Adipocytes disrupt the translational programme of acute lymphoblastic leukaemia to favour tumour survival and persistence

Abstract The specific niche adaptations that facilitate primary disease and Acute Lymphoblastic Leukaemia (ALL) survival after induction chemotherapy remain unclear. Here, we show Bone Marrow (BM) adipocytes dynamically evolve during ALL pathogenesis therapy, transitioning from cellular depletion in the leukaemia to a fully reconstituted state upon remission induction. Functionally, adipocyte niches elicit fate switch cells towards slow-proliferation quiescence, highlighting critical contribution of dynamic establishment resistance. Mechanistically, interaction targets posttranscriptional networks suppresses protein biosynthesis cells. Treatment with general control nonderepressible 2 inhibitor (GCN2ib) alleviates adipocyte-mediated translational repression rescues cell quiescence thereby significantly reducing cytoprotective effect against other extrinsic stressors. These data establish how driven restrictions proteome benefit tumours, preventing their elimination, suggest ways manipulate