leukemia

[Leukemia] Researchers describe the immunological features of the acute myeloid leukemia (AML) niche, with particular attention to the crosstalk between the AML blasts and the cellular components of the altered tumor microenvironment and the mechanisms of immune escape that hamper the therapeutic effects of the most advanced treatments.

[Oncogenesis] The authors identified that guanylate-binding protein (GBP)1 and GBP2 interacted with MCL-1, the key prosurvival member of the BCL-2 family, via its BH3 domain. GBPs induced caspase-dependent apoptosis in chronic myeloid leukemia and acute myeloid leukemia cells, where the proapoptotic BCL-2 member, BAK, was an indispensable mediator.

[Nature Cancer] Investigators provided direct evidence of a specific mechanism by which chemotherapy induced drug-resistance-associated mutations leading to relapse. Using genomic and functional analysis of relapsed acute lymphoblastic leukemia (ALL), they showed that thiopurine treatment in mismatch repair-deficient leukemias induced hotspot TP53 R248Q mutations through a specific mutational signature.

[Journal of Leukocyte Biology] The authors suggest that proteomic profiles at the early stage of chronic lymphocytic leukemia (CLL) can discriminate progressive from stable disease and that RNA splicing dysregulation underlies CLL evolution, which opens new perspectives in terms of biomarkers and therapy.

[Journal of Molecular and Cellular Cardiology] Investigators summarize emerging research on CHIP, the mechanisms underlying its important role in propagating inflammation and accelerating cardiovascular disease, and new studies detailing the role of associated risk factors and co-morbidities that increase CHIP prevalence.

[Blood] Researchers introduced sialic-acid-binding immunoglobulin-like lectin (Siglec)-6 as a novel target for CAR T-cells in acute myeloid leukemia (AML) and found that Siglec-6 was prevalently expressed on AML cell lines and primary AML blasts, including the subpopulation of AML stem cells.