64 results about "Oncogene" patented technology

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 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.

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

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 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 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 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.

The present application relates to the field of cancer cell identification, and particularly relates to a method and system for identifying different types of cancer cells of a renal pelvis cancer patient based on urine, the method comprising: collecting a urine sample, obtaining a detection sample by using the urine sample; sequencing the detection sample to obtain a cell expression profile of the detection sample; obtaining cell expression profile data of a mixed urothelial cell subpopulation by using the cell expression profile, the mixed urothelial cell subpopulation comprising normal urothelial cells and cancerous urothelial cells; extracting different proto-oncogene expression data from the cell expression profile data of the mixed urothelial cell subpopulation; analyzing the different proto-oncogene expression data to obtain a cancer cell ratio and identify different types of cancer cells. The present method quickly and accurately obtains different types of cancerous urothelial cells through non-invasive examination and proto-oncogene expression profile data, and provides a reference and basis for preoperative neoadjuvant therapy of renal pelvis cancer.

The invention discloses an application of DRAP1 as a biomarker in diagnosis and / or treatment of liver cancer, and particularly discloses an application of a reagent for detecting DRAP1 in preparation of a product for diagnosing liver cancer, and expression of DRAP1 is up-regulated in liver cancer patients. The invention provides application of DRAP1 as a liver cancer biomarker. Database analysis, cell experiments and clinical sample verification prove that DRAP1 is a cancer promoting gene of liver cancer. On the basis of various public databases such as a DRAP1 database and a GEO database, the application of DRAP1 as a biomarker in liver cancer diagnosis and liver cancer prognosis risk assessment is provided through a bioinformatics analysis result, efficacy verification is carried out by using a large number of clinical samples, and the application of DRAP1 as a biomarker in liver cancer diagnosis and liver cancer prognosis risk assessment is provided. It is proved that DRAP1 can be used as a liver cancer biomarker to provide a prevention scheme or a treatment scheme for subjects clinically, and precise molecular treatment of liver cancer is achieved.

The present disclosure relates to a composition for promoting the activation of bone marrow-derived stem cells, including C-C motif chemokine ligand 5 (CCL5), wherein, when CCL5 is administered together with growth-related oncogene beta (GROβ) and AMD3100, it not only increases the migration of hematopoietic stem cells from bone marrow to peripheral blood, but also enhances the engraftment efficiency when the hematopoietic stem cells are transplanted into recipients.

Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. Disclosed herein are compounds and methods to recover wild-type function of p53 mutants using x-ray co-crystal structures of mutant p53 and compounds of the disclosure. 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 to reduce the progression of cancers that contain a p53 mutation.

Described herein is the preparation and use of amino acid-modified lipids for delivery of a small interfering RNA (siRNA), mRNA, miRNA, shRNA, or oligonucleotide via formation of lipid nanoparticles (LNPs) comprising the siRNA, mRNA, miRNA, shRNA, or oligonucleotide and the amino acid-modified lipid. Use of the described lipid nanoparticles to silence overexpression of oncogenes is described.

This invention relates to antisense oligonucleotides targeting different subtypes of human papillomavirus (HPV) oncogenes and their applications. The ASO molecules are 14–40 bases in length and specifically pair with specific regions of target genes. This invention also relates to the following applications of the ASO molecules: (1) preparing preparations to inhibit HPV virus expression; or (2) preparing drugs or drug compositions for treating diseases related to HPV infection; or (3) treating diseases related to HPV infection; or (4) inhibiting the expression of HPV virus genes.

The present disclosure provides compounds of formula (I): which induce proteolysis of the proto-oncogene tyrosine protein kinase receptor (RET), which may be either wild-type or mutant RET (useful in the treatment of diseases and disorders mediated by said protein): This relates to the compound represented by TIFF2026506696000135.tif42150.

The present disclosure relates to methods of treating pancreatic cancer. In particular, methods of treating pancreatic cancer and limiting overexpression of oncogenes, activating tumor suppressor genes, or modulating signaling proteins in a patient are described, comprising administering a compound and a pharmaceutical combination as described herein.

The invention relates to the technical field of biological medicines, and particularly discloses a cancer suppression small interfering RNA (Ribonucleic Acid) capable of simultaneously targeting cancer genes PTTG1 and STMN1 and application of the cancer suppression small interfering RNA, and the technical key points are as follows: the positive-sense strand sequence of the small interfering RNA is GGGAGAUCUCAAGUUUCAATT, and the antisense strand sequence of the small interfering RNA is UUGAAACUUGAGAUCUCCCTT. The small interfering RNA provided by the invention can specifically silence the expression of PTTG1 and STMN1 at the same time. Compared with siRNA (such as siRNA for ASCC3 or TRAPPC4) targeting a single gene in the prior art, the siRNA provided by the invention has the advantages that synergistic inhibition on tumor proliferation and metastasis pathways is realized through double-targeting design, and the inhibition effect on tumor cell growth is more remarkable; compared with a method of physically mixing two single siRNAs, the method provided by the invention has higher cell apoptosis induction efficiency and better in-vivo tumor inhibition effect; the small interfering RNA is effective in various liver cancer cells, has a lasting effect in an animal model, and provides a core molecular entity for developing novel antitumor drugs.

The invention provides a lentiviral vector for constructing a cell model for detecting carcinogenicity of chemical substances, a recombinant cell as well as a preparation method and application of the lentiviral vector. The lentiviral vector comprises a human c-myc gene promoter, an operably connected reporter gene and a selection marker gene. Recombinant cells capable of stably expressing reporter genes can be obtained by transfecting host cells with the vector, the activation effect of chemical substances on c-myc channels can be sensitively reflected through signal changes of the reporter genes, and rapid and visual preliminary screening of carcinogenicity is achieved. Furthermore, the recombinant cell is combined with a CRISPR-Cas9 sgRNA library targeting DNA damage repair, epigenetic regulation, tumor inhibition and proto-oncogene to construct an integrated screening system, so that the carcinogenic potential of chemical substances can be evaluated, key genes and molecular mechanisms of genetic toxicity of the chemical substances can be systematically revealed, and the application prospect is broad. And an efficient tool is provided for toxicology risk assessment and mechanism research.

This disclosure relates to CRISPR-related systems and components for targeting, editing, and / or regulating the expression of the FLI-1 (Friend virus leukemia integration 1 transcription factor, Fli-1 proto-oncogene, ETS transcription factor) gene. This disclosure also relates to methods and applications relating to genetically modified cells, including T cells or T cell progenitor cells.

Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. 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 to reduce the progression of cancers that contain a p53 mutation.