224 results about "Blastoma" patented technology

PCT No. PCT / US97 / 11564 Sec. 371 Date Apr. 14, 1999 Sec. 102(e) Date Apr. 14, 1999 PCT Filed Jul. 8, 1997 PCT Pub. No. WO98 / 01132 PCT Pub. Date Jan. 15, 1998The present invention relates to specific adamantyl or adamantyl group derivative containing retinoid compounds induce apoptosis of cancer cells. These adamantyl retinoid derivatives are useful for the treatment of many cancers and solid tumors, especially androgen-independent prostate cancer, skin cancer, pancreatic carcinomas, colon cancer, melanoma, ovarian cancer, liver cancer, small cell lung carcinoma, non-small cell lung carcinoma, cervical carcinoma, brain cancer, bladder cancer, breast cancer, neuroblastoma / glioblastoma, and leukemia. Also, the invention relates to novel adamantyl or adamantyl group derivative compounds which are useful as active agents for the treatment or prevention of keratinization disorders and other dermatological conditions, and other diseases.

The invention provides modified antibodies directed against GD2 that have diminished complement fixation relative to antibody-dependent, cell-mediated cytotoxicity, which is maintained. The modified antibodies of the invention may be used in the treatment of tumors such as neuroblastoma, glioblastoma, melanoma, small-cell lung carcinoma, B-cell lymphoma, renal carcinoma, retinoblastoma, and other cancers of neuroectodermal origin.

Methods of treating a malignant glioma in a subject are disclosed. The methods comprise administering to the subject a therapeutically effective amount of a viral vector comprising: (i) a first polynucleotide sequence encoding a Fas-chimera (Fas-c), said first polynucleotide sequence comprising SEQ ID NOs: 2 and 3; and (ii) a second polynucleotide sequence encoding an endothelial cell-specific promoter or a periendothelial cell-specific promoter.

Disclosed is an isolated or purified T cell receptor (TCR) having antigenic specificity for an HLA-A11-restricted epitope of mutated Kirsten rat sarcoma viral oncogene homolog (KRAS) (KRAS7-16), Neuroblastoma RAS Viral (V-Ras) Oncogene Homolog (NRAS), or Harvey Rat Sarcoma Viral Oncogene Homolog (HRAS). Related polypeptides and proteins, as well as related nucleic acids, recombinant expression vectors, host cells, populations of cells, and pharmaceutical compositions are also provided. Also disclosed are methods of detecting the presence of cancer in a mammal and methods of treating or preventing cancer in a mammal.

Adenovirus types 11p and 4p show a higher binding affinity and infectivity than type 5 for endothelial and carcinoma cell lines. Adenovirus type 11p shows a stronger binding to cells for neural origin, such as glioblastoma, neuroblastoma and medulloblastoma. The fact that adenovirus type 11 has a comparatively low prevalence in society, together with its high affinity and infectivity, makes it very suitable for use in gene therapy.

The present invention provides a number of gene markers whose expression is altered in various gliomas. In particular, by examining the expression these markers, one can accurately classify a glioma as glioblastoma multiforme (GM), anaplastic astrocytoma (AA), anaplastic oligodendroglioma (AO) or oligodendroglioma (OL). The diagnosis may be performed on nucleic acids, for example, using a DNA microarray, or on protein, for example, using immunologic means. Also disclosed are methods of therapy.

Adenovirus types 11p and 4p show a higher binding affinity and infectivity than type 5 for endothelial and carcinoma cell lines. Adenovirus type 11p shows a stronger binding to cells for neural origin, such as glioblastoma, neuroblastoma and medulloblastoma. The fact that adenovirus type 11 has a comparatively low prevalence in society, together with its high affinity and infectivity, makes it very suitable for use in gene therapy.

The present invention concerns prognosis for glioblastoma and / or assessment of the response of an individual to therapy for glioblastoma treatment. In particular, expression analysis of two or more specific genes provided in the invention is determined to predict outcome for the individual and / or to predict if the individual will respond to therapy, such as chemoradiation, for example. In specific embodiments, a multigene set from a sample from the individual is compared to a reference set of housekeeping genes.

The present invention provides antibodies useful as therapeutics for treating and / or preventing diseases associated with cells expressing GT468, including tumor-related diseases such as breast Cancer, lung Cancer, gastric Cancer, ovarian Cancer, hepatocellular Cancer, colon Cancer, pancreatic Cancer, esophageal Cancer, head & neck Cancer, kidney Cancer, in particular renal cell Carcinoma, prostate Cancer, liver cancer, melanoma, sarcoma, myeloma, neuroblastoma, placental choriocarcinoma, cervical cancer, and thyroid Cancer, and the metastatic forms thereof. In one embodiment, the rumor disease is metastatic cancer in the lung.

Disclosed are enriched preparations of neuroblastoma tumor initiating cells (NB TICs). The NB TICs are capable of self-renewal, initiating neuroblastoma tumor growth in vivo and are capable of being passaged in high frequency. These NB TICs have chromosomal abnormalities and are capable of giving rise to secondary tumor spheres. Methods are also disclosed for preparing the enriched preparations of NB TICs, such as from neuroblastoma tumor tissue and metastasized bone marrow. Also disclosed are methods of screening candidate substances to identify therapeutic agents for the treatment of neuroblastoma. Methods are also provided for screening a sample for neuroblastoma, as well as for screening a sample to identify the stage of neuroblastoma present. Kits are also provided for selecting appropriate anti-neuroblastoma compounds for a patient, and utilize isolated compositions of the patients' neuroblastoma tumor initiating cells. In this manner, a customized medicinal profile for the patient may be devised.

The present invention provides methods to manipulate differentiation of a neuroblastoma cell line (IMR-32) such that predominant Nav expression is either Nav1.3 in IMR-32 cells exposed to retinoic acid or Nav1.7 in cells grown under non-differentiating conditions. The cells of the present invention are useful for the discovery of new compounds that modulate the function of either Nav1.3 and / or Nav1.7.

The present invention provides antibodies useful as therapeutics for treating and / or preventing diseases associated with cells expressing GT468, including tumor-related diseases such as breast cancer, lung cancer, gastric cancer, ovarian cancer, hepatocellular cancer, colon cancer, pancreatic cancer, esophageal cancer, head & neck cancer, kidney cancer, in particular renal cell carcinoma, prostate cancer, liver cancer, melanoma, sarcoma, myeloma, neuroblastoma, placental choriocarcinoma, cervical cancer, and thyroid cancer, and the metastatic forms thereof. In one embodiment, the tumor disease is metastatic cancer in the lung.

The present disclosure involves compositions and methods for treating brain cancers having mutations in the retinoblastoma (Rb) pathway using an oncolytic adenovirus comprising an alteration in the Rb binding site of E1A, and a targeting motif inserted in the Ad fiber protein. The adenovirus is able to kill the tumor cells without harming cells with a wild-type retinoblastoma pathway.

A method is provided for assessing allelic losses and hypermethylation of genes in CpG tumor promotor region on specific chromosomal regions in cancer patients, including melanoma, neuroblastoma breast, colorectal, and prostate cancer patients. The method relies on the evidence that free DNA and hypermethylation of genes in CpG tumor promotor region may be identified in the bone marrow, serum, plasma, and tumor tissue samples of cancer patients. Methods of melanoma, neuroblastoma, colorectal cancer, breast cancer and prostate cancer detection, staging, and prognosis are also provided.

The invention relates to the use of dichloroacetate and chemical equivalents thereof for the treatment of cancer by inducing apoptosis or reversing apoptosis-resistance in a cell Preferably, the dosage is 10-100 mg / kg Preferably, sodium dichloroacetate is used. The dichloroacetate may optionally be given in combination with a pro-apoptotic agent and / or a chemotherapeutic agent Preferably, the cancers treated are non-small cell lung cancer, glioblastoma and breast carcinoma.

A targeted osmotic lysis (TOL) of tumor cells that over-express voltage-gated sodium channels (VGSCs) has been developed that uses a combined therapy of a drug that blocks sodium, potassium-adenosine triphosphatase (Na+, K+-ATPase) that is then followed by an activation of VGSCs, for example, by electrical or pharmacological stimulation. Activation of VGSCs conducts sodium into the cancer cells in much greater amounts than non-cancer cells. Water follows this sodium gradient into the cancer cells, causing swelling and lysis. Because non-cancerous cells do not over-express VGSCs, less sodium and less water will enter the cells, and the non-cancerous cells will not lyse. This method is applicable to all cells that over-express VGSCs, including, but not limited to, highly invasive breast cancer, prostate cancer, small cell lung cancer, non-small cell lung carcinoma, lymphoma, mesothelioma, neuroblastoma, and cervical cancer.

The invention provides a furanocoumarin-Base derivative, wherein the structural formula of the derivative is as shown in the following formula 6 or 7; the derivative is synthesized by performing ringformation and coupling reaction on parabromoaniline,paraformaldehyde, 4-hydroxycoumarin, isonitrile and n-butyllithium; and the synthesis process is mild in reaction condition, short in reaction timeand high in yield. The Base derivative containing a coumarin fragment has excellent luminescent property and high bioactivity; some of the products have anti-tumor activity, show high-selectivity inhibition on human triple negative breast cancer cells (MDA-MB-231) and have research value of being further developed into anti-tumor medicines; and the other products can be applied to synchronous detection on neuroblastoma metabolites homovanillic acid (HVA) and vanilmandelic acid (VMA) and have the potential of being developed into a high-efficiency fluorescent probe for human neuroblastoma earlywarning and definite diagnosis.

The present invention provides antibodies useful as therapeutics for treating and / or preventing diseases associated with cells expressing GT468, including tumor-related diseases such as breast cancer, lung cancer, gastric cancer, ovarian cancer, hepatocellular cancer, colon cancer, pancreatic cancer, esophageal cancer, head & neck cancer, kidney cancer, in particular renal cell carcinoma, prostate cancer, liver cancer, melanoma, sarcoma, myeloma, neuroblastoma, placental choriocarcinoma, cervical cancer, and thyroid cancer, and the metastatic forms thereof. In one embodiment, the tumor disease is metastatic cancer in the lung.

The invention discloses a marker METTL3 (Methyltransferase Like 3) for glioblastoma and application thereof. The METTL3 is obviously highly expressed in a glioma cell; further, the extent of the expression of the METTL3 has obvious relevance with a clinical scale; the METTL3 is most highly expressed in the glioblastoma with the highest malignant degree; the expression of the METTL3 is knocked downto be capable of inhibiting the growth of the glioblastoma, and the METTL3 is prompted to be capable of becoming a target spot for treating the glioblastoma.

The invention relates to a visualization method for quantifying glioma invasiveness based on a kernel density function, which is a method for quantifying glioblastoma invasiveness established by usinga kernel density estimation algorithm on the basis of Image J software and an R language platform. According to the method, a nuclear density estimation graph of cell nucleus distribution is deducedby utilizing a nuclear density estimation algorithm packaged by an R language ggplot2 packet and an MASS packet and a visualization function. The method can help to effectively judge the invasion condition of the tumor from the pathological section in scientific research work, the tumor nuclear density of each region is counted by utilizing the nuclear density, the invasion trend of the tumor canbe roughly judged from a visual graph, and the tumor invasion ability is reflected from the section.

A γ-butyrolactone compound as shown in Formula (I) and pharmaceutical composition thereof: wherein X═N, O, S, Se; and A and B are selected from substituents having the following formula: wherein R1, R2, R3, R4, and R5 are selected from a hydrogen atom, a halogen atom, a hydroxyl group, a mercapto group, an amino group, an alkoxy group, and a nitro group. The γ-butyrolactone compound and pharmaceutical composition thereof butyrolactone have inhibitory effects on hepatoma, ovarian cancer, breast cancer, lung cancer, malignant glioblastoma or colorectal carcinoma, and are cytotoxic with high specificity to inhibit Paclitaxel-resistant tumour cells at later stage of chemotherapy without any damage on normal cells.

Provided herein are novel compositions and methods to inhibit Olig2 activity. The Olig2 inhibitors and methods of using the same are useful, inter alia, for treating cancer. In particular the Olig2 inhibitors may be used to treat glioblastoma. Further, provided are peptide compositions capable of inhibiting Olig 2.

This invention relates to a method for detecting, (i) malignant astrocytoma from normal brain tissue (ii) glioblastoma and anaplastic astrocytoma (iii) primary glioblastoma and secondary glioblastoma (iv) progressive pathway and denovo pathway comprises determining the level of expression of miRNAs listed in table 2, 3, 4, 5, wherein a higher or lower level of expression of miRNAs in the test sample as compared to the control sample differentiates and kit for characterizing a) malignant astrocytoma from normal brain tissue cell comprising reagent capable of specifically detecting the level of expression of the genes of miRNAs and instructions for using said kit for characterizing malignant astrocyoma from normal brain tissue cells b) glioblastoma from anaplastic astrocytoma comprising reagent capable of specifically detecting the level of expression of the genes of miRNAs and instructions for using said kit for characterizing glioblastoma from anaplastic astrocyoma c) primary glioblastoma from secondary glioblastoma comprising reagent capable of specifically detecting the level of expression of the genes of miRNAs and instructions for using said kit for characterizing primary glioblastoma from secondary glioldastoma, d) progressive pathway from denovo pathway comprising reagent capable of specifically detecting the level of expression of the genes of miRNAs and instructions for using said kit for characterizing progressive pathway from denovo pathway.

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 present invention relates to glioblastoma inhibiting compounds, in particular gambogic acid amid and derivatives thereof for the treatment of glioblastoma. Moreover, methods for determining whether a treatment with the compounds of the invention is suitable for a patient are disclosed.

The present invention provides compositions and methods useful for treating cancers such as glioblastoma. SapC-DOPS was found to be synergistically effective at inducing cell death when administered in conjunction with rapamycin. SapC-DOPS / rapamycin combination therapy allows physicians to give lower doses of each drug and achieve better therapeutic efficacy. The compositions also allow for less toxicity and fewer off-target effects. Related methods and materials are also provided herein.

The invention discloses a polygenic expression characteristic spectrum based glioblastoma individual prognosis evaluation method. The method comprises the steps of obtaining a prognosis risk gene listand a gene weight of a glioblastoma; building a prognosis evaluation model by utilizing a tumor tissue transcriptome and survival data of a glioblastoma patient; calculating a risk score of the patient based on a gene expression spectrum of tumor tissues of the glioblastoma patient; and calculating the annual survival probability of the patient based on the risk score of the patient. A fact thatannual survival probability of the glioblastoma patient obtained by the method is highly consistent with the actual annual survival rate (the linear correlation R2=0.963, and P value=1.38 E-13) provesthat the method has very high prediction accuracy and is highly consistent with the actual survival state. At the same time, for each tumor patient, the polygenic expression characteristic spectrum based glioblastoma individual prognosis evaluation method can work out the special survival probability curve of the patient.

The present invention provides compositions and methods for the diagnosis and treatment of glioblastoma, particularly tumor propagating cells within the glioblastoma.