Disclosed are methods for treating Set1/COMPASS-associated cancers characterized by expression of Set1B/COMPASS. The methods typically include administering a therapeutic amount of an inhibitor of the Set1B/COMPASS pathway and/or an agonist for a target that is negatively regulated by the Set1B/COMPASS pathway.

Inhibitory RNA molecules that specifically inhibit mammalian RIZ2 expression, with therapeutic effect in cell proliferative diseases, such as cancer.

The invention provides compositions and methods for generating improved T cells having increased Ezh2 activity and methods of use thereof in the treatment of cancer and chronic infection.

The present invention relates to methods of suppressing the transcriptional expression of one or more genes by methylating the chromatin histone proteins of the one or more genes. Specifically, a viral SET domain histone lysine mehtyltransferase (vSET or vSET-like protein) methylates lysine 27 of a gene's histone protein 3 (H3-K27) thereby suppressing the transcription of the gene.

The object of the present invention is to provide a detecting agent for specifically detecting a tumor cell, a tumor antigen peptide-specifically presented on a tumor cell, a pharmaceutical composition useful for the prevention and/or treatment of cancer, the pharmaceutical composition containing the tumor antigen peptide as an active ingredient, etc. The above object has been achieved by a tumor antigen peptide or its motif-substituted product, the tumor antigen peptide comprising 8 to 14 consecutive amino acids in an amino acid sequence of a protein encoded by a gene selected from the group consisting of PVT1, SUV39H2, ZNF724P, SNRNP40, and DYRK4, the tumor antigen peptide having an HLA binding ability.

Provided herein are H1.0K180me2 antibodies, H1.0K180me2 proteins, and H1.0K180me2 peptides and methods of use for diagnostics and therapeutics. These H1.0K180me2 antibodies, H1.0K180me2 proteins, and H1.0K180me2 peptides may be used in the treatment of methylated H1.0-related diseases or conditions in an individual. These H1.0K180me2 antibodies, H1.0K180me2 proteins, and H1.0K180me2 peptides may also be used for the detection and quantification of a histone H1.0 protein or fragment thereof, comprising a dimethylated lysine at lysine residue 180 (H1.0K180me2); such compositions and methods are useful for detecting replicative senescence, DNA damage, genotoxic stress, radiation exposure, Alzheimer's disease, are useful for monitoring therapeutic regimens, patient stratification, drug screening, and may serve as a marker of biological aging in a system.

A product comprising two or more artificial transcription repressors (ATRs), or polynucleotides encoding therefor, selected from groups (a), (b), (c) or (d): (a) an ATR comprising a DNA-binding domain operably linked to a KRAB domain or homologue thereof; (b) an ATR comprising a DNA-binding domain operably linked to a DNMT3A, DNMT3B or DNMT1 domain or homologue thereof; (c) an ATR comprising a DNA-binding domain operably linked to a DNMT3L domain or homologue thereof; and (d) an ATR comprising a DNA-binding domain operably linked to a SETDB1 domain or homologue thereof, wherein at least two of the ATRs are selected from different groups (a), (b), (c) or (d).

Methods and systems for obtaining inhibitors of Nuclear receptor SET Domain containing protein 2 (NSD2) are disclosed where the methods involve designing compounds that resemble the NSD2 transition state.

The present disclosure provides compositions with a modulating gene expression and methods for modulating transcription.

The present invention provides methods and compostions to improve the efficiency of somatic cell nuclear transfer (SCNT) and the consequent production of nuclear transfer ESC (ntESC) and transgenic cells and/or non-human animals. More specifically, the present invention relates to the discovery that trimethylation of Histone H3-Lysine 9 (H3K9me3) in reprogramming resistant regions (RRRs) in the nuclear genetic material of donor somatic cells prevents efficient somatic cell nuclear reprogramming or SCNT. The present invention provide methods and compositions to decrease H3K9me3 in methods to improve efficacy of SCNT by exogenous or overexpression of the demethylase Kdm4 family and/or inhibiting methylation of H3K9me3 by inhibiting the histone methyltransferases Suv39h1 and/or Suv39h2.