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Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture
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Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture
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Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture
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Paper
Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture
2019
Overview
Human B-lineage precursor acute lymphoid leukemias (BCP-ALLs) comprise a group of genetically and clinically distinct disease entities with features of differentiation arrest at known stages of normal B-lineage differentiation. We previously showed BCP-ALL cells display unique and clonally heritable DNA-replication timing (RT) programs; i.e., programs describing the variable order of replication and sub-nuclear 3D architecture of megabase-scale chromosomal units of DNA in different cell types. To determine the extent to which BCP-ALL RT programs mirror or deviate from specific stages of normal human B-cell differentiation, we transplanted immunodeficient mice with quiescent normal human CD34+ cord blood cells and obtained RT signatures of the regenerating B-lineage populations. We then compared these with RT signatures for leukemic cells from a large cohort of BCP-ALL patients of varied genetic subtype and outcome. The results identify BCP-ALL subtype-specific features that resemble specific stages of B-cell differentiation and features that appear associated with relapse. These results suggest the genesis of BCP-ALL involves alterations in RT that reflect biologically significant and clinically relevant leukemia-specific epigenetic changes that have potential as a novel genre of prognostic biomarkers.
DNA replication timing of >100 pediatric leukemic samples identified BCP-ALL subtype-specific genome alteration signatures.
Comparative analysis identified features that resemble specific stages of B-cell differentiation and features associated with outcome.
Publisher
Cold Spring Harbor Laboratory
Subject
