124 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 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 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 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 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.

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 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 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.

The application discloses an ecDNA recognition method based on scATAC-seq data. The ecDNA recognition method provided by the application can accurately detect copy number amplification, breakpoint quantity and ecDNA feature quantity on the whole cell level. The method provided by the application can recognize specific circular oncogenes carried in tumors, analyze the distribution characteristics of the circular oncogenes in the genome, and reveal the overall composition of all circular DNAs in a single cell and the specific composition of a single circular DNA. In addition, the method can also verify the existence of the circular DNA through a staining experiment, so that the reliability of the detection result is ensured.

A novel compound that is a protein degradation-inducing part of the proto-oncogene tyrosine protein kinase receptor (RET), wherein the RET may be wild-type RET or a mutant form of RET.

Methods and compositions for gene therapy of retinal degeneration related to mutations in MER proto-oncogene, tyrosine kinase (MERTK).

An mRNA vaccine composition is described. The vaccine composition includes an exosome comprising an expression cassette comprising mRNA encoding chimeric / fusion / hybrid oncogene (CFHON). Methods of treating or preventing cancer in a subject by administering a therapeutically effective amount of the mRNA vaccine composition are also described.

The application relates to a circular triplex-forming oligonucleotide, a preparation method and application in preparation of tumor-targeting drugs. The circular triplex-forming oligonucleotide (Cir-TFO) is composed of two oligonucleotide chains A and B, each of which comprises a first complementary sequence, a first connecting sequence, a target sequence, a second connecting sequence and a second complementary sequence from the 5' end to the 3' end. The first complementary sequences of the two oligonucleotide chains A and B are reversely and complementarily connected, and the second complementary sequences are reversely and complementarily connected to form a closed ring structure. The target sequence is a TFO sequence capable of forming a triplex structure with double-stranded DNA in the promoter region of a target gene through Hoogsteen hydrogen bonds, and the target gene is selected from a proto-oncogene, an anti-apoptotic gene or a tumor metabolism-related gene.

Provided are a method and a combination for one-tube simultaneous detection of tumor-specific gene mutation and methylation, and the use thereof. The method comprises searching a database to select mutation and methylation sites of a cancer driver gene and a cancer suppressor gene, synthesizing capture probes correspondingly paired with a target interval, performing hybrid capture on an amplification product of a sample treated with a restriction endonuclease by using a probe set comprising tumor-specific gene mutation and methylation capture probes, constructing a high-throughput sequencing library containing a target region, and performing high-throughput sequencing to obtain the sequence of a target fragment, so as to obtain the results of methylation, point mutations and indel variation of a cancer-associated gene. The provided method enables one-tube simultaneous detection of mutation and methylation states of a cancer-associated gene in one assay, requires a low content of a gene to be detected, can be used for methylation and mutation detection of a tumor-specific DNA, and has low detection costs and high efficiency.

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 present invention relates to a pharmaceutical composition comprising a Runx3 gene or protein as an active ingredient for prevention or treatment of K-Ras mutant lung cancer. Specifically, Runx3 gene-deleted, K-Ras gene-activated lung cancer mice established in the present invention were found to be completely cured without lung cancer recurrence likelihood when restoring the Runx3 gene, compared to the conventional approach of inhibiting the activated cancer gene. Thus, the composition comprising Runx3 protein, a polynucleotide coding therefor, a vector carrying the polynucleotide, or a virus or cell transformed with the vector as an active ingredient according to the present invention can be advantageously used as a composition for prevention or treatment of K-Ras mutant lung cancer.

The present disclosure relates to proteolysis-inducing compounds against the proto-oncogene tyrosine-protein kinase receptor (RET), which may be either wild-type RET or a mutant form of RET, which are useful in the treatment of diseases and disorders mediated by said protein, and have formula (I): TIFF2025540907000060.tif43113

The application relates to the technical field of molecular markers, and discloses an SNP site associated with turbot albinism, a molecular marker and application, wherein the SNP mutation site is a base T / A mutation at the 50th bp of a coding region of a gene KIT proto-oncogene, receptor tyrosine kinase a (kita); the SNP mutation site is a base A / T mutation at the 137th bp of a coding region of a gene cytochrome P450 3A40-like (LOC118311907); the SNP mutation site is a base G / T mutation at the 371st bp of a coding region of a gene kit ligand a (kitlga); and the SNP mutation site is a base G / A mutation at the 581st bp of a coding region of a gene frizzled class receptor 10 (fzd10). The SNP site associated with turbot albinism, the molecular marker and the application provide a precise screening method for turbot breeding. In the breeding process, the SNP molecular markers are used to determine whether the genotype is albinism or normal, to establish an excellent family with normal body color, to reduce the incidence of abnormal body color, and to improve the overall quality and economic benefits of turbot culture.

The invention belongs to the technical field of biological medicines, and discloses application of a CCT6A inhibitor in preparation of a medicine for treating colorectal cancer. CCT6A is determined to be a key cancer promoting gene of colorectal cancer for the first time, the CCT6A is remarkably and highly expressed in colorectal cancer tissues and cell lines, and high expression indicates poor prognosis of patients, so that a brand-new specific target is provided for targeted therapy of colorectal cancer. The invention discloses the cancer promoting effect of the compound in colorectal cancer and the association with 5FU drug resistance for the first time, enriches the development of colorectal cancer and the molecular mechanism research of chemotherapy drug resistance, and provides a new theoretical basis and research direction for the fundamental research in the field. Experiments prove that the inhibitor can significantly reduce the mRNA level of CCT6A in colorectal cancer cells so as to strongly inhibit tumor cell proliferation and increase the sensitivity of the colorectal cancer cells to 5-FU, and a novel therapeutic drug with high specificity and high curative effect is provided for treatment of colorectal cancer.

The invention discloses an application of CUTA as a biomarker in diagnosis and / or treatment of liver cancer, and particularly discloses an application of a reagent for detecting CUTA in preparation of a product for diagnosing liver cancer, and the expression of the CUTA in a liver cancer patient is up-regulated. The invention provides application of CUTA as a liver cancer biomarker. Database analysis, cell experiments and clinical sample verification prove that CUTA is a cancer promoting gene of liver cancer. Based on a plurality of public databases such as a TCGA database and a GEO database, the invention provides the application of the CUTA as a biomarker in liver cancer diagnosis and liver cancer prognosis risk assessment according to a bioinformatics analysis result, and a large number of clinical samples are used for performing efficacy verification, so that the application of the CUTA in liver cancer diagnosis and liver cancer prognosis risk assessment is realized. It is proved that the CUTA can serve as the liver cancer biomarker to provide a prevention scheme or a treatment scheme for subjects clinically, and precise molecular treatment of the liver cancer is achieved.

Provided herein are compounds of formula (I) and salts and compositions thereof which find utility as modulators of Cbl-b in the treatment of various forms of cancer.

The present disclosure relates to methods of selecting and / or treating a subject for treatment of a cancer with a G4-stabilizing ligand based on expression of oncogene with a G4 motif comprising GxN1-7GxN1-7GxN1-7GxN1-7 (SEQ ID NO: 15) where N refers to any base and x≥3 in the subject. The disclosure also provides methods of detecting a cancer cell susceptible to growth inhibition with a G4-stabilizing ligand and methods of treating a cancer in a subject with a G4-stabilizing ligand.

Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes methods of recovering wild-type function to p53 mutants by treating a tumor with a compound and a second agent. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used in combination with an MDM2, PI3K, or AKT inhibitor to reduce the progression of cancers that contain a p53 mutation.

The present invention relates to gene editing agents (e.g., CRISPR / Cas) that target mutated oncogenes (e.g., a mutated oncogene a cancer is addicted to) and uses thereof (e.g., for inactivation of mutated oncogenes and / or treatment cancer). In some embodiments, the mutated oncogene is a mutated KRAS. In some embodiments, the cancer is pancreatic ductal adenocarcinoma, non-small cell lung cell, or colorectal cancer.

This disclosure describes a machine learning (ML) framework, including a graph convolutional neural network (GCN), for identifying gene expression signatures associated with cancer driver events. The model is trained to identify the TP53 mutation status of cancer samples from gene expression, utilizing a comprehensive, curated graph structure of gene interactions. Quantitative scores are generated to rank the severity of driver events in each sample. Very high AUC results for unknown data across several tumor types are achieved in this method. A strong correlation with protein function exists. The Signature in Transcriptome Associated with Mutant Proteins (STAMP) model can also predict driver events in many combinations of key oncogenes / pathways and several tumor types, based on well-established annotations from the literature. Thus, the STAMP model can identify and quantify driver events, which may lead to improved targeted therapy selection and prioritization in cancer patients.

TIFF2025540906000076.tif4057 The present disclosure relates to protein-binding compounds of the proto-oncogene tyrosine-protein kinase receptor (RET), which may be either wild-type RET or a mutant form of RET, that are useful for the treatment of diseases and disorders mediated by said protein and have formula (I):

This invention relates to the field of biomedical technology, specifically disclosing a plant-derived exovesicle preparation for treating liver cancer, its preparation method, and its application. The plant-derived exovesicle preparation is used to prepare drugs for treating liver cancer, and includes Uncaria rhynchophylla exovesicles and tea exovesicles. The plant-derived exovesicle preparation provided by this invention treats liver cancer by inhibiting liver cancer cell proliferation, promoting liver cancer cell apoptosis, and inhibiting oncogene expression.