Disease-specific epigenetic deregulation of enhancers, transposons, and polycomb targets in acute promyelocytic leukemia.

ABSTRACT:

Background

Acute promyelocytic leukemia (APL) is a subtype of acute myeloid leukemia (AML), characterized by a fusion between the PML and RARA genes and by a block in the myeloid maturation at the promyelocytic stage.

Methods

This study investigates the epigenetic landscape of APL by integrating ChIP-seq data on eight histone modifications and RNA-seq in APL as well as non-APL AML. APL showed a distinct chromatin profile that differed from non-APL AML.

Results

We describe APL-specific changes in H3K27ac, H3K9me3, and H3K27me3 with impact on enhancer activity, repression of transposable elements, and Polycomb regulated gene repression. The APL-specific H3K27ac pattern identifies APL-specific enhancer and super-enhancer regions, including a subset of enhancers that are

SUBMITTER: Zhong X 

PROVIDER: S-EPMC12573822 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature