Abstract: The present invention relates to a method of identifying epigenetic reprogramming. Identifying epigenetic reprogramming comprises detecting large organized heterochromatin lysine (K)-9 modified domains (LOCKs) and large DNA hypomethylated blocks in a sample containing DNA from a subject having cancer, for example, PDAC.

Abstract: The present invention relates to a method of identifying epigenetic reprogramming. Identifying epigenetic reprogramming comprises detecting large organized heterochromatin lysine (K)-9 modified domains (LOCKs) and large DNA hypomethylated blocks in a sample containing DNA from a subject having cancer, for example, PDAC.

Abstract: Provided herein are tissue-specific differential methylated regions (T-DMRs) and cancer-related differential methylated regions (C-DMRs) and methods of use thereof. In one embodiment of the invention, there are provided methods of detecting a cell proliferative disorder by detecting altered methylation in one or more DMRs identified herein. In another embodiment of the invention, there are provided methods of determining clinical outcome by detecting altered methylation in one or more DMRs identified herein.

Abstract: The present disclosure provides computational methods for epigenetic analysis as well as systems for implementing such analyses.

Abstract: Provided herein are tissue-specific differential methylated regions (T-DMRs) and cancer-related differential methylated regions (C-DMRs) and methods of use thereof. In one embodiment of the invention, there are provided methods of detecting a cell proliferative disorder by detecting altered methylation in one or more DMRs identified herein. In another embodiment of the invention, there are provided methods of determining clinical outcome by detecting altered methylation in one or more DMRs identified herein.

Abstract: Provided herein is a method of detecting cancer through generalized loss of stability of epigenetic domains as well as compositions useful therein. The present invention is based on the discovery that generalized loss of stability of epigenetic domains was determined to be a characteristic across various cancer types. Genome-scale bisulfite sequencing of cancers revealed a surprising loss of methylation stability in the cancer methylome, involving both CpG islands and shores, as well as large (up to several megabases) blocks of hypomethylation affecting more than half of the genome, with concomitant stochastic variability in gene expression.

Abstract: Provided herein are tissue-specific differential methylated regions (T-DMRs) and cancer-related differential methylated regions (C-DMRs) and methods of use thereof. In one embodiment of the invention, there are provided methods of detecting a cell proliferative disorder by detecting altered methylation in one or more DMRs identified herein. In another embodiment of the invention, there are provided methods of determining clinical outcome by detecting altered methylation in one or more DMRs identified herein.

Abstract: The present invention is directed to a method for determining risk of autism spectrum disorder (ASD) in an offspring subject. The method includes analyzing DNA methylation status in a sample containing sperm from the prospective paternal parent, wherein a methylation pattern that is different from the pattern found in a sample not associated with ASD, is indicative of a risk of ASD in the offspring.

Abstract: Provided herein is a method of detecting cancer through generalized loss of stability of epigenetic domains as well as compositions useful therein. The present invention is based on the discovery that generalized loss of stability of epigenetic domains was determined to be a characteristic across various cancer types. Genome-scale bisulfite sequencing of cancers revealed a surprising loss of methylation stability in the cancer methylome, involving both CpG islands and shores, as well as large (up to several megabases) blocks of hypomethylation affecting more than half of the genome, with concomitant stochastic variability in gene expression.

Abstract: The present invention relates to a method of identifying targets for epigenetic reprogramming comprising detecting large organized heterochromatin lysine (K)-9 modified domains (LOCKs) and large DNA hypomethylated blocks in a sample containing DNA from a subject having cancer, for example, PDAC. The invention also provides for the use of differentially expressed genes to identify metastatic propensity in primary tumors, wherein the genes are selected from genes in the Tables herein, oxidative stress genes, EMT genes, immunological response genes, DNA repair genes, glucose metabolism genes, oxPPP genes, and PGD genes. Further, the invention provides a method for identifying agents or compounds to affect epigenomic changes, including inhibition of oxPPP comprising analyzing a sample from a subject before and after contacting with the agent or compound and determining the effect of the agent or compound on the epigenomic changes.

Abstract: Disclosed herein is a method for determining risk of autism spectrum disorder (ASD) in an offspring subject. The method includes analyzing DNA methylation status in a sample containing sperm from the prospective paternal parent, wherein a methylation pattern that is different from the pattern found in a sample not associated with ASD, is indicative of a risk of ASD in the offspring.

Abstract: The present invention provides a method for identifying a subject having or at risk of having a metabolic disease, such as diabetes or obesity. The invention is based on an approach to identify candidate genes involved in metabolic diseases, such as obesity and type 2 diabetes (T2D) through epigenetic mechanisms. The method includes identifying in the subject genetic markers correlating differentially methylated regions (DMRs) in the genome with genetic risk loci for the subject and comparing methylation patterns of the markers with a control sample from a subject not having the disease. In another embodiment, the invention also provides a method of treating a subject having or at risk of having a metabolic disease. In another embodiment, the invention provides a method of providing a prognostic evaluation of a subject having or at risk of having a metabolic disease.

Abstract: The invention relates to methods and compositions for identifying subjects having, or predisposed to having, a neoplastic or cell proliferation or neoplastic disorder. The methods are applicable to any type of tissue sample and can be conducted on otherwise normal tissue.

Abstract: The invention relates to methods and compositions for identifying subjects having, or predisposed to having, a neoplastic or cell proliferation or neoplastic disorder. The methods are applicable to any type of tissue sample and can be conducted on otherwise normal tissue.

Abstract: Provided herein is a method of detecting cancer through generalized loss of stability of epigenetic domains as well as compositions useful therein. The present invention is based on the discovery that generalized loss of stability of epigenetic domains was determined to be a characteristic across various cancer types. Genome-scale bisulfite sequencing of cancers revealed a surprising loss of methylation stability in the cancer methylome, involving both CpG islands and shores, as well as large (up to several megabases) blocks of hypomethylation affecting more than half of the genome, with concomitant stochastic variability in gene expression.

Abstract: Provided are methods and models for an alternative source of disease risk, which identifies not genetic variants for a phenotype per se, but variants for variability itself. Also provided are methods and models for a genome-scale, gene-specific analysis of DNA methylation in the same individuals over time, in order to identify a personalized epigenomic signature that may correlate with common genetic disease. Also provided are methods and models for simulating stochastic epigenetic variation as a driving force of development, evolutionary adaptation, and disease.

Abstract: Provided herein are differentially methylated regions (DMRs) of multipotent progenitor cells (MPPs) and oligopotent progenitor cells and methods of use thereof. The invention provides methods for detecting and analyzing alterations in the methylation status of DMRs in such progenitor cells as well as methods for differentiating such cells.

Abstract: Provided herein are differentially methylated regions (DMRs) of reprogrammed iPS cells (R-DMRs) and methods of use thereof. The invention provides methods for detecting and analyzing alterations in the methylation status of DMRs in iPS cells, somatic cells and embryonic stem (ES) cells as well as methods for reprogramming somatic cells to generate an iPS cell.

Abstract: Provided is a method for isolating methylated CpG islands. The method includes identifying an imprinted gene adjacent to the methylated CpG island, and identifying a disease which is preferentially transmitted by one parent and which is genetically linked to region of genomic DNA which contains the imprinted gene, whereby the imprinted gene is thereby indicated as a candidate gene involved in transmitting the disease.

Abstract: The present invention provides methods and kits for identifying an increased risk of developing cancer in a subject. The methods include analyzing a first biological sample, such as a blood sample, from the subject for loss of imprinting of the IGF2 gene. According to the methods a loss of imprinting is indicative of an increased risk of developing cancer. The method can include analyzing genomic DNA from the sample for altered methylation of the IGF2 or the H19 gene. The altered methylation for example includes hypomethylation of a differentially methylated region of IGF2, corresponding to SEQ ID NO:1 and/or a polymorphism or fragment thereof, or hypomethylation of a differentially methylated region of H19 corresponding to SEQ ID NO:6, or a polymorphism, or fragment thereof. In certain aspects, hypomethylation of the H19 DMR or the IGF2 DMR indicates an increased risk of developing colorectal cancer.