73 results about "Ganglioglioma" patented technology

The invention discloses gene engineering tumor targeted polypeptide and a preparation method and application thereof. The method separates a polypeptide, a sequence of the a polypeptide is an amino acid sequence shown in SEQ ID NO: 1. A primer that the gene engineering relates to inserts a nucleotide sequence of KCT-W1 into an expression vector pGEX-6p-1 to form recombinant expression plasmids; the recombinant expression plasmids transform colon bacillus Rossetta(DE3) and then obtain recombinant KCT-W1 polypeptide through cell lysis and GST affinity chromatography, the cutting of small intestine kinase and chromatogram purification. Cy5.5NHS easter is used to mark the KCT-W1 polypeptide to obtain a steady KCT-W1 polypeptide fluorescence complex. The KCT-W1 polypeptide fluorescence complex has special target function for neuroglioma transplanted under the oxter of a big mouse, and can perform accurate tracing and positioning to tumor. The invention also discloses a use of the KCT-W1 polypeptide fluorescence complex in the preparation of medicine used to treat or prevent incipient tumor. The method is simple and easy, convenient in operation, highly efficient and sensitive.

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.

Eflornithine is an agent that can be used to treat glioma, especially glioma of WHO Grade II or Grade III such as anaplastic glioma. Eflornithine can suppress or prevent mutations in glioma which can cause the glioma to progress to a higher grade. Compositions and methods can include eflornithine or a derivative or analog of eflornithine, together with other agents such as conventional anti-neoplastic agents for treatment of glioma, inhibitors of polyamine transport, polyamine analogs, or S-adenosylmethionine decarboxylase inhibitors.

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.

The present invention provides a new drug to treat malignant glioma, which is the most prevalent type of primary tumor of the central nervous system (CNS). The present invention indeed shows that the isolated NFL-TBS40-63 peptide is highly specific for glioma cells, in which it triggers apoptosis. It is therefore presented here for use in a method for treating malignant glioma. The present invention further relates to the use of the NFL-TBS40-63 peptide for detecting specifically glioma cells either in vivo, or in vitro, or for addressing chemical compounds to said tumor 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 present invention provides a TOP2A inhibition by temozolomide useful for predicting glioblastoma patient's survival. Glioblastoma (GBM) is the most common, malignant primary adult brain tumor. The conventional treatments for GBM, include surgery, radiation, and chemotherapy which have only modestly improved patient survival. The patients with GBM expressing higher TOP2A transcript levels had better prognosis. More interestingly, the present invention reports that temozolomide is an inhibitor of TOP2A activity in vitro. The present invention further shows that siRNA knock down of TOP2A rendered a glioma cell line resistant to temozolomide chemotherapy.; Thus it is demonstrated for the first time that temozolomide is a TOP2A inhibitor and establishes that TOP2A transcript levels determines the chemosensitivity of glioblastoma to temozolomide therapy thus explaining the very high levels of TOP2A transcript being a good prognostic indicator in GBM patients receiving temozolomide chemotherapy.

Provided herein are methods of treating an IDH mutant cancer in a subject comprising administering to the subject a therapeutically effective amount of a composition comprising an all-trans retinoic acid (ATRA). In some embodiments, the methods increase an NK-cell-mediated immune response and / or a T cell-mediated immune response to the cancer. In some embodiments, the cancer is a glioma or a chondrosarcoma. In some embodiments, the expression of one or more NKG2D ligands (e.g., ULBP1 and ULBP3) is increased in a tumor microenvironment of the cancer. In some embodiments, CCL2 production, the number of NK cells, and / or apoptosis of tumor cells is increased in a tumor microenvironment of the cancer. In some embodiments, the subject has an IDH1 mutation at arginine 132 or an IDH2 mutation at arginine 172. In some embodiments, method reduces growth of a tumor.

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 a clerodane type diterpene compound for treating neuroglioma, belongs to the field of medicine, and specifically relates to a novel clerodane type diterpene compound which is separated from dry nearly-matured fruits of cardamom, a preparation method and medical applications thereof. The compound is reported for the first time and is extracted from the dry nearly-matured fruits of cardamom, the extract is separated and purified, and the purity is high. The in-vitro experiment results show that the compound can inhibit human brain malignant glioblastoma U251 cell by inhibiting cell proliferation and inducing apoptosis and can be further developed to prepare drugs for treating neuroglioma.

A method of treating a patient suffering from a glioma. The method comprises delivering electrical energy to a glia at a margin of the glioma, thereby stimulating the glioma.

Using gene array technology, we observed that an increase of the α4 chain-containing Laminin-8 correlated with poor prognosis for patients with brain gliomas. We established that inhibition of Laminin-8 expression by a new generation of highly specific and stable antisense oligonucleotides (Morpholino™) against chains of Laminin-8 could slow or stop the spread of glioma. This was demonstrated in an in vitro model using human glioblastoma multiforme cell lines M059K and U-87MG co-cultured with normal human brain microvascular endothelial cells (HBMVEC). Using Western blot analysis and immunohistochemistry, we con-firmed that antisense treatment effectively blocked laminin-8 protein synthesis. Antisense oligonucleotides against both α4 and β1 chains of laminin-8 blocked significantly the invasion of co-cultures through Matrigel. The results show that Laminin-8 may not only contribute to glioma progression and recurrence as part of the neovascularization process but also by directly increasing the invasive potential of tumor cells.

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 present invention relates to a method of treating glioma in a subject. The method comprises selecting a subject having a glioma, providing an inhibitor of binding between a PAR-1 receptor and a ligand of the PAR-1 receptor, and administering the inhibitor to the selected subject under conditions effective to treat the glioma and / or prevent spread of tumor cells. Methods for inhibiting proliferation of glioma cells and / or precursors thereof and a method of screening for compounds suitable for treating glioma in subjects are also disclosed.

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 invention relates to a medicine combination for treating human neuroglioma during nursing. The medicine combination comprises an effective quantity of compound and a pharmaceutically acceptable carrier, and the compound is of a structure in the specification. The compound of the medicine combination has growth inhibition activity on human neuroglioma cells.

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.

The invention discloses usages of CNTN3 protein, application of the CNTN3 protein in preparation of drugs for diagnosis and prognosis judgement or treatment of neuroglioma, and application of mRNA encoding the CNTN3 protein in preparation of the drugs for diagnosis and prognosis judgement or treatment of neuroglioma. By detecting the CNTN3 protein / mRNA in a tissue sample, the prognosis of a gliomapatient can be judged effectively. The usages of the CNTN3 protein disclosed by the invention can provide strong technical support for prognosis analysis of a neuroglioma patient, are beneficial fora clinician to choose a reasonable subsequent therapeutic schedule, improve postoperative living quality of the neuroglioma patient, increase survival rate of the patient, have profound clinical significance, and are suitable for clinical popularization and application.