TRIM33 performs an essential function in B cell acute lymphoblastic leukemia through an association with a single cis element.

Convergent transcription and stalling of transcription are enriched at DNA breakpoints found in acute lymphoblastic leukemia and associate with DNA structures and sequences that mediate genetic instability.

A comprehensive analysis of long noncoding RNAs in the hematopoietic system reveals their dynamic regulation and a loss-of-function screen identifies some required for leukemia progression and involved in normal myeloid differentiation.

Editors' Summary: This Replication Study has reproduced important parts of the original paper.

A general framework captures the evolutionary routes leading to the formation and progression of tumors.

Anti-targets are proteins that cause problems when inhibited along with an intended target and our novel chemical strategy affords unprecedented selectivity in the context of FLT3 vs. KIT inhibition for treatment of a devastating blood cancer.

Editors' Summary: This Replication Study has reproduced important parts of the original paper.

The human leukemia virus HTLV-1 causes abnormal chromatin looping in tens of thousands of infected T cell clones in each host, and abnormal host transcription both flanking the integrated provirus and at distant loci in cis.