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Brian Krug

New work in Nature Genetics on how H3K27me3 spreading organises chromatin architecture

Lead author, with the Lu lab at Columbia.

H3K27me3 spreading organizes canonical PRC1 chromatin architecture to regulate developmental programs

Nature Genetics

Awarded a ChadTough Defeat DIPG Foundation postdoctoral fellowship

Supporting work on diffuse midline glioma through 2027.

Presented recent work at the EpiCypher chromatin meeting

Poster presentation.

Aberrant EZHIP expression drives tumorigenesis in osteosarcoma

Nature Communications

Immune landscape of oncohistone-mutant gliomas reveals diverse myeloid populations and tumor-promoting function

Nature Communications

Pediatric glioma histone H3.3 K27M/G34R mutations drive abnormalities in PML nuclear bodies

Genome Biology

K27M in canonical and noncanonical H3 variants occurs in distinct oligodendroglial cell lineages in brain midline gliomas

Nature Genetics

Loss of MAT2A compromises methionine metabolism and represents a vulnerability in H3K27M mutant glioma by modulating the epigenome

Nature Cancer

Histone H3.3 K27M and K36M mutations de-repress transposable elements through perturbation of antagonistic chromatin marks

Molecular Cell

Polycomb repressive complex 2 in the driver's seat of childhood and young adult brain tumours

Trends in Cell Biology

Oncohistones: a roadmap to stalled development

The FEBS Journal

H3K27M in Gliomas Causes a One-Step Decrease in H3K27 Methylation and Reduced Spreading within the Constraints of H3K36 Methylation

Cell Reports

Stalled developmental programs at the root of pediatric brain tumors

Nature Genetics

Pervasive H3K27 Acetylation Leads to ERV Expression and a Therapeutic Vulnerability in H3K27M Gliomas

Cancer Cell

H3K27M induces defective chromatin spread of PRC2-mediated repressive H3K27me2/me3 and is essential for glioma tumorigenesis

Nature Communications