Remodeling of the DNA methylation landscape of CD34+ cells from fetal liver / cord blood upon upon CRISPR mediated t(4:11) rearrangements.

ABSTRACT: The prognosis of infant B-cell acute lymphoblastic leukemia (iB-ALL) remains dismal, especially in patients harboring the MLL-AF4 (KTM2A-AFF1) rearrangement, which arises prenatally in early hematopoietic stem/progenitor cells (HSPCs). MLL-AF4+ B-ALL shows a bimodal localization of the MLL gene breakpoint within the MLL break cluster region, and two subgroups of patients based on the gene expression pattern of the HOXA/MEIS cluster have been identified. The pathogenic mechanisms in MLL-AF4+ B-ALL are challenging to study functionally due to the absence of faithful human cellular models recapitulating the disease phenotype and latency. Here, we assess the molecular contribution and leukemogenic capacity of MLL breakpoints occurring in either intron 10 (MLLi10, centromeric) or intron 12 (MLL

ORGANISM(S): Homo sapiens

SUBMITTER: Mario Fraga F. 

PROVIDER: E-MTAB-12806 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress