombinant sulfhydryl oxidase 1 protein; firstly, lentivirus for overexpression of sulfhydryl oxidase 1 is constructed, and then target cells are transfected; and the dosage forms of the sulfhydryl oxidase 1 agonist comprise an oral preparation, an injection or a sustained release preparation and the like. The lentivirus for overexpression of QSOX1 and sorafenib are used for acting on liver cancer cells at the same time, QSOX1 can inhibit the activity of the liver cancer cells, the GSH content can be more obviously reduced, the free ferrousions in the cells and the lipid peroxidation level are increased, and thus cell ferroptosis is promoted; and therefore, the lentivirus for overexpression of QSOX1 is combined with sorafenib, so that the inhibition effect on tumor growth is promoted synergistically, and a stronger killing effect is achieved.

The invention provides phthalimide compounds with an antiangiogenic activity, and the compound is as shown in a formula (I). According to the invention, the new phthalimide compounds 4,6-dihydroxyisoindol-1,3-dione and 4,6-dihydroxyisoindol-1-one isolated from traditional Chinese medicine peeled puffball fruiting body are subjected to a full synthesis and a derivative reaction at the same time, and seven new compounds are obtained. The compounds provided by the invention has no cytotoxic activity to human lung carcinoma A549 cells, can inhibit VEGF secretion level of the human lung carcinoma A549 cells, and thus can control growth of tumors through blocking or interfering signal transduction pathways of the VEGF / VEGFR. Pharmacological activity shows that the compound system provided by the invention is low in toxicity and high in security, and has important significance in inhibiting the growth of the tumors through an antiangiogenic mechanism.

The invention relates to a quinoline compound which is used as a c-Met depressant and is expressed by the general formula (I) below, a pharmaceutically acceptable salt or pharmaceutically acceptable solvate and a preparation method of the compound, a medicament combination containing the compound and application of the compounds in the preparation of medicaments for preventing or treating diseases relevant to abnormal cell proliferation, morphological change and hyperkinesia with respect to hepatocyte growth factor receptors (HGFR) in an organism as well as diseases relevant to angiogenesis or cancerometastasis, especially medicaments for treating or preventing growth and metastasis of tumors.

The invention discloses a CCL1-containing fusion protein, a preparation method and application, the fusion protein sequentially comprises an IgE signal peptide, CCL1, a linker and an antigen from an N terminal to a C terminal, or the IgE signal peptide, CCL1, the linker, the antigen and a T2 fragment, and the amino acid sequence of the T2 fragment is shown as SEQ ID NO: 4. According to the invention, different antigen proteins are transferred and crossly presented to the surface of the DC cell by utilizing the chemotactic binding capacity of CCL1 and surface receptors of immune cells such as the DC cell, so that the efficiency of phagocytosis, processing and presentation of various antigen proteins by the DC cell is improved, and the effect of preventing and treating related diseases is improved. Experiments prove that the T2 sequence disclosed by the invention has a very strong immune enhancement effect, and can further excite body fluid and cellular immune response in the process of promoting antigen presentation, so that the effect of inhibiting growth of related tumors is finally achieved.

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.

A genetically modified NOD.Cg-Prkdcscid Il2rgtm1Wjl / SzJ mouse is provided by the present invention wherein the genome of the mouse includes a mutated Rhbdf2 gene such that the mouse expresses a mutant iRhom2 protein, wherein the mutant iRhom2 protein differs from wild-type iRhom2 protein due to one or more mutations selected from p.I156T, p.D158N and p.P159L, and wherein the mouse is characterized by hairless phenotype and increased growth of an exogenous tumor compared to a mouse of the same genetic background which express wild-type iRhom2 protein.

Tumor infiltrating lymphocytes (TILs) are white blood cells that are actively recruited to the tumor site to mount an immune response against tumor growth and metastasis. The disclosure provides methods for treating cancer that comprise steps of isolating CD8+ T cells from a sample derived from a subject, expanding the CD8+ T cells in the presence of interleukin-10, and administering the expandedCD8+ T cells to the subject. Methods of treating cancer may be used in combination with inhibitors of the complement signaling pathway.

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 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.

To study the mechanism of βig-h3 modulation of the anti-tumoral immune response in pancreatic cancer, Inventors took advantage of engineered mouse models of spontaneous pancreatic neoplasia and cancer to evaluate the effect of depleting βig-h3 on the modulation of anti-tumor immunity and its subsequent impact on tumour growth alone and in combination with an immune checkpoint inhibitor. This association proved to be effective in vivo in this model showing a synergic effect of the therapeutic combination. Accordingly, the present invention relates to a combination of (i) an immune checkpoint inhibitor, and (ii) a βig-h3 antagonist, for simultaneous or sequential use in the treatment of a patient suffering from solid tumor, e.g. a pancreatic cancer. The present invention also provides a βig-h3 antagonist, for use in a method for enhancing sensitivity of a patient suffering from a solid tumor to an immune checkpoint inhibitor.