38 results about "Astrocytoma resection" patented technology

The present invention provides a recombinant toxin and monoclonal antibody which specifically binds to glial-derived or meningioma-derived tumor cells. Also provided are various methods of screening for malignant gliomas and meningiomas. Further provided are methods of treating malignant gliomas, including glioblastoma multiforme and astrocytomas.

Disclosed are transgenic animals and transfected cell lines expressing a protein associated with Alzheimer's Disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas. Also disclosed is the use of such transgenic animals and transfected cell lines to screen potential drug candidates for treating or preventing Alzheimer's disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas. The invention also relates to new antisense oligonucleotides, ribozymes, triplex forming DNA and external guide sequences that can be used to treat or prevent Alzheimer's disease, neuroectodermal tumors, malignant astrocytomas, and glioblastomas.

The invention relates to a glioma typing system based on IDH1-R132H and ATRX expression. The system comprises: (1) glioma patients' tumor paraffin embedding kit and optional kit application instruction; (2) a kit for immunohistochemical detection of ATRX protein expression level of tumor of glioma patients and optional kit application instruction; and (3) a kit for immunohistochemical detection of IDH1-R132H protein expression in tumor of glioma patients and optional kit application instruction. When IDH1-R132H and ATRX losses are combined as diagnostic markers for distinguishing primary glioblastoma, WHO grading II/III oligodendroglioma, WHO grading II/III astrocytoma and secondary glioblastoma, diagnostic specificity is obviously higher than diagnostic specificity of the two single markers of IDH1-R132H or ATRX losses.

The invention relates to the identification of astrocytoma markers, astrocytoma stem cells and markers of such stem cells, and diagnostic, prognostic and therapeutic methods based on an understanding of the markers and cells.

The disclosure provides methods of treating glioblastoma, methods of screening for compounds that treat glioblastoma, and pharmaceutical compositions useful in the treatment of glioblastoma.

Disclosed is a method of diagnosing the presence of higher grade astrocytoma/glioblastoma (GBM) or lower-grade grade astrocytoma (DA or AA) in a human subject using secreted or plasma membrane associated biomarkers, which involves the detection of the expression levels of said genes, alone or in combination, in either tumor tissue samples or body fluids and a diagnostic kit thereof.

The invention discloses a monoclonal antibody for mouse anti-human type BRAF V600E mutant protein. The monoclonal antibody is high in specificity, stable in expression and high in potency, can be applied to BRAF V600E mutant protein in malignant tumors, and has a certain medicine-based research value. The invention also relates to application of the monoclonal antibody to preparation of an immunohistochemical detecting tool for detecting the BRAF V600E mutant protein. According to the monoclonal antibody and the application of the monoclonal antibody disclosed by the invention, an immunohistochemical technology based on the BRAF V600E monoclonal antibody is built and is used in auxiliary diagnosis, selection of treatment schemes and prognosis of the malignant tumors, wherein the malignanttumors mainly comprise malignant melanoma, lung adenocarcinoma, colorectal carcinoma, gastrointestinal stromal tumors, papillary thyroid carcinoma, astrocytoma, hairy cell leukemia, lynch syndrome andthe like. Based on simple operation and less charging of the immunohistochemical method, the method can be used as a first-choice detection method of BRAF V600E gene mutation in clinic work.

The present invention relates to the use of a compound that specifically binds to JAM-C or JAM-B for the treatment of gliomas. More specifically the invention relates to the use of an antagonist of JAM-B or JAM-C for the treatment of glioma, in particular astrocytoma.

The present invention provides radiosensitizer compositions, in controlled-release formulations or other acceptable formulations, particularly nitrohistidine radiosensitizer compositions, which may be administered by any suitable means including oral, intravenous, arterial infusion, intraperitoneal, intramuscular, subcutaneous, surgical, and topical. Optionally, radiosensitizer compositions may be formulated with other agents, including chemotherapy agents and agents that provide a synergistic radiosensitizing effect. Methods of potentiating radiotherapy cancer treatment of cancers in humans, particularly of astrocytomas, are also presented, wherein a radiosensitizer composition is administered and radiotherapy is directed to the site of the tumor. Chemotherapy regimens may also be used as adjuvant therapy.

The present invention relates to melanoma-associated chondroitin sulfate proteoglycan (MCSP) epitopes recognized by T cells, especially by CD4⁺ T lymphocytes (short T-cells) and CD8⁺ T cells, on human melanoma cells. In more detail, the present invention relates to novel T-cell stimulatory tumour antigenic peptides corresponding to said epitopes (MCSP peptides); to fusion proteins comprising said MCSP peptides; to the use of said MCSP peptides, fusion proteins or of the full length MCSP protein itself or fragments thereof to induce an immune response, especially a T-cell response; to the use of said MCSP peptides, fusion proteins or full length MCSP protein itself or fragments thereof to prepare immune cells, such as mature dendritic cells (DCs) loaded with anyone of the peptides according to the invention, or peptide-specific T-cell clones, especially CD4⁺ or CD8⁺ T cell clones; to the use of said MCSP peptides, fusion proteins or MCSP itself or fragments thereof for research and development on/of a cancer treatment; to the use of said MCSP peptides, fusion proteins or MCSP itself or fragments thereof for preparing a medicament for inducing a T cell response in a patient, preferably for the treatment of cancer, more preferably for the treatment of melanoma, including cutaneous and ocular melanoma, and other MCSP expressing tumours such as breast cancer, notably lobular breast carcinoma, astrocytoma, glioma, glioblastoma, neuroblastoma, sarcoma and certain types of leukaemia; to the use of said MCSP peptides, fusion proteins or full length MCSP protein or fragments thereof for the preparation of a medicament, and a diagnostic agent for the treatment and prophylaxis as well the diagnosis of an immune response against tumours; and to the use of said peptide-specific T-cell clones for diagnosing or treating cancer.

The present disclosure relates to methods of treating EPAS1-related diseases such as cancer, metastases, astrocytoma, bladder cancer, breast cancer, chondrosarcoma, colorectal carcinoma, gastric carcinoma, glioblastoma, head and neck squamous cell carcinoma, hepatocellular carcinoma, lung adenocarcinoma, neuroblastoma, non-small cell lung cancer, melanoma, multiple myeloma, ovarian cancer, rectal cancer, renal cancer, clear cell renal cell carcinoma (and metastases of this and other cancers), gingivitis, psoriasis, Kaposi's sarcoma-associated herpesvirus, preemclampsia, inflammation, chronic inflammation, neovascular diseases, and rheumatoid arthritis, using a therapeutically effective amount of a RNAi agent to EPAS1.

The present invention relates to somatic mutations in the Multiple Tumor Suppressor (MTS) gene in human cancers and their use in the diagnosis and prognosis of human cancer. The invention further relates to germ line mutations in the MTS gene and their use in the diagnosis of predisposition to melanoma, leukemia, astrocytoma, glioblastoma, lymphoma, glioma, Hodgkin's lymphoma, CLL, and cancers of the pancreas, breast, thyroid, ovary, uterus, testis, kidney, stomach and rectum. The invention also relates to the therapy of human cancers which have a mutation in the MTS gene, including gene therapy, protein replacement therapy and protein mimetics. Finally, the invention relates to the screening of drugs for cancer therapy.

The present invention relates to novel primers for identification of astrocytoma, it's grades and glioblastoma prognosis. Further, disclosed is a method of diagnosing the presence of different grades of diffuse astrocytoma and glioblastoma, in a human subject, which involves detection of the expression levels of said genes in tumor tissue samples in comparison to normal brain. Also disclosed is a method of distinguishing between the two types of Glioblastoma—the progressive and de novo types. Also disclosed is a method of prognosis of glioblastoma based on the expression of the gene PBEF1, wherein the higher level of expression of the gene in the tumor sample, indicates poorer survival of the human subject. The disclosed compositions are useful, for example, in the diagnosis, prevention, treatment and/or prognosis of astrocytoma. The invention further provides kits for the detection and prognosis of the said diseases.

The invention provides methods for diagnosing tumors in mammals using a reagent that bind to LEDGF/p75 or to a nucleic acid encoding LEDGF/p75. For example, the tumor may be located in the CNS, the prostate, the skin, the bone marrow, or the gut of the mammal. Also provided are methods for diagnosing brain tumors such as medulloblastomas, meningiomas, astrocytomas, glioblastomas multiforme, and ependymomas by examining LEDGF/p75 or a nucleic acid encoding LEDGF/p75 localization. The invention also involves methods for diagnosing cancers involving cancerous epithelial cells such as colon cancer. The instant invention also provides methods for isolating stem cells from a heterogeneous population of cells, as well as methods for identifying neuroepithelial stem cells, newly differentiated neurons, and astrocytes in a subject. Also provided are methods for inducing the differentiation of neuroepithelial stem cells into astrocytes or neurons and methods for screening candidate compounds that regulate the differentiation of neuroepithelial stem cells.

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.