227 results about "Oncogene" patented technology

The invention relates to an oncogene prediction method based on graph variation self-coding, and belongs to the field of bioinformatics. The method is based on a dual-path neural network framework: a main path processes an original network and features enhanced by a variational auto-encoder (VAE) by using a graph attention network (GAT) so as to capture a complex relationship between nodes; the auxiliary path generates an auxiliary network and features containing global information through an APPNP algorithm, and the auxiliary network and features are aggregated through GraphSAGE to retain structural information. The model introduces jump connection and residual connection to relieve gradient disappearance and enhance feature complementarity. And finally, integrating dual-path information output prediction through a linear layer. The method is verified on a plurality of biological network data sets, the prediction accuracy, robustness and hidden relation recognition capability are remarkably improved, and a reliable tool is provided for cancer research.

The invention relates to the technical field of medical information, in particular to a construction method and system of a liver cancer gene database and a medium, and the method comprises the following steps: constructing a spatial neighborhood relationship based on cell space coordinates, and defining mutually communicated cell populations as spatial neighborhood hyperedges; labeling functional modules according to the gene expression values, and associating cell nodes in the same functional module as functional module hyperedges; constructing a space-time dynamic hypergraph structure based on the spatial neighborhood hyperedge and the functional module hyperedge; and carrying out local aggregation on node features of the space-time dynamic hypergraph structure to obtain a gene expression correlation weight matrix between a target node and a domain node so as to construct a liver cancer gene database. According to the method, a high-quality data support and analysis platform is provided for liver cancer mechanism research by comprehensively describing a spatial interaction network of liver cancer cells, dynamic evolution of functional modules and gene expression correlation.

The present disclosure relates to compounds that elicit degradation of proteins directed against the protooncogene tyrosine protein kinase receptor (RET), which may be a wild-type RET or a mutant form of RET, including compounds of formula (I), for use in the treatment of diseases and conditions mediated by said proteins. # imgabs0 #

The invention discloses a multi-target anti-tumor active rutaecarpin derivative or a pharmaceutical salt thereof. The structural general formula of the rutaecarpin derivative or the pharmaceutical salt thereof is shown as a formula I or a formula II: # imgabs0 #, wherein R1 is selected from C1-C5 alkoxy, hydroxyl and hydrogen; r2 is selected from hydrogen and halogen; according to the present invention, the enzyme inhibition activity and in vitro anti-tumor activity test results show that the compound of the present invention has strong inhibition activity on topoisomerase 1, topoisomerase 2 and c-MYC oncogenes, such that the new approach is developed for the deep research and the development of the new structure type anti-tumor drug, and the new strategy is provided.

The invention discloses an ecDNA (ectodeoxyribonucleic acid) identification method based on scATAC-seq (scATAC-Seq) data. The ecDNA recognition method provided by the invention can be used for accurately detecting copy number amplification, breakpoint quantity and ecDNA feature quantity on the whole cell level. According to the method provided by the invention, the specific carried annular oncogene in the tumor can be identified, the distribution characteristics of the annular oncogene in the genome can be analyzed, and the overall composition of all annular DNAs in a single cell and the specific composition of the single annular DNA can be disclosed. In addition, according to the method, the existence of the circular DNA can be verified through a dyeing experiment, and the reliability of a detection result is ensured.

The invention discloses a method, a system and equipment for detecting internal tandem repeat and a storage medium, and the key points of the technical scheme are as follows: obtaining a first reference sequence according to at least one target exon sequence corresponding to a protooncogene, and obtaining a second reference sequence according to at least one target intron sequence corresponding to the protooncogene; comparing the sequencing data of the to-be-detected sample to the second reference sequence to obtain a first comparison result, extracting an uncompared sequence from the sequencing data according to the first comparison result, and comparing the uncompared sequence to the first reference sequence to obtain a second comparison result; and determining a first detection result according to the second comparison result and a first reference sequence, and performing false positive filtering on the first detection result to obtain a second detection result. According to the invention, false positive can be reduced so as to ensure the accuracy and reliability of subsequent analysis.

The invention relates to a hepatocellular carcinoma gene knockout target library based on multiple omics and a screening method of the hepatocellular carcinoma gene knockout target library, and the gene knockout target library for precise treatment of hepatocellular carcinoma is finally obtained through data collection and integration, data screening and target verification in sequence. According to the invention, through multi-omics data integration and bioinformatics analysis, key driving genes of hepatocellular carcinoma are systematically screened, and the important effects of the genes in occurrence, development, metastasis, drug resistance and immune escape of hepatocellular carcinoma are disclosed; the genes not only deepen the understanding of the hepatocellular carcinoma molecular mechanism, but also provide important theoretical basis and potential intervention targets for the development of targeted therapy and personalized therapy strategies.

The invention discloses application of ZMYM1 as a biomarker in liver cancer diagnosis and / or treatment. The expression of ZMYM1 in liver cancer patients is up-regulated. Database analysis, cell experiments and animal model experiments prove that ZMYM1 is a cancer promoting gene of liver cancer, ZMYM1 interacts with METTL3 to promote migration of tumor cells and improve the inflammation level in a tumor microenvironment, and finally the effect of promoting the progress of liver cancer is achieved. Based on TCGA, GEO, ICGC and NGDC databases, the application of the ZMYM1 as a biomarker in liver cancer diagnosis, liver cancer prognosis risk assessment, liver cancer immunotherapy effect prediction and targeted drug therapy effect prediction is provided according to a bioinformatics analysis result, so that a prevention scheme or a treatment scheme is clinically provided for a subject, and the clinical application of the ZMYM1 in liver cancer diagnosis, liver cancer prognosis risk assessment, liver cancer immunotherapy effect prediction and targeted drug therapy effect prediction is promoted. The precise molecular treatment of the liver cancer is realized.

The invention provides an SNP (Single Nucleotide Polymorphism) site related to turbot non-ocular side blackening, a primer pair and application, and belongs to the technical field of molecular markers. Wherein an SNP (Single Nucleotide Polymorphism) site related to turbot blackening is positioned at the 277th site of a coding region of the gene notumpectinacetylesterase 2, the basic group of the SNP site is mutated into C from T, and the amino acid is mutated into histidine from tyrosine; one SNP site related to turbot blackening is located at the 1154th site of a coding region of a gene KIT progene-oncogene, and the other SNP site related to turbot blackening is located at the 1154th site of a coding region of a gene KIT progene-oncogene receptor kinase b, the basic group of the SNP site is mutated from A to G, and the amino acid of the SNP site is mutated from aspartic acid to glycine. Researches show that genotype distribution of the SNP site between normal turbots and blackened turbots has significant difference.

The invention relates to a method for forming a hair follicle-like structure by co-culturing an immortalized hair papilla cell line derived from human hair follicles and keratinocytes. Specifically disclosed is a hair papilla cell line (SV40T-hTERT DPC) which is immortalized by forced expression of SV40T, which deactivates a cancer suppressor gene, in human hair follicle-derived hair papilla cells and hTERT gene, which is a telomerase elongase promoting gene, and keratinocytes, are co-cultured three-dimensionally. From the result, it has been confirmed that a hair follicle-like structure is formed in which a cuticle grows so that a hair follicle analogue in combination with a primary-cuticle hair follicle-derived cell has a shape similar to that of the primary-cuticle hair follicle-derived cell. Therefore, the method can be applied to multiple fields of animal replacement experiments, efficacy evaluation of materials for preventing alopecia / promoting hair follicle growth and the like. Through immortalized hair papilla cells, higher result consistency can be ensured compared with that in the prior art, and stable hair follicle-derived cell supply can be realized, so that the problem of high entry barriers of efficacy evaluation of alopecia materials based on cells is expected to be solved.

The invention relates to the technical field of gene and immune molecule detection, in particular to a method for predicting lung cancer EGFR genotype and immune molecule expression level, and the method specifically comprises the following steps: S1, obtaining a CT image: obtaining the CT image of a non-small cell lung cancer patient, the CT image comprising a tumor area and a peritumor area; s2, image omics characteristics are extracted, wherein the image omics characteristics are extracted from the tumor area and the peritumor area respectively; s3, extracting deep network features: extracting the deep network features from the CT image by using a deep neural network based on an attention mechanism; and S4, constructing a prediction model: inputting the radiomics characteristics and the deep network characteristics into the prediction model, and outputting prediction results of EGFR genotypes and immune molecule expression levels. The method for predicting the lung cancer EGFR genotype and immune molecule expression level has the advantages of non-invasiveness, high efficiency, accurate prediction, clinical practicability, model interpretability and technical compatibility and flexibility.

The present invention relates to an N-containing heteroaryl derivative and a pharmaceutical composition comprising same as an active ingredient for the prevention or treatment of cancer. The derivative exhibits high inhibitory activity against various protein kinases, particularly excellent ret proto-oncogene (RET) enzyme inhibitory ability, and has an excellent effect of inhibiting the proliferation of medullary thyroid cancer cells and lung cancer cells, which express RET fusion genes, and thus the derivative can be effectively used in the treatment of cancer, for example, medullary thyroid cancer or lung cancer, and particularly, can be effectively used in the treatment of cancer in which RET fusion genes are expressed.

The invention belongs to the technical field of biological medicine and molecular biology, and provides application of GJB6 in preparation of an esophageal squamous cell carcinoma prognosis evaluation reagent and screening of drugs for targeted treatment of esophageal squamous cell carcinoma. The low expression of the GJB6 is applied to preparation of an esophageal squamous cell carcinoma prognosis evaluation reagent. GJB6 is low in expression in ESCC patients, and ESCC prognosis is poor. And the prognosis of patients with high expression of GJB6 is better. Overexpression of GJB6 inhibits ESCC cell proliferation, migration and invasion and in-vivo tumor enlargement. The GJB6 plays a role of a cancer suppressor gene in ESCC and inhibits cell proliferation, migration and invasion. The AKT signal channel is one of downstream channels for GJB6 to regulate the occurrence and development of ESCC. The AKT inhibitor effectively inhibits GJB6 low-expression ESCC malignant phenotypes, including enhancement of cell proliferation and migration invasion ability and in-vivo tumor enlargement. The AKT is a key therapeutic target of the GJB6 low expression type ESCC.

The invention provides a bladder cancer gene mutation prediction system based on deep learning, and the system comprises a histopathologic image collection module which is used for collecting an original to-be-detected histopathologic image; the preprocessing module is used for preprocessing the original to-be-detected histopathologic image by adopting an HE staining method and a full-slide imaging scanner to obtain WSI with HE stained bladder tissue; the cloud server module is used for calling a bladder cancer deep learning prediction model to perform bladder cancer gene expression state prediction, bladder cancer gene methylation state prediction and bladder cancer gene mutation state prediction on the WSI to generate corresponding prediction results; and the report generation module is used for automatically generating a bladder cancer gene mutation prediction auxiliary diagnosis report according to the corresponding prediction result and feeding back the report to the specified terminal.

The invention provides an application of a GABA-A receptor negative regulator in preparation of a medicine for treating pan cancer, and belongs to the technical field of medicines. The research finds that in the tumor microenvironment of panthenic cancer, the GABA-A receptor negative regulator acts on the key cancer-promoting gene target of cancer cells for drug therapy, abnormal overexpression of the key cancer-promoting gene causing cancer occurrence and development can be controlled, the inhibition effect of the cancer cells on immune cells is reduced, and the cancer-promoting effect of the cancer cells is improved. The medicine can be used for treating cancer cells, so that an immunosuppressive tumor microenvironment beneficial to cancer cell growth is destroyed, immune infiltration of the cancer tumor microenvironment is readjusted, a normal immune system of an organism is activated to treat the cancer cells, and the medicine can also be used for reducing NF-kb signal channels of the cancer cells to reduce inflammatory factor expression of the cancer cells and promote apoptosis of the cancer cells. The GABA-A receptor negative regulator acts on key cancer promoting gene targets of cancer cells, so that accurate and effective targeted therapy can be carried out on cancers on the molecular level.

The invention discloses an oncolytic virus and application of the oncolytic virus in preparation of tumor inhibition drugs. The oncolytic virus is a lentiviral vector, and the lentiviral vector comprises polynucleotide encoding p16 protein or a bioactive part of the p16 protein containing CDKN2A gene, and can effectively inhibit growth of cancer related to CDKN2A gene mutation, so that the problem that the existing oncolytic virus has biological safety risk in delivery of cancer suppressor genes is effectively solved.

The invention as disclosed herein relates to bispecific antibodies that comprises a first variable domain that can bind an extracellular part of epidermal growth factor receptor (EGFR) and a second variable domain that can bind an extracellular part of MET Proto-Oncogene, Receptor Tyrosine Kinase (cMET). The antibody may comprise a common light chain. It may be a human antibody. The antibody may be a full length antibody. In some embodiments the bispecific antibody is an IgG1 format antibody having an anti-EGFR, anti-cMET stoichiometry of 1:1. In some embodiment the antibody has one variable domain that can bind EGFR and one variable domain that can bind cMET.

Provided herein are methods related to treating or delaying progression of cancer in an individual. In some embodiments, the methods comprise detecting one or more TMPRSS2-ERG gene rearrangements in one or more samples from an individual having prostate cancer; and administering to the individual an effective amount of a treatment that comprises an anti-cancer agent.

The present invention relates to the use of compounds of formula (I) as RAS inhibitors and as a medicament, in particular for use in treating proliferative disorders, inflammatory diseases and / or genetic disorders. The present invention relates further to a pharmaceutical composition comprising the compounds of formula (I). Moreover, the present invention relates to a method of inhibiting growth, proliferation or metastasis of cancer cells in a subject in need thereof, in particular which may encompass subsets of patients defined by their mutational status of the RAS oncogene or patients who might have developed resistance to the standard of care or treatment with RAS mutation specific inhibitors. The present invention also relates to a method of inhibiting RAS molecules in treating genetic disorders like RASopathies or inflammatory disorders like Adenomyosis where KRAS gene is mutationally activated. In addition, the present invention relates to a method of inhibiting proliferation and or secretion of factors from a cell population sensitive towards inhibiting RAS activation in vitro, in particular sensitive towards inhibiting KRAS. HRAS and NRAS activation in vitro. Furthermore, the present invention relates to a kit containing a formulation comprising a pharmaceutical composition comprising a compound of formula (I).

The utility model discloses a portable sampling device for endometrial cancer gene methylation detection in the technical field of sampling devices, which comprises an extraction cylinder, one end of the extraction cylinder is fixedly inserted with a connecting pipe, the inner wall of the connecting pipe is movably inserted with a detachable extraction pipe, and the inner wall of the detachable extraction pipe is movably inserted with a connecting pipe. A plurality of guide blocks are fixedly arranged on the outer wall of the end, inserted into the connecting pipe, of the detachable extraction pipe, the guide blocks are in sliding fit with the inner wall of the connecting pipe, and two toothed plate sealing pieces used for blocking the connecting pipe are movably arranged on the inner wall of the extraction cylinder; after the device is used, the grab handle is firstly detached, then the detachable extraction pipe is detached, and at the moment, the guide block slides along the inner wall of the connecting pipe, so that the connecting pipe drives the transmission gear to rotate reversely, and the two toothed plate sealing pieces are reset along with the reverse rotation of the transmission gear to seal the connecting pipe; therefore, the possibility that external sundries enter the extraction barrel through the connecting pipe when the device is not used is reduced.

Mutations in oncogenes and tumor suppressor factors contribute to the development and progression of cancer. This disclosure describes compounds and methods for restoring DNA-binding affinity of p53 mutants, as well as their use in diagnostic assays to guide the treatment of subjects with said compounds for cancer. The compounds of this disclosure can bind to mutant p53 and restore the ability of p53 mutants to bind to DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers containing p53 mutations.

Provided is reproducible means that enables production of nucleus pulposus progenitor cells (preferably, an active nucleus pulposus progenitor cell phenotype) from desired cells such as terminally differentiated cells and stem cells having pluripotency or multipotency. A nucleus pulposus progenitor cell inducer according to the present invention comprising an effective amount of a gene of Brachyury (T) or a homolog thereof, at least one selected from the group consisting of SRY-box6 (SOX6) or a homolog thereof and Forkhead Box Q1 (FOXQ1) or a homolog thereof, and MYC Proto-Oncogene, BHLH Transcription Factor (cMyc) or a homolog thereof (nucleus pulposus progenitor cell master regulator transcription factor), or a product thereof.

The present disclosure features chemical entities (e.g., compounds or pharmaceutically acceptable salts thereof) that degrade the proto-oncogene VAV1 protein (VAV1). The chemical entities are useful, for example, for treating subjects (e.g., human subjects) with inflammatory or autoimmune disorders.

The present invention discloses a method and system for mining potential proto-oncogenes based on the three-dimensional structure of chromatin, which relates to the field of computational biology technology. The method comprises: obtaining multiple mutation insulation regions based on chromatin data and cancer mutation data, and inputting the regions into a trained binding site predictor to obtain prediction results and destroyed insulation regions; obtaining multiple differentially expressed gene sets based on cancer gene expression data, intersecting the multiple differentially expressed gene sets to obtain a final differentially expressed gene set; intersecting the final differentially expressed gene set and the genes in the destroyed insulation regions to obtain intersection genes; performing survival analysis to obtain analysis results, screening the intersection genes based on the analysis results to obtain genes associated with poor prognosis; and screening the intersection genes to obtain potential proto-oncogenes. This improves the accuracy and reliability of mining potential proto-oncogenes while saving time and economic expenses.

The invention discloses an immortalized rabbit liver cell line as well as a construction method and application thereof, and the construction method is characterized in that an exogenous oTERT gene is introduced into rabbit embryo liver cells, so that the rabbit embryo liver cell line is immortalized. The successfully immortalized rabbit embryo liver cell line can be stably subcultured for more than 10 generations, and does not have an aging phenomenon. Compared with a traditional method (introducing exogenous immortalized genes such as cancer suppressor genes p53 and SV40TAg into cells), the TERT-mediated cells belong to normal cells, the growth characteristics of the TERT-mediated cells are kept consistent with those of the normal cells, the TERT-mediated cells belong to immortalization in a real sense, and a scientific and stable cell material can be provided for subsequent RHDV research. The construction method is simple, easy to implement and easy to popularize.

The present invention includes a method and kit for method for detecting anti-Ro antibody negative Sjögren's syndrome / Sjögren's disease without performing a lip biopsy comprising: obtaining a biological sample from a patient suspected of having an anti-Ro antibody negative Sjögren's syndrome / Sjögren's disease; and detecting if the biological sample has autoantibodies to at least one of: Geminin DNA Replication Inhibitor (GMNN), Kelch Domain Containing 8 A (KLHDC8A), Microtubule Associated Protein RP / EB Family Member 1 (MAPRE1), Nucleoporin 50 (NUP50), or SKI Like Proto-Oncogene (SKIL).

The present disclosure provides antibodies specifically binding N-terminal or C -terminal regions of Cell Adhesion Molecule-Related / Down-Regulated By Oncogenes (CDON) polypeptide, methods of making the same, and methods of treating humans having tumors by administering the antibody.

The invention belongs to the technical field of biological medicines, and particularly relates to application of a cancer suppressor gene SLC26A11 in hyperleukocyte acute B lymphocytic leukemia. The invention discloses an application of a cancer suppressor gene SLC26A11 as a specific molecular marker in preparation of induction treatment reaction, prognosis and risk assessment of high leukocyte acute B lymphocytic leukemia of children, and an application in improvement of sensitivity of chemotherapeutic drugs for high leukocyte acute B lymphocytic leukemia of children. The SLC26A11 is used as a potential target, so that a personalized treatment scheme is provided for HALL patients, the toxic and side effects of chemotherapeutic drugs are reduced, and the treatment effect is improved.

Disclosed herein is a system that addresses all of the current challenges described above by combining three existing technologies and an improved nuclear RNA delivery system to generate a first-in-class cellular therapy that can secrete a cancer specific suicide gene for the treatment of several cancers. Also disclosed herein is a 'Trojan-Horse' like genetic construct aimed at engineering a chemo-sensitive dominant clone for adaptive therapy in cancers, such as leukemia. In some embodiments, cells, such as cancer cells from a subject, are engineered with suicide genes to promote a bystander effect in neighboring cancer cells once returned to the subject. In some embodiments, these cells are further engineered to be clonally dominant, e.g. by deleting or mutating tumor suppressor genes in the cells, overexpressing oncogenes, or any combination thereof. Once the engineered cells have reached a target clonal dominance, the suicide gene can be induced, thereby promoting the bystander effect.

Disclosed herein are polypeptide fragments and polynucleotides based on mutant capicua transcriptional repressor (CIC), catenin beta 1 (CTNNB1), v-erb-b2 erythroblastic leukemia viral oncogene homolog B (ERBB2), kirsten rat sarcoma (KRAS), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA), phosphatase and tensin homolog (PTEN), splicing factor 3b subunit 1 (SF3B1), SRY-box transcription factor 17 (SOX17), tumor protein 53 (TP53), and cytomegalovirus (CMV) sequences, vectors, host cells, viruses, methods for generating CD8+ T-cells, and methods of treatment. Also disclosed herein are T-cell receptors (TCRs), polynucleotides, vectors and cells comprising the TCRs, and methods of treatment.