58 results about "PTEN" patented technology

The invention belongs to the technical field of molecular biology and biomedicine, and relates to a method for increasing the efficiency of CRIPSR/Cas9 target knock-out genes NHEJ. According to the method for increasing the efficiency of CRIPSR/Cas9 target knock-out gene NHEJ, small molecule interference RNA that efficiently interferes with expression of PTEN genes is screened out; by using CRISPR/Cas9 system to target knockout genes, the small molecule RNA is cotransfected into the target gene, thus the NHEJ efficiency of target genes is effectively improved and the NHEJ of target gene in cell multiple targets is significantly improved. The method has the advantages of low cost, simple operation and high efficiency, and has a good promoting effect on the efficiency and application of CRISPR/Cas9 technology.

The invention relates to the field of tumor gene, and discloses a high-flux sequencing detection method for tumor-targeted drugs related genes mutation, a group of primer pairs and a reagent thereof. The method is used for detecting mutation of tumor-targeted drugs related genes in an acceptor, the related genes comprise BRAF, EGFR, KRAS, NRAS, TP53, FGFR3, KIT, PIK3CA, RET, PTEN, and CTNNB1. The method comprises the following steps: extraction of sample DNA, target gene enrichment, primer sequence removal, joint connection, PCR amplification, library homogenization, library detection and high flux sequencing. The disclosed primer pairs enable multiple PCR enrichment and amplification on the tumor-targeted drugs related genes, the method can be used for detecting 115 mutation sites in the above 11 genes, a detection result can be a medication guidance for the tumor-targeted drugs, and provides a basis for exploitation of novel cancer drugs.

A transgenic animal having a somatic cell in which at least one allele of an endogenous p53 and Pten gene is functionally disrupted is provided. The cell of the animal may be heterozygous or, more preferably, homozygous for the gene disruptions. The animals of the invention can be used to evaluate the efficacy of novel therapeutics and to identify novel points of therapeutic intervention for cancer. In certain embodiments, the transgenic animal is a transgenic mouse having functionally disrupted endogenous p53 and Pten genes. This mouse can be used to identify agents that inhibit the development of cancers, namely bladder cancers in humans in vivo. Nucleic acid constructs for functionally disrupting an endogenous p53 and Pten gene in a host cell, recombinant vectors including the nucleic acid construct, and host cells into which the nucleic acid construct has been introduced are also encompassed by the invention

The invention relates to an in-situ hybridization detection kit for a PTEN gene. The kit comprises a hybridization probe and a marker, wherein the hybridization probe has a sequence shown as SEQ ID NO.1. The invention also provides an in-situ hybridization detection method for the PTEN gene. In addition, the invention provides application of the kit to the preparation of medicaments for detecting cancers. The invention has the advantages that: the kit has the characteristics of high sensitivity and specificity; and the detection method is convenient and easy to operate and can be universally used and popularized in hospitals of district-level or above.

The invention relates to methods of predicting the clinical outcome of brain cancer patients based on the LOH levels of the PTEN gene and on the expression levels or the polysomy/amplification levels of EGFR gene in a sample from said patients.

The invention relates to a biomarker for typing non-small cell lung cancer, and application thereof, and belongs to the technical field of medical detection. The biomarker comprises at least five genes such as TP53, STK11, PTEN, NFE2L, KRAS and the like. When squamous cell carcinoma and adenocarcinoma in small cell carcinoma of lung are subjected to typing by utilizing the biomarker, the AUC of a typing diagnosis ROC curve is 0.700 when the at least five markers are used, the AUC of the typing diagnosis ROC curve is 0.734 when the number of the markers is further increased to 10, and the AUC can reach 0.786 when all the biomarkers are used, so that the biomarkers have excellent diagnosis capability.

The invention relates to mRNA of PTEN genes. The nucleotide sequence is shown as SEQ ID NO.1. The invention further provides PTEN gene overexpression recombinant adenoviral vectors, namely, the mRNA of the PTEN genes is inserted into multiple cloning sites of the adenoviral vectors, and the invention further provides a construction method and purposes of the PTEN gene overexpression recombinant adenoviral vectors. The PTEN gene overexpression recombinant adenoviral vectors constructed through the method can cause overexpression of the PTEN genes, can promote oxidative metabolism of fatty acid, and can effectively increase and determine assembly and secretion of VLDL. Moreover, the PTEN gene overexpression recombinant adenoviral vectors can enhance transport capacity of triglyceride and can be used for treating fatty liver in dairy cows.

The invention discloses a method for detecting esophagus cancer susceptibility gene PTEN polymorphism with Hae III. Primer sequences are shown as SEQ ID NO:1 and SEQ ID NO:2. The method includes the steps that genomic DNA of a sample is extracted; a forward primer and a reverse primer for amplifying sequences near the human PTEN gene polymorphism rs701848 site are provided, PCR amplification is conducted with the extracted genomic DNA to be detected as the template, and an amplification product is obtained; the obtained amplification product is subjected to digestion with the restriction enzyme Hae III, and a corresponding digestion product is obtained; the digestion product is subjected to electrophoresis with 3% agarose gel so as to judge the genotypes of PTEN gene polymorphism rs701848. The method is simple, easy to implement, rapid, efficient and low in cost, the digestion result is easy to identify, and a simple way is provided for genotyping of esophagus cancer susceptibility gene PTEN polymorphism rs701848.

The present disclosure relates to a method of treating cancer using a composition comprising Nelfinavir, Metformin, Rosuvastatin, optionally along with a pharmaceutically acceptable excipient. The said composition is used for the treatment of cancer caused due to aberration in PTEN gene, optionally along with aberration in TP53 gene and related genes selected from group comprising PI3K, CDKN2A, MDM2 and MDM4.

The invention discloses an application of an ER and Ki-67 expression ratio in endometrial tissues in fertility function retention treatment prognosis of endometrial cancer (EC) and atypical endometrial hyperplasia (AH). According to the invention, 53 EC patients and 68 AH patients orally take MPA or MA, then gonadotropin is combined to release a hormone agonist and/or a levoynorethindrone intrauterine sustained release system, the patients are divided into a recurrence group and a non-recurrence group according to whether recurrence occurs after complete remission, then ER, PR, P16, P53, PTEN, Ki-67 and the like are subjected to immunohistochemical analysis, and statistical analysis is carried out. Results show that the expression rate of the Ki-67 is of great significance in predicting recurrence after the EC and AH retention fertility function treatment, and the optimal critical value (3.55) of ER/Ki-67 can predict recurrence after the EC and AH retention fertility function treatment better than that of a single immunohistochemical marker. The method has an important application value.

The evolutionary origin of high-grade serous ovarian carcinoma remains largely unknown. The vast majority of tumor-specific genomic alterations from ovarian cancers are present in fallopian tube STIC lesions (average of 55 sequence alterations per tumor), including those affecting TP53, BRCA1, BRCA2 or PTEN genes. A quantitative evolutionary analysis indicated that tumors of the fallopian tube were the likely precursors of ovarian cancer and could directly give rise to metastatic lesions. These analyses suggest that there may be less than two years between the development of a STIC and the initiation of fallopian tube tumors, ovarian tumors or other metastases. Thus there may be a short window between the development of a STIC and the initiation of ovarian tumors or other metastases, highlighting the importance of the prevention, early detection and therapeutic intervention of this disease.

The invention discloses a mutant gene group, library and kit for evaluating female malignant tumor risk, and belongs to the technical field of biomedical molecular detection. The mutant gene group forevaluating the risk of female malignant tumors comprises one or more selected from a group consisting of the following 25 genes: ATM, BRCA1, BRCA2, BRIP1, CDH1, CHEK2, EPCAM, MLH1, MSH2, MSH6, NBN, NF1, PALB2, PMS2, PTEN, RAD51C, RAD51D, STK11, TP53, BARD1, MRE11A, MUTYH, RAD50, XRCC2 and FANCC5. According to the invention, female malignant tumor related genetic markers can be widely screened andinspected, accuracy is higher, and a basis is provided for prediction, prevention and diagnosis of female malignant tumor onset risks.

The invention provides a method for screening a glioma biomarker based on a PTEN gene state. The method comprises the following steps of: (1) obtaining the PTEN gene states of glioma patients; (2) dividing the glioma patients into a PTENWT subgroup and a PTENmutant subgroup; (3) screening subgroup-specific DEGs for the patients of the subgroups respectively; (4) fitting the subgroup-specific DEGswith the survival time of the subgroup patients to obtain subgroup-specific OPRDEGs; (5) constructing a risk score of each subgroup patient, observing the relationship between the risk score and the malignant degree of the tumor, and predicting the survival rate of each subgroup patient; (6) screening OPRDEGs of independent prognosis of each subgroup; and (7) screening potential targeting drugs. The independent optimal prognostic gene of the PTEN mutation subgroup with high malignant degree is analyzed through multi-factor COX, and further guiding significance is provided for diagnosis, prognostic prediction and treatment of PTEN mutation glioma.

The invention discloses a method for efficiently expressing an AFP3-PTEN fusion protein, and belongs to the technical field of biology. The method comprises the steps of cloning an HBx gene to a constructed expression vector, enabling the constructed vector to be transfected with human liver cancer cells, after expressing HBx proteins in the liver cancer cells, enabling the third structured domainof AFP and an overall-length PTEN gene to be connected to the expression vector and transfected into the human liver cancer cells expressing the HBx proteins, expressing the HBx proteins in the livercancer cells, promoting efficient secretory expression of a human AFP3-PTEN fusion protein through the HBx proteins, and concentrating and purifying culture mediums to obtain the AFP3-PTEN fusion protein. The AFP3-PTEN fusion protein expressed by the liver cancer cells can restrain cell proliferation and can enable the cell proliferation capacity of NIH 3T3 cells to be reduced by 15%-60%. But a reference protein AFP enables cell proliferation capacity to be obviously increased by 22-125%. Serum proteins do not have notable capacity for promoting NIH 3T3 cell proliferation. The obtained AFP3-PTEN fusion protein can be used for researching tumor treatment.

The invention discloses a regulating effect of zuojin wan (ZJW) on a ROCK/PTEN/PI3K signal pathway of human gastric cancer drug-resistant cells and application of ZJW. The influence of ROCK and PI3K signals on ZJW inducing apoptosis and a cycle of the gastric cancer drug-resistant cells is inhibited, and the results show that ZJW can induce apoptosis of SGC7901/DDP cells. No significant change occurs when Y27623 is applied alone. Apoptosis induction of ZJW and Y27623 combination to the SGC7901/DDP cells is significantly lower than that of ZJW alone, and it is indicated that activation of the ROCK signals is an important factor for ZJW to induce apoptosis. LY294002 applied alone significantly increases apoptosis of the SGC7901/DDP cells, and it is indicated that the PI3K signals are inhibitory signals of apoptosis. The induction effect of apoptosis of the SGC7901/DDP cells by combined use of ZJW and LY294002 is further increased rather than ZJW alone, and it is indicated that the two treatment methods have a synergistic effect.

The invention discloses lung cancer targeted drug and chemotherapy drug genomes and an application thereof in lung cancer clinical drug treatment. The targeted drug genome comprises AKT1, ALK, BRAF, CCND1, CDKN2A, DDR2, EGFR, ERBB2, ERBB4, FBXW7, FGFR1, FGFR2, FGFR3, HRAS, IGF1R, KDR, KIT, KRAS, MAP2K1, MET, NF1, NRAS, NTRK1, NTRK3, PDGFRA, PIK3CA, PTEN, RET, ROS1, STK11 and TP53; and the chemotherapy drug genome comprises ABCB1, CDA, CEP72, CYP1B1, CYP2C8, DPYD, ERCC1, ERCC2, GSTM, GSTP1, MTHFR, RRM1, SLCO1B1, TEKT4, TPMT, TYMS, UMPS, XPC and XRCC1. The lung cancer targeted drug and chemotherapy drug genomes disclosed by the invention are applied to guidance of clinical precise chemotherapy of the lung cancer or auxiliary diagnosis of the lung cancer and curative effect and after-healingmonitoring, can provide the most effective drug selection for lung cancer patients with drug resistance or toxic and side effect intolerance caused by conventional drugs and targeted and chemotherapydrug requirements, improve the drug treatment effect, and reduce the toxic and side effects of the drugs.

A method of providing a diagnosis for a subject having Cowden-like syndrome or PTEN germline mutations is described. The method includes the steps of: (a) obtaining a biological sample from a subject; (b) conducting a germline PTEN mutation and deletion analysis of genomic DNA from the biological sample; (c) determining the level of copy number variation in the genomic DNA; (d) comparing the level of copy number variation in the genomic DNA to a control value for copy number variation; and (e) diagnosing the subject as having an increased risk of developing a neurodevelopmental disorder if the copy number variation level is higher than the control value.

The invention discloses a kit for detecting abnormity of BRCA1 and PTEN genes and detection method. The kit includes a first group of probes and a second group of probes, which aim to the BRCA1 gene, and/or a third group of probes and a fourth group of probes, which aim to the PTEN gene. Each group of probes is labeled with a fluorescent dye, wherein the color of the fluorescent dye on the probes in the same group is same while the color of the fluorescent dye on the probes in different groups are different. The four groups of probes respectively are amplification products by amplifying a primer with corresponding BAC cloning as a template. The FISH probes are produced through repeated comparison and selection and then utilization of optimized BAC cloning as the template and through amplification by designing a primer aiming to a non-repeated and highly-conserved sequence, so that the kit has excellent specificity and lower background noise. The kit can achieve the optimal balance between detection specificity and hybridization time length, so that not only are specificity and sensitivity of a result ensured, but also hybridization time is reduced, thereby increasing detection efficiency.

As described below, the present invention features compositions and methods of treating cancers characterized by the loss of Pten, Zbtb7a/Pokemon, p53, Pml and other tumor suppressors by inhibiting the expression or activity of CXCL17; and methods for identifying CXCL17 antagonists using a murine platform.