34 results about "Dna breaks" patented technology

The present invention relates to the treatment of cancer with compounds that inhibit the activity of endo-exonuclease. Endo-exonuclease has been shown to be necessary for the repair of damaged DNA. Compounds that inhibit the activity of endo-exonuclease have been shown to be particularly effective for treating cancer when used in combination with drugs that induce DNA breaks such as cisplatin and mitomycin C. These compounds have a synergistic effect when used in combination for inhibiting tumour growth. The invention includes pharmaceutical compositions for inhibiting tumour growth comprising a compound that inhibits endo-exonuclease activity. These pharmaceutical compositions preferably include compounds that induce DNA breaks. The invention includes methods of treating cancer with these pharmaceutical compositions and uses of these compositions to treat cancer. The preferred compounds that inhibit the activity of endo-exonuclease have low toxicity. One such compound is pentamidine. The invention also includes a method for diagnosing cancer and monitoring its progression. This aspect of the invention involves isolating serum from a patient; measuring the concentration of endo-exonuclease in said serum and determining whether said concentration is above a predetermined mean.

Methods and means are provided to modify in a targeted manner the genome of a plant in close proximity to an existing elite event using a double stranded DNA break inducing enzyme. Also provided are plants, in particular cotton plants showing tolerance to a field dose of at least 1× of at least one HPPD inhibitor, and methods for making such plants.

The present invention relates to the treatment of cancer with compounds that inhibit the activity of endo-exonuclease. Endo-exonuclease has been shown to be necessary for the repair of damaged DNA. Compounds that inhibit the activity of endo-exonuclease have been shown to be particularly effective for treating cancer when used in combination with drugs that induce DNA breaks such as cisplatin and mitomycin C. These compounds have a synergistic effect when used in combination for inhibiting tumour growth. The invention includes pharmaceutical compositions for inhibiting tumour growth comprising a compound that inhibits endo-exonuclease activity. These pharmaceutical compositions preferably include compounds that induce DNA breaks. The invention includes methods of treating cancer with these pharmaceutical compositions and uses of these compositions to treat cancer. The preferred compounds that inhibit the activity of endo-exonuclease have low toxicity. One such compound is pentamidine. The invention also includes a method for diagnosing cancer and monitoring its progression. This aspect of the invention involves isolating serum from a patient; measuring the concentration of endo-exonuclease in said serum and determining whether said concentration is above a predetermined mean.

The invention relates to a method for rapid detection of in vitro DNA break damage strength by plasma, and the method is used for determining the damage strength of plasma mutagenesis methods including atmospheric and room temperature plasma (ARTP) on DNA. The method includes the steps of: 1) treating DNA coated microspheres by plasma mutagenesis method, and setting a control group without plasma treatment; 2) performing washing, and then dyeing the DNA coated microspheres with a dye; 3) determining the fluorescence value of the dyed DNA coated microspheres by a fluorescence detector; and 4) calculating the DNA relative content of the control group and the plasma mutagenesis treated microspheres according to the fluorescence value, and judging the gene damage strength of plasma. The invention utilizes DNA coated microspheres to establish a rapid detection method for in vitro DNA damage strength so as to realize direct and effective evaluation of plasma caused damage strength to DNA.

Methods are disclosed for correcting a mutant allele of a gene of interest in a primate cell. The methods include a) introducing a non-naturally occurring targeted nuclease and site-specific nucleotide-binding guide that act together to introduce double-stranded breaks in the mutant allele into the primate cell, wherein: i) the primate cell is undergoing mitotic cell division; ii) the primate cell comprises a genome that is heterozygous for the mutant allele, such that the genome comprises one copy of the mutant allele and one copy of a wild-type allele; iii) single-stranded oligonucleotides homologous to the wild-type allele are not introduced into the primate cell. The methods also include b) allowing the primate cell to activate homology-directed repair of the double-stranded DNA breaks in the mutant allele, thereby correcting the mutant allele using the normal wild-type allele as a repair template and producing a primate cell that is homozygous for the wild-type allele. The primate cell can be a one-cell embryo and/or a human cell.

The present invention provides compositions and methods for inducing DNA breaks in specifically-targeted cells, in particular cancer and HIV-infected cells, thereby promoting cell death.

The present invention provides a cancer vaccine comprising DNA repair-deficient cancer cells, wherein the cancer cells are contacted with a PARP inhibitor to induce DNA breaks. In another aspect, a method of treating a subject afflicted with a cancer comprising administering to the subject a therapeutically effective amount of a cancer vaccine comprising DNA repair-deficient cancer cells, wherein the cancer cells are contacted with a PARP inhibitor to induce DNA breaks, is provided. The present invention also provides a kit comprising DNA repair-deficient cancer cells modified as described herein, PARP inhibitors, immune checkpoint inhibitors, and combinations thereof, packaged in a suitable container.

A process for evaluating the sensitivity of a tissue taken from an individual to the DNA-breaking toxic effect of at least one chemical or biochemical agent, or of a combination of chemical and/or biochemical agents, comprising the following steps: (a) a working concentration is set for said at least one chemical or biochemical agent, or for chemical and/or biochemical agents included in said combination of chemical and/or biochemical agents; (b) cells are taken from a tissue to be evaluated of an individual; (c) said cells are dispersed and/or amplified so as to obtain a cell sample; (d) saidcell sample is brought into contact with said at least one chemical or biochemical agent (or said combination of chemical and/or biochemical agents) in the working concentration thereof defined in step (a), for a predetermined period of time; (e) the number of double-stand breaks of the DNA, and/or a biomarker representing this number, and/or the number of micronuclei is detected, in the knowledge that steps (b), (c), (d) and (e) must be carried out one after the other, and that step (a) must be carried out before step (e).

Methods are provided to mutate, in a targeted manner, the genome of a plant cell using a double stranded DNA break inducing enzyme. Also provided are plants, in particular Brassica plants that yield seeds producing oils having a reduced total saturated fatty acid content, and method for making such plants.

The present invention relates to the technical fields of genetic engineering and bioinformatics, in particular, to a method for creating a new gene in an organism in the absence of an artificial DNA template, and a use thereof. The method comprises simultaneously generating DNA breaks at two or more different specific sites in the organism's genome, wherein the specific sites are genomic sites capable of separating different genetic elements or different protein domains, and the DNA breaks are ligated to each other through non-homologous end joining (NHEJ) or homologous repair to generate a new combination of the different gene elements or different protein domains that is different from the original genome sequence, thereby creating a new gene. The new gene of the invention can change the growth, development, resistance, yield and other traits of the organism, and has great value in application.

The present disclosure provides the quantification of double-strand breaks in DNA molecules using terminal deoxynucleotidyl transferase using a preliminary step of nick gap and repair. This preliminary step comprising contacting the DNA molecules with both a DNA ligase and a DNA polymerase to repair DNA nicks and remove DNA gaps prior to using the terminal deoxynucleotidyl transferase.

The invention discloses a DNA breaking instrument. According to the DNA breaking instrument, a water tank with a shell layer is mounted on a machine box of the DNA breaking instrument, a temperature control system capable of accurately controlling the temperature is connected to the shell layer of the water tank, L-shaped sample seat assemblies for placing sample tanks are mounted on the front side and the rear side of the water tank, the sample seat assemblies are foldable, when the sample seat assemblies are unfolded, sample tubes in the mounted sample tanks can be suspended in the water tank, microelectrode arrays are installed on the left side and the right side of the machine box through assemblies, and the two microelectrode arrays are connected with a power source and a controller of a liquid phase plasma device; and when the breaking instrument is used, the sample seat assemblies are unfolded, the sample tubes are placed on the sample tanks, water is filled in the water tank, and a centrifugal tube is in contact with the water, so that non-contact liquid-phase plasma of a sample in the sample tube can be broken. The breaking instrument is simple in structure and wide in application, is mainly used for breaking DNA required by sequencing, and can also be used for preparing DNA and DNA terminal protein compounds and the like.

The invention relates to a fusion protein, a method for homologous recombination using it and its application in homologous recombination of exogenous DNA molecules into target sequences. The fusion protein of the present invention includes CRISPR protein, TALEN or ZFN protein, biotin-binding protein and linker; it realizes exogenous Efficient and precise insertion of DNA sequences; compared with the traditional CRISPR gene editing technology, the fusion protein of the present invention and the homologous recombination method using it greatly improve the homologous recombination efficiency.

A process for evaluating the response of a tumour to a DNA-breaking treatment using a sample of cells from said tumour, in which: (a) a cell sample is prepared from the cells taken from said tumour; (b) said cell sample is subjected to a DNA-breaking treatment characterized by a dose D, (c) the average number of nuclear foci obtained with a marker pH2AX at the observation times t (these average numbers being respectively called NpH2Ax(t)) is determined on said cell sample, said observation times t being the time t=0 min (called tO, state before administration of the dose D) and at least one observation time selected from t = t1, t2, t3 and t4 after administration of the dose D; (d) at least one parameter or score which makes it possible to characterize the response of the sample to said DNA-breaking treatment is determined using at least the average numbers NpH2Ax(t), and in which process t4 is a fixed value which represents the time for which the level of DNA breaks reaches its residual value, t3 is a fixed value which represents the time after which approximately 25% of the double-strand breaks (DSBs) are repaired in control cells from radioresistant patients, t2 is a fixed valuewhich represents the time after which approximately 50% of the DSBs are repaired in control cells from radioresistant patients, t1 is a fixed value which represents the time after which the number ofrecognized DSBs reaches its maximum in control cells from radioresistant patients.

Methods are provided to mutate, in a targeted manner, the genome of a plant cell using a double stranded DNA break inducing enzyme. Also provided are plants, in particular Brassica plants that yield seeds producing oils having a reduced total saturated fatty acid content, and method for making such plants.