Abstract: The present invention provides for a method or methods of targeted genetic recombination or mutagenesis in a host cell or organism, and compositions useful for carrying out the method. The targeting method of the present invention exploits endogenous cellular mechanisms for homologous recombination and repair of double stranded breaks in genetic material. The present invention provides numerous improvements over previous mutagenesis methods, such advantages include that the method is generally applicable to a wide variety of organisms, the method is targeted so that the disadvantages associated with random insertion of DNA into host genetic material are eliminated, and certain embodiments require relatively little manipulation of the host genetic material for success. Additionally, it provides a method that produces organisms with specific gene modifications in a short period of time.

Abstract: The present invention provides for a method or methods of targeted genetic recombination or mutagenesis in a host cell or organism, and compositions useful for carrying out the method. The targeting method of the present invention exploits endogenous cellular mechanisms for homologous recombination and repair of double stranded breaks in genetic material. The present invention provides numerous improvements over previous mutagenesis methods, such advantages include that the method is generally applicable to a wide variety of organisms, the method is targeted so that the disadvantages associated with random insertion of DNA into host genetic material are eliminated, and certain embodiments require relatively little manipulation of the host genetic material for success. Additionally, it provides a method that produces organisms with specific gene modifications in a short period of time.

Abstract: The present invention provides for a method or methods of targeted genetic recombination or mutagenesis in a host cell or organism, and compositions useful for carrying out the method. The targeting method of the present invention exploits endogenous cellular mechanisms for homologous recombination and repair of double stranded breaks in genetic material. The present invention provides numerous improvements over previous mutagenesis methods, such advantages include that the method is generally applicable to a wide variety of organisms, the method is targeted so that the disadvantages associated with random insertion of DNA into host genetic material are eliminated, and certain embodiments require relatively little manipulation of the host genetic material for success. Additionally, it provides a method that produces organisms with specific gene modifications in a short period of time.

Abstract: The present disclosure provides a method for cancer relapse prediction that provides higher resolution grading than Gleason score alone. In particular, the method provides for prediction of prostate cancer relapse that correlates gene expression of each individual signature gene and deriving a prostate cancer gene expression (GEX) score in the plurality of prostate cancer tissue samples; and correlating said GEX score with the clinical outcome for each prostate carcinoma tissue sample. A set of signature genes is provided that encompasses all or a sub-combination of GI_2094528, KIP2, NRG1, NBL1, Prostein, CCNE2, CDC6, FBP1, HOXC6, MKI67, MYBL2, PTTG1, RAMP, UBE2C, Wnt5A, MEMD, AZGP1, CCK, MLCK, PPAP2B, and PROK1.

Abstract: The present invention provides for a method or methods of targeted genetic recombination or mutagenesis in a host cell or organism, and compositions useful for carrying out the method. The targeting method of the present invention exploits endogenous cellular mechanisms for homologous recombination and repair of double stranded breaks in genetic material. The present invention provides numerous improvements over previous mutagenesis methods, such advantages include that the method is generally applicable to a wide variety of organisms, the method is targeted so that the disadvantages associated with random insertion of DNA into host genetic material are eliminated, and certain embodiments require relatively little manipulation of the host genetic material for success. Additionally, it provides a method that produces organisms with specific gene modifications in a short period of time.

Abstract: The present disclosure provides a method for cancer relapse prediction that provides higher resolution grading than Gleason score alone. In particular, the method provides for prediction of prostate cancer relapse that correlates gene expression of each individual signature gene and deriving a prostate cancer gene expression (GEX) score in the plurality of prostate cancer tissue samples; and correlating said GEX score with the clinical outcome for each prostate carcinoma tissue sample. A set of signature genes is provided that encompasses all or a sub-combination of GI_2094528, KIP2, NRG1, NBL1, Prostein, CCNE2, CDC6, FBP1, HOXC6, MKI67, MYBL2, PTTG1, RAMP, UBE2C, Wnt5A, MEMD, AZGP1, CCK, MLCK, PPAP2B, and PROK1.

Abstract: The present invention provides a method for identification of differentially methylated genomic CpG dinucleotide sequences within genomic target sequences that are associated with cancer in an individual by obtaining a biological sample comprising genomic DNA from the individual measuring the level or pattern of methylated genomic CpG dinucleotide sequences for two or more of the genomic targets in the sample, and comparing the level of methylated genomic CpG dinucleotide sequences in the sample to a reference level of methylated genomic CpG dinucleotide sequences, wherein a difference in the level or pattern of methylation of the genomic CpG dinucleotide sequences in the sample compared to the reference level identifies differentially methylated genomic CpG dinucleotide sequences associated with cancer. As disclosed herein, the methods of the invention have numerous diagnostic and prognostic applications.

Abstract: The present invention provides a method for identification of differentially methylated genomic CpG dinucleotide sequences within genomic target sequences that are associated with cancer in an individual by comparing the level of methylated genomic CpG dinucleotide sequences in the sample to a reference level of methylated genomic CpG dinucleotide sequences.

Abstract: The present invention provides a method for preparing a reference model for cancer relapse prediction that provides higher resolution grading than Gleason score alone.

Abstract: The present invention provides a method for preparing a reference model for cancer relapse prediction that provides higher resolution grading than Gleason score alone.

Abstract: The present invention is directed to compositions and methods for multiplex analyses of nucleic acids from archival tissues.

Abstract: The present invention provides a method for preparing a reference model for cancer relapse prediction that provides higher resolution grading than Gleason score alone.

Abstract: The present embodiments relate to a system and method of measuring the methylation level of DNA. Some embodiments relate to a system and method of measuring methylation level of DNA with a gene array.

Abstract: The present invention provides a method for identification of differentially methylated genomic CpG dinucleotide sequences within genomic target sequences that are associated with cancer in an individual by obtaining a biological sample comprising genomic DNA from the individual measuring the level or pattern of methylated genomic CpG dinucleotide sequences for two or more of the genomic targets in the sample, and comparing the level of methylated genomic CpG dinucleotide sequences in the sample to a reference level of methylated genomic CpG dinucleotide sequences, wherein a difference in the level or pattern of methylation of the genomic CpG dinucleotide sequences in the sample compared to the reference level identifies differentially methylated genomic CpG dinucleotide sequences associated with cancer. As disclosed herein, the methods of the invention have numerous diagnostic and prognostic applications.

Abstract: The present invention provides a method for identification of differentially methylated genomic CpG dinucleotide sequences within genomic target sequences that are associated with cancer in an individual by obtaining a biological sample comprising genomic DNA from the individual measuring the level or pattern of methylated genomic CpG dinucleotide sequences for two or more of the genomic targets in the sample, and comparing the level of methylated genomic CpG dinucleotide sequences in the sample to a reference level of methylated genomic CpG dinucleotide sequences, wherein a difference in the level or pattern of methylation of the genomic CpG dinucleotide sequences in the sample compared to the reference level identifies differentially methylated genomic CpG dinucleotide sequences associated with cancer. As disclosed herein, the methods of the invention have numerous diagnostic and prognostic applications.

Abstract: The present invention provides a method for identification of differentially methylated genomic CpG dinucleotide sequences associated with cancer in an individual by obtaining a biological sample comprising genomic DNA from the individual measuring the level or pattern of methylated genomic CpG dinucleotide sequences for two or more of the genomic targets in the sample, and comparing the level of methylated genomic CpG dinucleotide sequences in the sample to a reference level of methylated genomic CpG dinucleotide sequences, wherein a difference in the level or pattern of methylation of the genomic CpG dinucleotide sequences in the sample compared to the reference level identifies differentially methylated genomic CpG dinucleotide sequences associated with cancer. As disclosed herein, the methods of the invention have numerous diagnostic and prognostic applications.

Abstract: The present invention is directed to compositions and methods for multiplex analyses of nucleic acids from archival tissues.