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Genome sequencing analysis dissects the origins and evolution of cancer transmission between clam species in the Seas of Southern Europe.

Non-core RAG regions, especially RAG1, maintain V(D)J recombination accuracy and genomic stability, reducing malignant characteristics and off-target recombination in BCR-ABL1⁺ B-cell acute lymphoblastic leukemia.

FLT3-ITD/STAT5A signaling is more sensitive to Dot1L inhibition than the canonical MLL-fusion activated drivers of leukemogenesis, providing a potential therapeutic avenue for one of the most frequent lesions in leukemia.

PPM1D-mutant leukemia cells exhibit a dysregulated redox landscape, a diminished response to oxidative stress, and rely on SOD1 for their survival.

Cellular and molecular analyses of human AML cells reveal a novel pathway activated by the bone marrow microenvironment that confers resistance to FLT3 inhibition and can be exploited to improve the efficacy of FLT3 inhibitor therapy for AML.

Inhibition of FGF2-FGFR1 signaling in bone marrow stroma attenuates secretion of FGF2-laden exosomes and subsequent protection of leukemia cells.

Scaffolding protein RAPSYN can exert its NEDD8 E3 ligase activity to neddylate and stabilize oncogenic BCR-ABL by competing proteasomal degradation in Ph⁺ leukemia.

Single-cell analysis of CML patients bone marrow at diagnosis reveals coexistence of CD26^-CD35⁺ healthy stem cells and CD26⁺CD35^- CML stem cells, and how the ratio between these impacts TKI response.

The identification of key determinants of LSC “stemness” and LSC differentiation that is reversible through an epigenetic mechanism may have considerable implications in understanding leukemia and designing effective therapies.

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.