73 results about "Ganglioglioma" patented technology

The present invention embraces microRNA-antagonists and activators of homeobox D10 protein; Zinc finger, MYND domain containing 11 protein; or RB1-inducible coiled-coil 1 protein for use in decreasing glial tumor cell proliferation and treating glioma.

The invention is based on observing that LIF is capable of activating the self-renewal of tumor stem cells in cancer, in particular gliomas, which indicates that the inhibition of LIF, and generally of IL-6 type cytokines, can be used in therapeutic compositions for the treatment of diseases associated with unwanted proliferation. The invention also relates to a method for the identification of compounds capable of blocking/inhibiting the proliferation of stem cells, and to an in vitro method for the diagnosis of diseases associated with unwanted cell proliferation in a subject or for determining the predisposition of a subject to suffer said disease associated with unwanted cell proliferation, or for prognosis of average life expectancy of subjects suffering from said tumors.

The present invention is directed to methods of treating a primary brain tumor and preventing the migratory spread of a primary brain tumor in a subject. These methods involve utilizing the CD24 surface protein selectively expressed on tumor progenitor cells as a therapeutic target as well as a means for directing oncolytic therapeutics directly to the tumor site. The present invention further relates to methods of diagnosing the presence of a brain tumor and monitoring the status of the brain tumor in a subject based on CD24 expression in tumor progenitor cells.

Disclosed are compounds that are effective for selectively killing cancer cells. Compounds have been demonstrated to be especially effective for killing glioma cells, while exhibiting low toxicity to normal cells.

The invention relates to a medicinal diterpenoid compound separated from dried aerial parts of Callicarpa nudiflora and a preparation method of the compound. The diterpenoid compound is reported for the first time, adopts a novel structure, and can be obtained through extraction from the dried aerial parts of the Callicarpa nudiflora, separation and purification. In-vitro tests prove that the compound plays a role in inhibiting human brain glioblastoma U251 cells by inhibiting cell proliferation and inducing cell apoptosis and can be developed into drugs for treating neuroglioma.

Disclosed are compositions of matter, therapeutic protocols, and immunization means to induce an active immune response to vasculature feeding glioma or other brain neoplasia. In one embodiment the invention provides administration of placental derived endothelial cells at concentrations of 10 million to 50 million administered in a manner to stimulate immunity toward blood vessels supplying glioma or other brain neoplastic malignancies. The invention provides means of blocking augmenting efficacy of immunotherapy, chemotherapy, and radiotherapy.

The invention relates to fusion protein (Arg)9-LDP and reinforced fusion protein (Arg)9-LDP-AE thereof. The fusion protein consists of cell-penetrating peptide (Arg)9, lidamycin apoprotein LDP and carboxyl terminal hexamerichistidine tail, wherein the full length of gene is 387bp, and 129 amino acids are encoded; the reinforced fusion protein is formed by fusion protein (Arg)9-LDP with molecular weight of about 14.5kDa and activated enediyne chromophore AE with molecular weight of 843Da; in-vivo and in-vitro experiment results prove that the fusion protein and reinforced fusion protein thereof have intense killing effect on glioma cells, and have remarkable curative effect in in-vivo animal experiments, and are expected to be developed into clinic efficient glioma treating medicament.

The invention discloses a neuroglioma 1p/19q co-deletion detection system based on next generation sequencing. The system comprises an SNP locus screening device, an SNP detection device without a check sample and/or an SNP detection device with a check sample, wherein the SNP locus screening device is used for screening SNP loci on the first chromosome and nineteenth chromosome of the human according to an existing database to obtain a first group of SNP loci, and the SNP detection device without the check sample comprises a first sequencing module used for sequencing a to-be-sequenced sampleand a group of negative samples, a first SNP detection module, a first gSNP locus screening module, a second SNP detection module, a first calculating statistics module and a first judgement module.The system is utilized and combined with information on 1q and 19 p to correct information of 1p and the 19q, the detection accuracy is improved, and 1p/19q co-deletion can be identified efficiently,conveniently and accurately.

Provided are methods of targeting patient-specific oncogenes in extrachromosomal DNA (ecDNA) to treat glioma in a human. The present methods include identifying a drug that targets against an oncogene present in ecDNA of a human suffering from glioma, such as glioblastoma. The identified oncogenes present in ecDNA include MET, MET/CAPZA2, MDM2, CDK4, SOX2, PIK3CA, MECOM, PDGFRA, EGFR, MYCN, MYC, TERT, SMARCA4, RP56, FBXW7, CDK6, CCND2, ERBB2, BRCA1, and BAP1. The present methods include identifying a drug targeted against the ecDNA oncogene, which drug inhibits the function of the identified oncogene, so as to inhibit tumor growth or progression of the glioma in the human. Also provided are PDX mouse models to further identify and/or confirm patient-specific drugs that target the identified oncogene(s) present in ecDNA. Also provided are methods of diagnosing gliomas or recurrent gliomas and methods of screening or monitoring for recurrence of gliomas. Further provided are methods of validating a predicted presence of ecDNA in a brain tumor using fluorescence in situ hybridization (FISH). Also provided are methods of screening drug candidates for a patient by implanting different identified drugs that target an identified oncogene into PDX mouse models.

There is presently provided a nucleic acid molecule comprising a glial-specific promoter; a coding sequence for a transgene; and a plurality of miRNA target sites. Each miRNA target site binds an miRNA that is down-regulated in .a glioma cell compared to a normal glial cell, and the glial-specific promoter and the plurality of miRNA target sites are both operably linked to the coding sequence for the transgene.

The invention discloses application of RDH10 gene to brain glioma diseases. The RDH10 gene is highly expressed in brain gliomas, and the RDH10 gene is closely related to the brain glioma grade and thesurvival time of a patient. In-vitro lentivirus-mediated shRNA RDH10 gene knockout significantly inhibits proliferation and apoptosis of glioma cells, increases and induces S-G2/M cell cycle arrest and inhibits the invasion functions of the glioma cells. RDH10 gene knockout also slows growth of neurogliomas of a nude mouse. Researches find that both in vivo and in vitro, the RDH10 gene plays an important role in occurrence and progression processes of the brain gliomas, and according to high expression results of the RDH10 gene in brain glioma tissues, a powerful method is provide for biological targeted treatment to the gliomas in the further.

The invention discloses application of a RDH10 (retinol dehydrogenase 10) gene to preparation of a TWEAK-NF-kappaB signal pathway blocking agent. A positive correlation exists between RDH10 gene expression and the glioma grade, and RDH10 gene knockout regulates proliferation of neuroglioma cells in vitro, causes S and G2/M cell cycle arrest, inhibits the RDH10 gene to cause growth retardation of the glioma cells, and causes decrease in cell invasion ability of the glioma cells. RDH10 gene knockout changes related expression of the TNFRSF12A (TWEAKR), TRAF1, TRAF3, BMPR2, TNFAIP3, NFKBIA, NFKBIE and IKBKB, and such a result shows that the RDH10 may affect the proliferation, the apoptosis and the cell cycle of the glioma cells by regulating a TWEAK-NF-kappaB signal pathway. Researches find that the RDH10 plays an important role in occurrence and progression processes of the gliomas. Studies on the functions of the RHD10 gene provide a powerful method for targeted treatment to human neurogliomas.

The invention belongs to the field of biotechnology and medicine, relates to oligoden droglioma (OG) markers, and particularly relates to a protein marker MAP2 (microtubuleassociated protein 2) protein which can differentiate OG that clinically has sensitivity to chemotherapy and 1P loss of heterozygosity (1P LOH), and use thereof. According to the invention, the protein marker MAP2 protein which can differentiate the OG that clinically has sensitivity to chemotherapy and 1P loss is determined through the iTRAQ-LC-MS/MS technology. The MAP2 protein has 90% accuracy for the prognosis of the 1P loss. The marker not only can explain the mechanism for the sensitivity to chemotherapy of an OG sample with the 1P LOH, but also can prognose the sensitivity to chemotherapy of an OG patient with the 1P LOH through a decision tree model. The MAP2 protein can be further used for preparing a clinical kit so as to offer help for the diagnosis, the prognosis and the treatment of the OG.

The invention discloses a construction method of an in-vitro glioblastoma (GBM) invasion model based on biological three-dimensional printing, which belongs to the field of tissue engineering and biological three-dimensional (3D) printing. According to the method, hydrogel containing cells is used as biological ink, and an in-vitro GBM invasion model is constructed by using a biological three-dimensional printer. The model structure is formed by printing hydrogel carrying normal human brain glial cells, and is inoculated with glioma cell clusters. The model has important significance for researching invasive growth of GBM, and is expected to provide help for researching a treatment method of polymorphic glioblastoma.

The present invention relates generally to therapeutic agents, formulations comprising them and their use in the treatment, amelioration and/or prophylaxis of glioma brain tumours and related conditions. The therapeutic agent comprises two fused 6-membered rings with at least a nitrogen at position 1 and a hydroxyl at position 8.