70 results about "Glioblastoma cell" patented technology

The invention provides antibodies to a mutant form of the epidermal growth factor receptor known as EGFRvIII found only or primarily on the surface of glioblastoma cells, and on cells of breast, ovarian and non-small cell lung carcinomas. The antibodies provided by the invention have the complementarity determining regions (“CDRs”) of the scFv designated MR1, but with mutations at positions 98 and 99 in the CDR3 of the heavy chain variable region and, optionally, in other CDRs. In particular, the invention provides an antibody, designated MR1-1, which mutates MR1 in the CDR3 of the VH and VL chains. The invention provides additional antibodies in which MR1 is mutated in the CDR1 and 2 of VH or VL, or both.

Viability of cancer cells (e.g., glioblastoma cells) can be reduced by administering ABT-751 to the cancer cells and applying an alternating electric field with a frequency between 100 and 400 kHz (e.g., 200 kHz) to the cancer cells. Notably, experiments show that the combination of ABT-751 and the alternating electric field produces synergistic results for certain glioblastoma cell lines.

The invention is based on the discovery that STM/Hop promotes proliferation of human glioblastoma-derived cells but not of normal astrocytes and that the proliferation requires the binding of STM/Hop to PrP^C. The invention is directed to methods for treating cancer which rely on interfering with the Hop-PrP^C interaction and to peptides, and antibodies raised against the peptides, which directly provide that interference. The invention is further based on the discovery that STI1_230-245 peptide and its human homologue Hop23o-245 provide the desired interference with the STI1/Hop-Pre interaction and inhibit the STI 1/Hop-induced proliferation of glioma and glioblastoma cells. The invention is thus further directed to methods of treating cancer that employ these peptides and functional derivatives thereof, and antibodies directed to the peptides and derivatives. The invention is further directed to means of treating cancer which involve reducing the effective amount of Hop or reducing the expression of Hop. The invention is further directed to means of alleviating or eliminating the side effects of drug therapy and radiotherapy used in treating patients with brain cancers.

A method for purifying an immunosuppressant protein (HISP) has the steps of obtaining supernatant from hNT cells; exposing the supernatant to preparative polyacrylamide gel electrophoresis to produce 20 isoelectric fractions, including active isoelectric fraction #10; placing the active isoelectric fraction on a Blue Sepharose column to bind albumin; and collecting the free fraction containing the concentrated, isolated HISP. Also disclosed is a method of treating inflammation, using an effective amount of an HISP. The HISP is anionic, has a molecular weight of 40-100 kDa, an isoelectric point of about 4.8 and is obtained from the supernatant of hNT cells, but not from NCCIT embryonal carcinoma cells, T98G glioblastoma cells or THP-1 monocytic leukemia cells. HISP can maintain T cells in a quiescent G₀/G₁ state without lowering their viability. HISP loses activity when treated with heat, pH2, pH11, or mixed with trypsin or carboxypeptidase, but not with neuraminidase. HISP can suppress proliferation of responder peripheral blood mononuclear cells in allogeneic mixed lymphocyte cultures; HISP can suppress T-cell proliferation and IL-2 production in response to phorbol 12-myristate 13-acetate (PMA), ionomycin and concanavalin-A. HISP does not bind to heparin-sepharose CL-B gel; or to albumin-binding resin Blue Sepharose. HISP is concentrated with YM10 ultrafiltration. HISP does not act through the T-cell receptor-CD3 complex or via altered accessory signal cells. A method of treating inflammation comprises administering an effective amount of hNT neuronal cells.

Geldanamycin derivatives that block the uPA-plasmin network and inhibit growth and invasion by glioblastoma cells and other tumors at femtomolar concentrations are potentially highly active anti-cancer drugs. GA and various 17-amino-17-demethoxygelddanamycin derivatives are disclosed that block HGF/SF-mediated Met tyrosine kinase receptor-dependent uPA activation at fM levels. Other ansamycins (macbecins I and II), GA derivatives, and radicicol required concentrations several logs higher (≧nM) to achieve such inhibition. The inhibitory activity of tested compounds was discordant with the known ability of drugs of this class to bind to hsp90, indicating the existence of a novel target(s) for HGF/SF-mediated events in tumor development. Methods of using such compounds to inhibit cancer cell activities and to treat tumors are disclosed. Such treatment with low doses of these highly active compounds provide an option for treating various Met-expressing tumors, in particular invasive brain cancers, either alone or in combination with conventional surgery, chemotherapy, or radiotherapy.

The invention belongs to the technical field of medicines, and discloses a construction method and application of a glioblastoma organ model. The method for constructing the glioblastoma organ model comprises the following steps: pretreating a glioblastoma cell line to obtain single glioblastoma cells, and transplanting the single glioblastoma cells into cerebral cortex organs cultured for 30 days. The method provided by the invention can simulate the growth characteristics of glioblastoma and the microenvironment of tumors clinically to realize simulation of the growth process of tumor cellsin the normal brain tissues. Furthermore, in order to observe the growth of glioblastoma cells in organoids, a red fluorescent dye is used for marking tumor cells instead of lentiviral transfection oftumor cells. The method is simple and feasible. The influence of lentivirus transfection labeling on the cell growth state is avoided. Meanwhile, the culture time of the system is shortened, the fluorescence labeling difficulty is reduced, and conditions are provided for rapidly applying a tumor sample to experimental researches clinically.

The invention belongs to the technical field of medicine and particularly relates to a pharmaceutical composition for treating glioma.The pharmaceutical composition comprises a component A, a component B, a component C and a component D, wherein the component A is diterpenoids (I) extracted from callicarpa nudiflora, the component B is withanolides (II) extracted from the dried whole herb of asiatic plantain, the component C is triterpenoid saponins echinoside A purchased from the market, and the component D is flavonoids (IV) extracted from the overground part of vervain.In-vitro experiment prove that the pharmaceutical composition can inhibit the human brain malignant glioblastoma U251 cells by inhibiting cell proliferation and inducing cell apoptosis and can be developed into medicine for treating the glioma.

The invention discloses a drug-tolerant glioblastoma cell line of primary temozolomide and bevacizumab, a construction method and application of the cell line. The construction method comprises the following steps: obtaining tissue specimens of patients with drug-resistant glioblastoma cell of primary temozolomide and bevacizumab through clinical screening, primarily culturing tumor cells through an enzyme digestion method, and continuously extending generation to 50 generations to obtain a strain of drug-tolerant glioblastoma cell line of primary temozolomide and bevacizumab; the microbial preservation number of the drug-tolerant glioblastoma cell line of primary temozolomide and bevacizumab is CGMCC No.8205. The glioblastoma cell line, disclosed by the invention, is stable in characteristics, stably heritable and high in tolerance to temozolomide and bevacizumab; the cell generation cycle lasts about 48 hours; the glioblastoma cell line has strong invasiveness and tumorigenicity. The glioblastoma cell line constructed by the construction method has important application prospect in aspects of screening medicines for treating glioblastoma and researching nosogenesis of the glioblastoma, and the like.

The present invention discloses a dual-targeting drug carrier and a method for fabricating the same, wherein WGA- and FA-modified MPEG-PLA nanoparticles of the carrier enable the anticancer drugs encapsulated thereinside to pass through BBB and target human glioblastoma cells. The dual-target drug carrier is fabricated in an emulsion-solvent evaporation technology and verified with an in-vitro BBB model formed of HBMECs, HAs and HBVPs. The present invention can increase the permeability of the in-vitro BBB model to the dual-target drug carrier and promote the glioblastoma-inhibition effect. Therefore, the present invention would contribute to the clinical therapy of brain cancers substantially in the future.

The invention provides application of a non-nucleoside reverse transcriptase inhibitor dapivirine (TMC120) to preparation of drugs used for treating glioblastoma. According to the invention, in-vitro experiments are carried out to detect cytotoxic effect of dapivirine on a human glioblastoma cell strain U87 and influence of dapivirine on the migration and invasion ability of U87, on proliferation, apoptosis and autophagy of U87 cells, on expression of epithelial-mesenchymal transition-associated proteins and on signal channels in the U87 cells, so the potential antineoplastic effect of dapivirine is preliminarily revealed; and the in-vivo anti-glioblastoma activity of dapivirine is confirmed via a nude-mouse in-vivo transplantation tumor model. Dapivirine provided by the invention can be used for development of novel anti-glioblastoma drugs.

The invention provides an ultrasonic administration microbubble compound carrying an anti-tumor drug as well as a preparation method and application of the ultrasonic administration microbubble compound. The compound is prepared by connection of cationic microbubbles and an anti-tumor drug-PLGA nanoparticles through attraction of positive and negative charges. According to the preparation method, the GA-PLGA nano-particles are prepared by utilizing an ultrasonic emulsification effect, and the CMB and the GA-PLGA nano-particles are connected through charge attraction to form the CMBS-GA-PLGA micro-bubble compound due to the fact that the cationic micro-bubbles carry positive charges and the GA-PLGA nano-particles carry negative charges. The micro-bubbles generate a series of alternative changes such as expansion, shrinkage, oscillation and implosion under the effect of ultrasound, so that the permeability of a cell membrane is improved, the phenomenon is called as 'sound pore effect', gambogic acid can better act on glioblastoma cells by utilizing the 'sound pore effect' of the micro-bubbles under the action of ultrasound, and a new thought is expected to be provided for treatment of glioma.

The invention relates to an application of a bacillus subtilis protein AMEP412 with an amino acid sequence as shown in SEQ ID NO: 1 in inhibition of tumor cell proliferation. The tumor cells are any one of liver cancer cells, cervical cancer cells, pancreatic cancer cells, colon cancer cells, prostate cancer cells, lung cancer cells, uterine squamous cell carcinoma cells, gastric adenocarcinoma cells, malignant glioblastoma cells and breast cancer cells. According to the invention, the inhibition function of the protein AMEP412 on tumor cells is found; the protein can generate an inhibition effect on 10 kinds of tumor cells, has selective specificity on inhibition effects on different kinds of tumor cells, and has the best effect on breast cancer cells; transcriptomics research finds that the protein AMEP412 can cause the change of a plurality of pathways related to apoptosis and death in tumor cells, and a new material is accumulated for inhibiting the activity of the tumor cells.

The invention discloses application of cucurbitacin D in preparing a glioma cell activity inhibitor. The hemi-inhibitory concentrations of the cucurbitacin D on glioblastoma cell lines A172, U-87MG and U-251MG are 700nM, 150nM and 200nM, the cucurbitacin D has different degrees of inhibition on migration and multiplication of glioma cells under the two concentrations of 250nM and 500nM, and ATP enzyme activity can be reduced, so that a metaboilic level, a block cell cycle and apoptosis induction are influenced. An alternative proposal of a new chemotherapy drug is provided for treating brain malignant gliomas.

IDH1-mutant cell lines and xenografts (e.g., IDH1R132H heterozygous and IDH1R132H homozygous) are derived from human glioblastoma multiforme (GBM) samples. Methods use said cells and xenografts as tools for determining the impact of IDH1R132H on cancer properties including cellular morphology, tumorigenesis, DNA, apoptosis, and metabolic profiles. Methods also use these cell lines for the screening and identification of candidate therapeutic targets.

The invention discloses a siRNA capable of knocking down expression of a SRC-1 gene. A positive-sense strand and an antisense strand are separately as follows: the positive-sense strand: CAGCAGUCAUAGUAAUUCUTT and the antisense strand: AGAAUUACUAUGACUGCUGTT. By knocking down the SRC-1, cell proliferation of spongioblastoma and tumor growth can be inhibited, and sensibility of spongioblastoma cells to temozolomide can be increased. The siRNA can be used as a novel drug for treating spongioblastoma.

The invention belongs to the medical field and discloses an application of a grincamycin B compound in preparing anti-glioma drugs. According to the invention, the grincamycin B has selective action on glioblastoma cells, and also has very good biological activity; the grincamycin B acts in inducing the apoptosis of tumor cells and tumor stem cells and blocking cells at the stages G0-G1; the grincamycin B effectively inhibits glioma cloning; the grincamycin B effectively inhibits the formation of glioma stem cells; the grincamycin B effectively inhibits the expression of the dry gene of the glioma stem cells, and further is capable of effectively inhibiting the self-updating effect of the glioma stem cells; therefore, the grincamycin B is a potential anti-cancer drug and provides a new scheme and a new drug for oncotherapy of targeted cancer stem cells (CSC); and furthermore, the grincamycin B plays an important role in improving the oncotherapy effect and improving the life quality of a patient.

The invention relates to a research method for researching a function of an RBM8A gene for promoting glioblastoma proliferation. The method comprises the steps of 1) Western blot analysis of glioblastoma cell line RBM8A expression, 2) slow virus mediated knockout and overexpression of RBM8A, 3) effect of interfering RBM8A gene expression on glioblastoma cell proliferation, 4) observation of effectof knockout of RBMBA on glioblastoma proliferation at the animal level, 5) detection of the conditions of Notchl, phosphorylated STAT3 (p-STAT3), total STAT3 (STAT3), phosphorylated H3 (p-H3), totalH3 (H3) and actin in the glioblastoma cell line which interferes with RBM8A gene expression through Western blot analysis. The Notch/STAT3 pathway is a RBM8A-mediated cell proliferation mechanism of glioblastoma cells. The invention provides a new idea for treating the glioblastoma, and provides a new way for researching drug treatment targets of the glioblastoma.

The invention relates to an interference plasmid for knocking down expression of COPS5 protein in a glioblastoma cell line, application of the interference plasmid as a drug for solving the drug resistance problem of temozolomide in treatment, and application of a combined drug formed by the interference plasmid for knocking down expression of the COPS5 protein and temozolomide as a glioblastoma chemotherapeutics. The interference plasmids knock down expression of COPS5 protein and regulate the ferroptosis process of glioblastoma cells, specifically, the expression of ferroptosis promoting protein is increased, and the expression of ferroptosis inhibiting protein is reduced.

Provided is a method for producing a glioblastoma mouse model and the mouse model produced thereby, the method including the steps of: (a) dividing a glioblastoma tissue, isolated from a patient, into 4 or more sections, and collecting one or more pieces from each of the sections; (b) dissociating a mixture of the collected pieces into glioblastoma cells as single cells; and (c) orthotopically transplanting a graft sample containing the glioblastoma cells obtained in step (b), into the brain of an immunodeficient mouse. Further provided are a method of screening a glioblastoma therapeutic agent using the mouse model and a method of providing information for selection of a patient-specific glioblastoma therapy using the mouse model. The glioblastoma mouse model shows the same genetic, morphological and pathological characteristics as those of the parental tumor, and it allows screening patient-specific glioblastoma therapeutic agent or selecting safer and more effective patient-specific glioblastoma therapy.