35 results about "Tumor suppressor gene" patented technology

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 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.

Provided herein are methods and compositions for treating cancer in an individual comprising administering to the individual an effective amount of at least one CD122 / CD132 agonist, at least one immune checkpoint inhibitor and a viral composition comprising one or more viruses engineered to overexpress a tumor suppressor gene and / or an adenoviral death protein. Also provided herein are methods and compositions for treating cancer in an individual comprising administering to the individual an effective amount of at least one oncolytic viral composition and at least one CD122 / CD132 agonist and at least one immune checkpoint inhibitor. Also provided herein are methods of enhancing anti-tumor efficacy by administering the agents described above in combination with other cancer therapies. In highly aggressive forms of cancer, known to be generally resistant to immune therapies, these treatments unexpectedly resulted in complete tumor remissions and curative outcomes.

The invention discloses an elephant source bacillus licheniformis and application thereof. The preservation number of the bacillus licheniformis strain L517 is GDMCC 67825, the bacillus licheniformis strain L517 is classified and named as bacillus licheniformis, and the preservation date is February 26, 2026. Research finds that the bacillus licheniformis has a remarkable treatment effect on acute colitis of mice; and the traditional Chinese medicine composition also has a remarkable treatment effect on mouse subcutaneous colon cancer. The anti-cancer mechanism is that the infiltration of GZMB < + > CD8 < + > cytotoxic T cells in a tumor microenvironment is remarkably promoted in vivo through a supernatant metabolite of a culture medium, and a tumor suppressor gene P53 can be directly up-regulated. It is found for the first time that the elephant intestinal tract source bacillus licheniformis with evolutionary disease-resistant advantages shows good anti-proctitis and colon cancer activity, and can become an effective medicine for treating proctitis and colon cancer in the future.

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 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.

Methods for inducing basal cell carcinoma (BCC) or BCC tumors, as well as an inducible non-human animal models of BCC, are defined herein. The methods and animal models comprise targeting Ptch1 and / or a tumor suppressor gene via conditional expression of one or more short hairpin RNAs (shRNAs) in the skin of said animals.

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.

Application of TMOD3 and / or ADSL in non-small cell carcinoma. The present invention discloses the application of reagents for detecting the expression levels of TMOD3 and / or ADSL in the preparation of products for detecting non-small cell lung cancer. The present invention also discloses the application of an ADSL promoter in the preparation of a drug for treating non-small cell lung cancer. The present invention reveals that the new NSCLC oncogene TMOD3 and tumor suppressor gene ADSL play important roles in the malignant progression and ferroptosis of non-small cell lung cancer and their potential molecular mechanisms, which can provide a basis for the diagnosis, treatment and prognosis of NSCLC, and provide a new research direction and theoretical basis for precision treatment.

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.

The invention discloses an anti-BCL6 protein nano antibody, a fusion protein and application thereof, and belongs to the technical field of biology. According to the invention, the nano antibody specifically targeting BCL6 is designed by using an artificial intelligence technology, and the nano antibody has good specificity and high affinity, and can efficiently bind to a BCL6 antigen; furthermore, rational design of the nano-antibody is carried out through artificial intelligence, so that a nano-antibody mutant with higher affinity is obtained; furthermore, a nano antibody or a nano antibody mutant with high affinity and relatively good specificity is fused with an RBCC structural domain or a mutant thereof to obtain a fusion protein, and the fusion protein can utilize the specificity of the nano antibody structural domain to bind to a target protein and start a protein degradation pathway, so that targeted degradation of the BCL6 protein is realized, and the BCL6 protein can be degraded in a targeted manner. The expression of cancer suppressor genes p53 and cyclin p21 in cells is improved, and the method has a very great clinical application value.

To provide application of a tumor suppressor gene.SOLUTION: Two antibodies capable of binding to a mutated P53 protein are created to sandwich the P53 protein from both sides for detection. The entire molecule thus sandwiched constitutes a transcription factor. The transcription factor expresses a toxin.

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.

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 discloses an octopus-shaped CdS QDs net and multivalent Au-S bond mediated photoelectrochemical detection strategy method for TP53. The method comprises the following steps: (1) preparing a TiO2-MXene (at) Au photoelectrode; (2) carrying out target identification and signal amplification reaction; and (3) adding a reaction solution obtained in the step (2) to the TiO2-MXene (at) Au photoelectrode obtained in the step (1) as a working electrode, and carrying out PEC measurement by taking a platinum wire as a counter electrode. An octopus-shaped CdS QDs net is formed based on a terminal deoxynucleotidyl transferase (TdT) chain extension reaction and a biotin-streptavidin coupling reaction, and a large number of CdS QDs can be enriched to the surface of the electrode through multivalent Au-S bond anchoring, so that the output of photoelectric signals is enhanced, and the sensitive detection of the cancer suppressor gene TP53 is realized.

The present invention discloses a non-invasive early screening method and system for cancer based on the length distribution characteristics of cfDNA fragments. This method uses a relatively low-depth whole-genome sequencing method to statistically analyze the differences in the fragment length distribution characteristics of tumor-derived cfDNA and healthy individual-derived cfDNA, establish an early screening model for cancer, and achieve non-invasive early screening for cancer. The scheme of the present invention focuses on the characteristic of blood cfDNA fragment size to distinguish ctDNA from non-tumor-derived cfDNA. It does not rely on the mutation detection of oncogenes or tumor suppressor genes, and eliminates the interference caused by clonal hematopoietic mutations. Secondly, the data of the embodiments of the present invention show that the size characteristics of blood cfDNA fragments can be used to distinguish between healthy people and early-stage tumor patients. Finally, due to the use of low-depth whole-genome sequencing technology, the detection costs involved in the scheme of the present invention are greatly reduced, which is conducive to future applications in the field of early screening of malignant tumors.

The present invention relates to a use of untranslated RNA RP11-252E2.2 for predicting liver cancer metastasis or treating liver cancer metastasis. lncRNA which specifically decrease in expression in liver cancer tissues and cells were identified by analyzing lncRNA which specifically decrease in expression in liver cancer as compared to normal cells with respect to lncRNA showing the potential to function as tumor suppressor genes, and RP11-252E2.2 was found to be involved in the metastasis of liver cancer. Therefore, the untranslated RNA RP11-252E2.2 discovered in the present invention is highly likely to be effectively used for predicting or treating liver cancer metastasis.

The present invention belongs to the field of biotechnology, and specifically relates to a biomarker for breast cancer, the ZNF662 gene, and its detection method and application. The biomarker is the ZNF662 gene, and the sample to be tested is derived from a patient suspected of breast cancer. The nucleotide of the ZNF662 gene is SEQ ID NO: 1. The present application provides a method for detecting the methylation status of the ZNF662 gene promoter, and the specific steps are: ① extracting a DNA sample; ② designing primers, using a methylation detection reagent, and detecting the methylation level of the ZNF662 gene promoter in the DNA sample by the MSP method to determine whether the ZNF662 gene is methylated, thereby achieving breast cancer diagnosis. The present application is the first to confirm through in vivo and in vitro experiments that ZNF662 is a new tumor suppressor gene, and its expression is downregulated in breast cancer due to hypermethylation of the promoter, providing a new option for the screening of early diagnostic markers for breast cancer.

Provided are a corn peptide having an anti-tumor effect, and a preparation method therefor and a use thereof. The corn peptide can obviously eliminate reactive oxygen species in tumor cells, increase the concentration of free calcium ions in the cytoplasm of the tumor cells and reduce the mitochondrial membrane potential of the tumor cells, and also can enhance the expression levels of mRNA and proteins of an IP3R and calreticulin, and further affect the calcium homeostasis of the tumor cells. In addition, the corn peptide can up-regulate the expression of tumor suppressor genes PTEN, P21 and P27, down-regulate the expression of a cell proliferation marker PCNA and a tumor-promoting gene Akt, and mediate an anti-tumor effect by means of PTEN and Akt cell signaling pathways.

The present application relates to the technical field of biological diagnosis, and particularly relates to a mutant gene set for tumor molecular typing and application thereof, wherein the mutant gene set comprises 82 mutant genes including DNA methylation modification related genes, histone modification related genes, chromatin remodeling related genes, TCR signal pathway related genes, PI3K-AKT signal pathway related genes, JAK-STAT signal pathway related genes, immune escape related genes, P53 signal pathway related genes, tumor suppressor genes and NOTCH signal pathway related genes. The mutant gene set can be used for molecular typing, targeted therapy and overall survival prediction of intranodal peripheral T-cell lymphoma. The mutant gene set is verified by clinical trials, and is suitable for all primary and relapsed PTCL patients, relapsed or refractory peripheral T-cell lymphoma umbrella study based on genomics typing and PTCL patients receiving different treatment schemes, and has a very wide application range.

Mutations in oncogenes and tumor suppressor genes contribute to the development and progression of cancer. The present disclosure describes compounds and methods for restoring wild-type function to p53 mutants. The compounds of the invention can bind to mutant p53 and restore the ability of p53 mutants to bind 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 invention provides for inhibitory transporter ribonucleic acids (sup-tRNAs) that inhibit premature termination codons (PTCs) during translation and promote full length readthrough of cancer suppressor gene nonsense mutation transcripts, as well as the use of the sup-tRNAs to treat disease conditions of cancer that contain cancer suppressor gene nonsense mutations. In particular, Arg-tRNAUGA and Gln-tRNAUAG can restore the tumor suppressor gene function of tumor cells and indirectly regulate and control the expression of downstream target genes of the tumor suppressor genes, so that the clone number, the total clone area and / or the single clone area of in-vitro cultured tumor cells are reduced, and the volume and / or the weight of in-vivo tumors are reduced.

This invention discloses a dual-ion-based nanoparticle for treating p53-mutant tumors, its preparation method, and its application, relating to the field of tumor drug technology. The dual-ion-based nanoparticle comprises liposomes and Zn... 2+ Co 2+ The inner and outer tumor cell membranes; liposomes have a bilayer; Zn 2+ Encased within the liposome, the inner layer is the tumor cell membrane and Co 2+ The complex is formed and coated on the outer layer of the liposome, with the outer layer of tumor cell membrane covering the outside of the complex. This application connects mutant p53 and the cGAS-STING pathway, promoting the cGAS-STING innate immune pathway by reducing the expression of mutant p53, restoring the function of the p53 tumor suppressor gene, achieving better tumor treatment effects, and has good application value in tumor treatment.

The invention provides a recombinant oncolytic adenovirus based on PCV2 functional protein as well as a preparation method and application of the recombinant oncolytic adenovirus, and belongs to the technical field of biological medicines. The genome of the recombinant oncolytic adenovirus based on the PCV2 functional protein provided by the invention comprises a PCV2 Cap gene and / or a PCV2 Rep gene. According to the invention, the Cap and / or Rep genes of PCV2 are / is taken as brand new therapeutic transgenosis, the recombinant oncolytic adenovirus is successfully constructed, and brand new candidate entities and action target bases different from traditional cell factors or tumor suppressor genes are provided for oncolytic virus therapy. According to the invention, the recombinant adenovirus is used as an efficient delivery vector, so that the transduction and expression efficiency of the PCV2 functional gene is greatly improved, and the limitations of low natural infection efficiency and weak replication ability of the PCV2 wild type virus are overcome. The recombinant oncolytic adenovirus, especially the recombinant Rep adenovirus, provided by the invention realizes a multi-mechanism synergistic efficient anti-tumor effect.

The application discloses a kind of anti-BCL6 protein nanobody, fusion protein and its application, belong to biotechnology field.The application is designed by using artificial intelligence technology to specifically target the nanobody of BCL6, the nanobody has good specificity, high affinity, can efficiently combine BCL6 antigen;Further, the higher affinity nanobody mutant of the rational design of nanobody is obtained by artificial intelligence;Further, by the fusion of nanobody or nanobody mutant with high affinity and good specificity and RBCC domain or its mutant, the fusion protein is obtained, the fusion protein can utilize its nanobody domain specific binding target protein, start protein degradation pathway, realize the targeted degradation of BCL6 protein, improve the expression of intracellular anticancer gene p53 and cell cycle protein p21, has very big clinical application value.

This invention provides the application of the tumor suppressor gene COTL1 in the preparation of drugs for the diagnosis and prognosis of clear cell renal cell carcinoma. This invention discloses the application of a novel tumor suppressor gene, COTL1, and its encoded protein, specifically designing the COTL1 gene and / or its encoded protein for the preparation of drugs against clear cell renal cell carcinoma; and the application of kits and methods for detecting the mRNA or protein levels of the COTL1 gene in drugs for the diagnosis and / or prognosis of clear cell renal cell carcinoma. This invention discovers that the COTL1 gene is a novel tumor suppressor gene, particularly playing an important role in the development and progression of clear cell renal cell carcinoma, providing new targets and methods for cancer diagnosis, prognosis, treatment, and drug screening.

The present disclosure relates to a biliary tract cancer organoid and a method of producing the same. A new biliary tract cancer organoid system was developed in which CRISPR-Cas9 gene editing technology is applied to human chemically-derived hepatic progenitors to introduce mutations into some genes known as tumor suppressors or oncogenes, and the effects of the combined genetic mutations on human non-tumor, chemically-derived hepatic progenitors are analyzed to identify and screen the effects of the combined mutations on oncogenesis.

A method includes accessing a digital pathology image that depicts tumor cells sampled from a subject. A plurality of patches may be selected from the digital pathology image, wherein each of the patches depicts tumor cells. A mutation prediction may be generated for each of the patches, wherein the mutation prediction represents a prediction of a likelihood that an actionable mutation appears in the patch. Based on the plurality of mutation predictions, a prognostic prediction related to one or more treatment regimens for the subject may be generated. The prognostic prediction may be based on determining one or more mutational contexts of the digital pathology image as an unknown driver or a tumor suppressor, an oncogene driver mutation, or a gene fusion.

Provided herein are nucleic acid sequences for targeting one or more single point mutations within a target gene, wherein the target gene is one or more tumour suppressor genes; wherein the tumour suppressor gene is p53; and methods of treating cancer in a subject comprising administering the same.

The application discloses an anti-vascular composite gene vector and a preparation method and application thereof. The anti-vascular composite gene vector is prepared by coating the cationized tussah silk fibroin which is modified by an angiogenesis inhibitor, endostatin, on the surface of an adenovirus by electrostatic adsorption. The anti-vascular composite gene vector is in the form of spherical nano-particles, can effectively infect umbilical vein endothelial cells and liver cancer cells, express anticancer genes, inhibit the proliferation of vascular endothelial cells and tumor cells, and block the growth and metastasis of tumors. Different anticancer genes are coded in the vector, so that the anti-vascular composite gene vector can play the therapeutic effect of resisting tumors and preventing metastasis for different malignant tumors. Therefore, the anti-vascular composite gene vector can be used for preparing a medicine for treating tumors.