Elisa Ten Hacken

TL;DR: This work finds pervasive DNA damage in hematologic malignancies, including multiple myeloma, lymphoma and leukemia, which leads to activation of a p53-independent, proapoptotic network centered on nuclear relocalization of ABL1 kinase, and identifies a new synthetic-lethal strategy to selectively target cancer cells presenting with endogenous DNA damage and low YAP1 levels.

TL;DR: The cellular and molecular characteristics of CLL cells are reviewed, and the relevant novel treatment strategies, focusing on immunomodulatory agents and BCR signaling inhibitors and how these treatments disrupt CLL-microenvironment interactions are highlighted.

TL;DR: Regulators of lymphoid transcription and cellular energy metabolism are identified as drivers of venetoclax resistance in addition to the known involvement by BCL-2 family members, which were confirmed in patient samples.

TL;DR: Central components of the CLL microenvironment are reviewed, with a particular emphasis on BCR signaling, and the most relevant clinical advances with inhibitors that target the BCR-associated spleen tyrosine kinase/SYK (fostamatinib), Bruton's tyrosINE kinase /BTK (ibrutinib), and PI3Kδ (idelalisib) are summarized.

TL;DR: Findings show that HS1 is a central regulator of cytoskeleton remodeling that controls lymphocyte trafficking and homing and significantly influences the tissue invasion and infiltration in CLL.