176 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 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.

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.

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.

The present application relates to the technical field of biology, and relates to an siRNA targeting glioblastoma multiforme and a use thereof. Provided is an siRNA targeting glioblastoma multiforme. An antisense strand of this siRNA can specifically bind to a target nucleic acid to initiate degradation of the target nucleic acid, wherein the target nucleic acid comprises a pathogenic gene in glioblastoma multiforme, and the pathogenic gene in glioblastoma multiforme comprises a gene encoding ribonucleotide reductase subunit M2 and / or a gene encoding heat shock protein 47. Studies have shown that both the gene encoding the ribonucleotide reductase subunit M2 and the gene encoding the heat shock protein 47 have a significant correlation with the survival of patients with glioblastoma multiforme. The two genes can be used as therapeutic targets for glioblastoma multiforme. The siRNA capable of effectively knocking down the expression of the two genes in the patients with glioblastoma multiforme has great application prospects in the preparation of drugs for preventing and / or treating glioblastoma multiforme.

The invention provides a children nephroblastoma machine learning survival model developed based on a center queue, and belongs to the technical field of nephroblastoma prediction and evaluation. And analyzing and evaluating prognosis risk factors of the nephroblastoma, establishing an interpretable machine learning survival model based on the central queue, and finally, converting the model into a clinically friendly online prediction platform to promote the transformation of a prognosis evaluation tool from scientific research to clinical practice, so as to improve the prognosis evaluation efficiency. The method aims at providing dynamic risk assessment and individualized treatment decision support for clinicians, and finally the survival income of relapse / refractory child patients is improved.

Described herein are methods and compositions for treating a disease, e.g. cancer (including solid tumors), using glial cells (e.g. microglia cells and / or astrocytes) and / or macrophages (e.g., CNS-associated macrophages) infected with an oncolytic virus (e.g., vaccinia virus). The methods and compositions provided herein demonstrate a synergistic anti-cancer effect.

The application discloses an intervention strategy for targeting CACNA2D2 protein and application thereof, and belongs to the technical field of medicine and biotechnology.The application discloses for the first time that abnormal high expression of CACNA2D2 is related to poor prognosis of neuroblastoma, especially malignant progression, and provides that CACNA2D2 gene is used as a drug target to prepare a drug for treating neuroblastoma, and further provides application of CACNA2D2 siRNA in preparation of a drug for treating neuroblastoma.After down-regulation of CACNA2D2 gene expression, cell proliferation and clone formation ability of neuroblastoma cells are significantly inhibited.Therefore, the application provides a new direction for development of a drug for treating neuroblastoma, and provides a possibility for preparing a new drug for treating neuroblastoma, improving curative effect of patients, improving prognosis and survival.

The application discloses a double-targeted glioma composite nanomaterial and a construction method thereof, wherein the composite nanomaterial comprises, from inside to outside, modified mesoporous silica, a drug loading layer, a hybrid membrane layer and a specific modification layer; and the hybrid membrane layer is obtained by combining liposomes and glioma-specific dendritic cell membranes. The double-targeted glioma composite nanomaterial can realize double targeting of glioma cells due to the existence of the hybrid membrane layer and the specific modification layer, has no obvious immunogenicity, can efficiently release preloaded molecules or drugs in cells, and is expected to develop into a new nanomaterial for more effective treatment of glioma.

The application belongs to the technical field of biomedicine, and particularly relates to application of E33 region methylation level in evaluation of medulloblastoma prognosis. The nucleotide sequence of the E33 region is shown in SEQ ID NO:1; the medulloblastoma comprises G3 subtype medulloblastoma and / or G4 subtype medulloblastoma. The application finds that the low methylation state of the E33 region is directly related to the prognosis of the medulloblastoma Group 3 / 4 patient, the high / low methylation level of the E33 region can be detected to effectively predict the clinical result of the patient, and the methylation level of the E33 region is detected to lay a foundation for early prognosis evaluation and personalized treatment strategy of the medulloblastoma Group 3 / 4 patient.

The invention discloses 9-phenyl-10-cyclopropyl methoxy evodiamine quinazolinone with a structural formula as shown in a formula 3, and 9-phenyl-10-cyclopropyl methoxy evodiamine quinazolinone derivatives as shown in the formula 3. The preparation method comprises the following steps: (1) taking 10-hydroxy evodiamine (A) as a raw material; reacting with bromomethyl cyclopropane in the presence of a proper alkali catalyst under proper conditions to obtain 10-cyclopropyl methoxy evodiamine 1; (2) reacting the compound 1 with a bromination reagent under proper conditions to obtain 9-bromo-10-cyclopropyl methoxy evodiamine 2; and (3) reacting the compound 2 with an arylboronic acid reagent under proper conditions to obtain the 9-phenyl-10-cyclopropyl methoxy evodiamine quinazolinone derivative 3. The 9-phenyl-10-cyclopropyl methoxyl evodiamine quinazolinone derivative synthesized by the invention has the advantages that the 9-phenyl-10-cyclopropyl methoxyl evodiamine quinazolinone derivative is used for treating liver cancer cells in vitro; the neuroblastoma cells show good anti-cancer activity and can be applied to preparation of corresponding anti-tumor drugs.

It provides a bioengineered bacteriophage-lime nanoparticle, rQβ@b-3WJ, comprising a broccoli light-up aptamer including 3WJ RNA scaffold (b-3WJ) integrated with a nucleic acid bioproduction and self-packaging system to produce b-3WJ packaged Qβ VLPs. Also provided is a nanoparticle, TrQβ@b-3WJ, which is the TrQβ@b-3WJ with the conjugation of TAT peptide on the surface, which enhance cellular internalization for highly efficient gene silencing.

The invention belongs to the field of biomedicine, and particularly relates to application of a reagent for detecting the m6A modification level of an FKBP4 gene in preparation of a neuroblastoma diagnostic product. The invention provides a primer pair for detecting the m6A modification level of a partial region of the FKBP4 gene. High-risk neuroblastoma and medium-low-risk neuroblastoma are distinguished by detecting the m6A modification level of the FKBP4 gene, wherein the m6A modification level of the FKBP4 gene in the high-risk neuroblastoma is remarkably lower than that in the medium-low-risk neuroblastoma. Through MeRIP-seq and RNA-seq combined analysis and in combination with GEO database screening, it is determined that the m6A modification level of the FKBP4 gene is closely related to the risk degree of neuroblastoma. By detecting the m6A modification level of the FKBP4 gene, high-risk neuroblastoma and medium-low-risk neuroblastoma can be accurately distinguished.

The invention discloses an application of a flavonoid natural product Peruvianoside I in preparation of an anti-retinoblastoma drug, belongs to the field of medicinal chemistry, and has the following structure: the compound can selectively inhibit LSD1 enzyme activity and can be used as the anti-retinoblastoma drug. Experiments find that the anti-tumor action mechanism is related to inhibition of retinoblastoma cell migration. As a selective histone lysine specific demethylase LSD1 inhibitor, the compound has the potential of developing the retinoblastoma resisting medicine.

The invention belongs to the technical field of bioinformatics and medical detection, and particularly relates to a marker combination for neuroblastoma (NB) noninvasive risk level grading, a prediction model, a prediction method and application thereof. The marker combination is used for determining the sex, determining whether the month age is greater than 18 months, determining whether plasma MYCN is amplified, determining whether tumors are metastatic, and determining the content of neuron-specific enolase and lactic dehydrogenase; a machine learning algorithm is used for constructing an NB noninvasive risk degree grading prediction model, the comprehensive performance of the random forest model is optimal, the area value under a subject working characteristic curve reaches 0.956, the sensitivity is 92.9%, the specificity is 82.1%, the accuracy rate is 87.5%, the Kappa value is 0.75, the F1 score is 0.881, and NB middle and low risk patients and NB high risk patients can be effectively distinguished; the NB non-invasive risk level grading prediction model constructed by the invention can quickly, accurately and non-invasively perform NB risk level grading, and has a relatively good clinical application value.

The invention belongs to the field of biological medicine, and particularly relates to a biomarker for clinical diagnosis of high-risk neuroblastoma and application of the biomarker. A product capable of being used for clinical diagnosis of high-risk neuroblastoma comprises a reagent for detecting the expression level of a biomarker, and the biomarker is plasma exosome protein CHD1. By detecting the CHD1 expression level, existing clinical indexes can be supplemented, precise layering and precise treatment of neuroblastoma are achieved, and meanwhile the kit has important guiding significance for prognosis judgment of tumor children.

Monoclonal antibodies that bind glypican-2 (GPC2) with high affinity are described. Immunotoxins and chimeric antigen receptors (CARs) that include the disclosed antibodies or antigen-binding fragments thereof are further described. In some instances, the antibody or antigen-binding fragment is humanized. The disclosed GPC2-specific antibodies and conjugates can be used, for example, for the diagnosis or treatment of GPC2-positive cancers, including neuroblastoma, medulloblastoma and retinoblastoma.