236 results about "Blastoma" patented technology

A computer implemented method of distinguishing tumor progression from treatment-related necrosis in digital images of a subject implements a multimodal deep learning architecture from MRI data of a selected anatomical portion of the subject, such as a brain, and corresponding dPET data for the subject with a tracer applied to the anatomical portion of the subject. The computer stores co-registered MRI data frames with dPET data frames as three dimensional (3D) parametric PET maps to identify multi-modal image features of segmented tumor data. A convolutional neural network uses MRI data and selected multi-modal image features as inputs and the computer concatenates respective output latent feature vectors from the respective sections of the at least one CNN. Feeding concatenated feature vectors to fully connected layers of the multimodal architecture distinguishes tumor progression from treatment-related necrosis of the anatomical portion of the subject.

The invention relates to a biomarker of a glioblastoma invasion leading edge region and application of the biomarker, and belongs to the technical field of biological detection. In order to solve the technical problems of unknown tumor invasion mechanism, scarcity of treatment targets and inaccurate prognosis evaluation caused by lack of a GBM invasion leading edge region specific marker in the prior art, 12 GBM invasion leading edge region specific high-expression genes, namely CREG2, KIF5A, CELF4, TMEM132D, KHDRBS2, SNAP25, SYT1, ASIC2, PAK3, RBFOX1, STMN2 and CNTNAP2, are analyzed and screened through space transcriptomics. A COX multi-factor regression risk assessment system is developed and constructed based on the markers. According to the invention, a molecular basis is provided for accurate recognition of a GBM invasion range, patient layering and prognosis prediction, targeted therapy development and curative effect monitoring.

The invention relates to an anti-VEGF antibody, a heavy chain variable region sequence is shown as SEQ ID NO: 1, and a light chain variable region sequence is shown as SEQ ID NO: 2. According to the present invention, the monoclonal antibody capable of specifically binding to VEGF is prepared, the binding of VEGF and its receptor can be inhibited after the monoclonal antibody is bound to VEGF, the downstream signal transduction pathway of VEGF is blocked, and the animal test results show that the antibody can inhibit the growth of glioblastoma.

Provided herein are inhibitors of the TFPJ2-CD51-STAT6 signaling axis and methods for the treatment of cancer (e.g., glioblastoma) therewith. In particular, inhibitors of expression or activity of components of the TFPJ2-CD51-STAT6 signaling axis are provided, with or without an immune checkpoint inhibitor, for the treatment of glioblastoma.

The invention relates to the technical field of medicines, in particular to application of combined use of NK cells and a GD2 antibody in preparation of a medicine for treating neuroblastoma. The NK cell and the GD2 antibody are jointly used to prepare a medicine for treating neuroblastoma. In-vivo and in-vitro experiments find that the umbilical cord blood NK cell combined with the GD2 antibody can significantly enhance the tumor killing ability and inhibit the growth of neuroblastoma cells, provides a new therapeutic medication scheme for the treatment of neuroblastoma, and has a good application prospect in the prevention and treatment of neuroblastoma.

The present disclosure relates, inter alia, to the combination therapy of an oncolytic adenovirus for the treatment of retinoblastoma, Ewing's sarcoma or neuroblastoma with a topoisomerase I inhibitor or a prodrug thereof, such as topotecan or SN-38, or a prodrug of a topoisomerase inhibitor, such as irinotecan.

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.

The present invention provides a GD2-targeting CAR-T cell and its preparation and application. Specifically, the present invention provides a GD2-targeting CAR construct, which comprises the scFv fragment of the humanized GD2 antibody 3F8, the human Fc fragment, the ICOS transmembrane region, the ICOS and 4-1BB intracellular regions (co-stimulatory signals), and CD3ζ. The present invention also provides a CAR-T cell based on the above CAR, its preparation method and application. The CAR-T cell of the present invention can significantly inhibit the proliferation of tumor cells in a subcutaneous model of neuroblastoma, has a significant in vivo anti-tumor effect, and can be used for the targeted treatment of neuroblastoma.

The invention belongs to the field of neuroblastoma tissue analysis, and particularly discloses a child neuroblastoma tissue microarray chip and a preparation method thereof.The child neuroblastoma tissue microarray chip comprises a glass slide base material, and a plurality of neuroblastoma tissue samples arranged in a dot-matrix mode are arranged on the glass slide base material; by integrating a plurality of neuroblastoma samples including various pathological typing, grading and clinical staging types of neuroblastoma in a tissue block, efficient sample processing and analysis are achieved, comprehensiveness and representativeness of research are ensured, a large number of samples are analyzed simultaneously through a microarray technology, and the accuracy and accuracy of analysis are improved. The requirements for high-throughput screening of specific genes and expression proteins thereof in scientific research activities are met, the prediction capacity for tumor prognosis and the guidance accuracy for treatment schemes are improved, and neuroblastoma tissues are analyzed more efficiently and comprehensively.

The application belongs to the technical field of biomedical engineering, and specifically discloses a nano gene composition for treating brain glioma and a preparation method thereof, which is synthesized from bovine serum albumin loaded manganese dioxide particles, PLGA, DSPE-PEG3000 and DSPE-PEG-Angiopep2 as raw materials; the average particle size of the nano gene composition is 122.18±31.3 nm. The application also discloses a preparation method of the nano gene composition. The nano gene composition provided by the application encapsulates miRNA-138 in PLGA to avoid the degradation of miRNA-138 by RNA enzymes in the body, and simultaneously utilizes the targeting property of Angiopep2 to target the delivery of the nano gene composition to tumor tissues, to deliver microRNA into the brain while reducing tumor hypoxia and increasing the sensitivity of cells to X-ray irradiation, so as to realize multidirectional comprehensive treatment of glioblastoma.

GD2 specific chimeric antigen receptor effector cells for the treatment of solid tumors, possibly in combination with an enhancer of a Zeste homolog 2 (EZH2) inhibitor. The invention relates to a GD2-specific chimeric antigen receptor (GD2. CAR) effector cell for use in the treatment of solid tumors, in particular in the treatment of extracranial GD2 + tumors, such as soft tissue sarcoma and osteosarcoma, neuroblastoma, melanoma, lung cancer, bladder cancer and retinoblastoma, and brain tumors. In addition, the present invention also relates to the use of the GD2. CAR genetically modified effector cell in combination with an enhancer of a Zeste homolog 2 (EZH2) inhibitor for the treatment of solid tumors.

Methods of treating cancers are provided, the methods comprise administering a therapeutically effective amount of azeliragon, or a pharmaceutically acceptable salt thereof, and co-administering an effective amount of radiation therapy (RT), to a patient who has been diagnosed with a cancer. In another aspect, methods of treating glioblastoma are provided, those methods comprise administering a therapeutically effective amount of azeliragon, or a pharmaceutically acceptable salt thereof, and co-administering an effective amount of radiation therapy (RT), to a patient who has been diagnosed with glioblastoma.

This invention relates to a method for constructing a mouse orthotopic model of highly aggregated glioblastoma, belonging to the fields of biomedicine and experimental animal model technology. Glioblastoma cells are resuspended in a composite carrier of a specific ratio of matrix gel and serum-free culture medium, and a low-temperature injection technique is used. Utilizing the thermosensitivity of matrix gel in the mouse intracranial environment (i.e., its phase transition from liquid to gel at a certain temperature), precise colonization and physical locking of tumor cells at target coordinate points are achieved. This method improves upon existing glioblastoma mouse orthotopic model construction techniques that suffer from tumor cell diffusion and loss, low tumor formation rate, irregular tumor morphology, large intragroup variability, and needle reflux due to low viscosity of the inoculation carrier. It provides a good disease model for subsequent screening or evaluation of anti-glioblastoma drugs.

This disclosure provides compounds of formula (I) or pharmaceutically acceptable salts thereof, methods for preparing the same, and their use in the treatment and / or diagnosis of cancers such as neuroblastoma, prostate cancer, pancreatic cancer, leukemia, osteosarcoma, hepatoblastoma, lung cancer, colon cancer, breast cancer, skin cancer, thyroid cancer, and / or rhabdoid cancer. JPEG2026522940000099.jpg50170

This invention discloses an engineered CAR-T cell targeting HIF-1α and its application in tumor immunotherapy. The CAR-T cell expresses a chimeric antigen receptor regulated by the hypoxia-responsive element HRE promoter, with its extracellular domain specifically binding to HIF-1α and its intracellular domain employing the 4-1BB+CD3ζ signaling module. Simultaneously, through immune checkpoint knockout and cytokine / chemokine modification, it achieves hypoxia-dependent activation, anti-exhaustion, high infiltration, and strong killing effects. The CAR-T cells of this invention significantly improve the adaptability to the solid tumor microenvironment and therapeutic efficacy, reduce off-target toxicity, and can be used to prepare drugs for treating malignant tumors such as lung cancer, liver cancer, pancreatic cancer, colorectal cancer, and glioblastoma, possessing significant clinical translational value.

Disclosed herein are methods and systems for treating cancer including glioblastoma, recurrent glioblastoma, or newly diagnosed glioblastoma, using the administration of ultra-low radio frequency energy (u / RFE®), either alone or in combination with one or more conventional cancer therapies. In some embodiments, the one or more conventional cancer therapies include chemotherapy or an anti-angiogenic therapy or other therapies.

The invention relates to a tricyclic heterocyclic compound as well as a preparation method and medical application thereof. Specifically, the invention relates to a compound shown in a general formula (I), a preparation method of the compound, a pharmaceutical composition containing the compound and application of the compound as an MAT2A inhibitor. The compound and the pharmaceutical composition containing the compound can be used for treating and / or preventing diseases related to MAT2A activity, such as mesothelioma, neuroblastoma, rectal cancer, colon cancer, esophageal cancer and the like. Wherein the definition of each group in the general formula (I) is the same as that in the specification.

The present invention provides a method for analyzing molecular differences in glioblastoma and its application, belonging to the field of biotechnology. Using differential gene expression analysis, spatial transcriptomics analysis, deconvolution analysis, single-cell RNA sequencing data, and immunofluorescence, this application identified specific molecular signatures associated with pseudopalisading necrosis (PAN) and microvascular proliferation (MVP), revealing differences between these tissue structures. The results showed that PAN and MVP shared spatial expression of specific marker genes and were enriched for endothelial cells of distinct phenotypes. Single-cell trajectories inferred pseudotemporal trajectories of glioblastoma stem cells (GSCs) to EC differentiation. This study reveals distinct roles for endothelial cells in the PAN and MVP regions of GBM, highlighting the complexity and diversity of the tumor microenvironment and providing new insights into endothelial cell subpopulations and GSC differentiation into endothelial cells in GBM.

This invention discloses a class of 2-(2-(quinolin-4-yloxy)ethyl)pyridazine-3(2H)-one compounds, their preparation methods, and applications. The structure of these compounds is shown in general formula (I). This invention also discloses that the above compounds have a significant inhibitory effect on interleukin-1 receptor-associated kinase 1 (IRAK1). These compounds can inhibit the proliferation of various tumor cells, including liver cancer, lung cancer, pancreatic cancer, gastric cancer, kidney cancer, colon cancer, esophageal cancer, glioblastoma, leukemia, multiple myeloma, and other solid tumors and hematological malignancies. This invention provides a new option for tumor treatment.

The invention provides an application of dihydroergomine in preparation of a product for treating and / or preventing glioblastoma, and belongs to the technical field of medicines. Researches find that dihydroergomine is specifically combined with an RING structural domain of TRIM47, inhibits the activity of E3 ubiquitin linker enzyme of TRIM47, blocks the TRIM47 from inhibiting activation of STAT1 through ubiquitination modification of STAT1, and promotes activation of interferon on STAT1, so that tumor cell apoptosis is promoted, proliferation and migration are inhibited, and finally tumor growth is inhibited. Dihydroergomine has good anti-glioblastoma activity, has low toxicity to normal cells, and provides more choices and possibilities for treatment of glioblastoma.

The invention provides a method for preparing an antitumor drug by inducing differentiation of neuroblastoma through co-culture supernate of human embryonic stem cells and neuroblastoma cells. The human embryonic stem cells have the biological characteristics of multidirectional differentiation potential, infinite proliferation, self-renewal and the like, and the microenvironment of the human embryonic stem cells can reprogram cancer cells. The early neuroblastoma can naturally fade, and research shows that cancer cells of the neuroblastoma retain certain differentiation potential and can be differentiated towards neurons. The inventor discovers that the neuroblastoma cells and embryonic stem cells are subjected to direct contact co-culture, and the generated co-culture supernatant can induce the neuroblastoma cells to differentiate into neuronal cells, so that the proliferation, migration and invasion of the neuroblastoma cells are inhibited in vitro. The discovery shows that the co-culture supernate has huge potential in innovative biological treatment application of resisting neuroblastoma.

The present disclosure provides compounds according to Formula I and pharmaceutically acceptable salts thereof, as well as compositions including such compounds and a pharmaceutically acceptable carrier or excipient. Further provided are methods of inactivating SIRT6 with compounds of Formula I as well as compounds of Formula III, W2—R2—Y—R3, as described herein. In addition, the present technology provides methods of treatment using such compounds to lower LDL levels, lower triglyceride levels, and / or increase glucose tolerance in a subject, and / or to inhibit proliferation of ovarian, colorectal, hepatocellular, non-small cell lung, glioblastoma, osteosarcoma, pancreatic, and skin cancer cells, and / or inhibit liver and / or kidney fibrosis, and / or promote corneal epithelial wound healing.

The present invention belongs to the field of chemical medicine and discloses an EGFR proteolysis-targeted chimera, its preparation method, pharmaceutical composition, and application. The present invention provides an EGFR-degradable proteolysis-targeted chimera based on CP0371, a novel E3 ligase ligand with "molecular glue" functionality, and gefitinib, a target protein ligand. The EGFR proteolysis-targeted chimera prepared by the present invention can effectively induce EGFR degradation in cancer cell lines and has considerable bioavailability. It can be used to prepare EGFR inhibitors and can be used to form pharmaceutical compositions. It has a certain inhibitory effect on the proliferation of various tumor cells and is suitable for the development of cancer drugs for the treatment of colorectal cancer, lung cancer, esophageal cancer, glioblastoma, anal cancer, head and neck epithelial cancer, and other cancers.

The invention relates to application of a SelK gene or an expression product thereof as a biomarker for prognosis judgment of glioblastoma diseases. The invention discloses application of a SelK gene or an expression product of the SelK gene to preparation of a product for performing glioblastoma typing diagnosis, therapeutic schedule selection and / or prognosis evaluation by detecting the level of the SelK gene or the expression product of the SelK gene in a tumor sample obtained from an object. The research shows that the high-expression SelK gene and the protein expression product thereof are both in negative correlation with poor prognosis of glioblastoma, and survival analysis also proves that the overall prognosis of patients with low SelK expression is obviously superior to that of patients with high SelK expression, so that the SelK gene and the expression product thereof can be used as molecular markers for prognosis evaluation and treatment effect. The invention also provides an application of the targeted SKP2 / beta-TrCP1 / CDK4 axis signal channel in preparation, evaluation or screening of drugs for treating glioblastoma.

Disclosed herein are synthesis and use of covalent inhibitors selective for Transcriptional Enhancer Factor TEF-1 (TEAD1), which can be used for treatment of cancers such as glioblastoma, gastric cancer, colorectal cancer, pancreatic ductal adenocarcinoma (PDAC), and malignant pleural mesothelioma (MPM). Further disclosed herein are pharmaceutical compositions including the TEAD1 inhibitor and methods of treating cancers using the same.

A method and apparatus for detecting MGMT promoter methylation in glioblastoma, relating to the field of Raman spectroscopic detection. The method comprises: performing Raman spectral scanning on a glioma tissue sample to be detected to obtain Raman spectral data; preprocessing the Raman spectral data to obtain normalized Raman spectral data; extracting intensity values at characteristic shifts from the normalized Raman spectral data; and inputting the intensity values at the characteristic shifts into a classification model to calculate a classification prediction value, the classification prediction value being used for assisting in determining the MGMT promoter methylation state of said glioma tissue sample. The effect of the present application is that low-cost, non-destructive and accurate detection of the MGMT promoter methylation state of glioblastoma can be achieved.

The application provides application of MTA1 which is highly expressed in glioma stem cells (GSC) in treatment of glioblastoma (GBM). The application firstly proposes that GSC in GBM highly expresses MTA1 protein molecules, the highly expressed MTA1 is positively correlated with poor prognosis of GBM patients, and also promotes the stemness, cell proliferation and spheroid formation ability of GSC. Targeting the highly expressed MTA1 in GSC can inhibit the malignant progression of GBM. The application provides a new target and inhibitor for targeted treatment of GBM.

This invention belongs to the field of biomedicine, specifically relating to biomarkers and their applications for the clinical diagnosis of high-risk neuroblastoma. A product for the clinical diagnosis of high-risk neuroblastoma includes a reagent for detecting the expression level of the biomarker, which is a plasma exosomal protein called LAMP2. By detecting LAMP2 expression levels, this method can complement existing clinical indicators, enabling precise stratification and treatment of neuroblastoma, and also provides important guidance for the prognosis of children with tumors.

An epigenetic silencer factor (ESF) for use in the treatment of cancer, or a polynucleotide encoding the same, wherein the ESF comprises a transcription factor DNA-binding domain functionally linked to at least one epigenetic effector domain, the transcription factor is an oncogenic transcription factor or a cancer-related transcription factor, and the cancer is selected from the group consisting of glioma, glioblastoma, medulloblastoma, astrocytoma, neuroblastoma, epithelioma, meningioma, retinoblastoma, rhabdomyosarcoma, lung cancer, prostate cancer, breast cancer, liver cancer, pancreatic cancer (e.g., human pancreatic ductal adenocarcinoma), bladder cancer, oropharyngeal cancer, kidney cancer, colon cancer (e.g., colon adenocarcinoma), colorectal cancer (CRC), or metastases of any of the foregoing.