Shunsuke Kimura

TL;DR: In this paper, the authors describe a distinct subgroup of acute leukemia with expression of myeloid, T lymphoid, and stem cell markers driven by aberrant allele-specific deregulation of BCL11B, a master transcription factor responsible for thymic T-lineage commitment and specification.

TL;DR: An overview of the recent advances in the knowledge of genomic bases of BCP-all, T-ALL, and relapsed ALL is provided, and their clinical implications are discussed.

TL;DR: This work identifies a highly conserved distal enhancer (PE) that interacts with the PTEN promoter in multiple hematopoietic populations, including T-cells, and acts as a hub of relevant transcription factors in T-ALL.

TL;DR: A large pan-acute leukemia analysis of 2,573 samples revealed a new subtype of 60 samples with a distinct gene expression profile and immunophenotype that exhibited monoallelic expression of BCL11B which encodes a T-lineage transcription factor that is repressed in hematopoietic stem and progenitor cells (HSPCs), a putative cell of origin for ALAL.

TL;DR: A recent review of the genetic taxonomy of ALL with a focus on clinical implications and the implementation of genomic diagnostic approaches is presented in this article, where the authors identify risk-associated ALL subtypes (e.g., those with rearrangements of MEF2D, DUX4, NUTM1, ZNF384 and BCL11B) and genomic phenocopies such as Ph-like ALL.