The fatty acid binding protein (FABP) family of proteins plays a role in multiple myeloma cell survival and disease progression in vitro and in silico, and thus blocking the FABPs could have anti-cancer effects and prove beneficial for myeloma patients.

Among multiple myeloma stratified by Revised International Staging System, single-cell transcriptome atlas reveals novel heterogeneities with NKG7+ cytotoxic plasma cells (PCs) enriched in stage II, RRM2+ high proliferative PCs enriched in stage III, and MKI67 up-regulated in EBV-positive patients.

CBP/EP300 bromodomain inhibitors have a therapeutic application in oncology via targeting the IRF4 transcriptional program, a clinically validated network critical for multiple myeloma cell viability.

Histone acetyl-transferase Kat2a preserves leukemia stem cells through frequent transcriptional firing of metabolic and regulatory gene promoters and maintenance of a largely invariant self-renewal program.

Integrated analyses of acute myeloid leukemia genetics and epigenetics demonstrate that epigenetic evolution occurs in a convergent manner in the absence of DNA mutations at relapse post-chemotherapy.

Reduced expression of MYBL2 contributes to malignancies of the blood by permitting uncontrolled expansion of blood cell progenitors, implying a tumor suppressor function for this gene.

In the pancreas, reciprocal interactions between epithelial cells and myeloid cells determine the balance between tissue repair and carcinogenesis by regulating acinar cell plasticity through differential activation of EGFR/MAPK signaling.

The nodes of the cytosolic proteostasis network can control sensitivity to proteasome inhibitors and decreased levels of the 19S proteasomal regulator can lead to increased resistance to inhibitors.

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.

The ubiquitin ligase c-Cbl preferentially targets unique-region phosphorylated LynA for rapid degradation, regulating its expression and differentially tuning signaling responsiveness in macrophages and mast cells.