Blood: Molecular mechanisms of B-ALL hyperxaid cells with filament division and chromosomal defects

B-cell acute lymphoblastic leukemia (B-ALL) is the most common childhood cancer, and hyper-hyperphee (HyperD) is the most common subtype of B-ALL in childrenAlthough HyperD is the initial carcinogenic event of B-ALL in children, there is still a lack of characteristics associated with fission disdivision and chromosomal defects associated with HyperD B-ALL (HyperD-ALL)in this study, Oscar et alused samples from 54 primary children b-ALL to characterize potential cellular-molecular mechanisms for fissoprosy/chromosome defects, which are predicted to be early causal factors in HyperD-ALLfound that HyperD-ALL mother cells had low proliferation, showed early filamental prostake delay, which was associated with chromosomal alignment defects on the mid-stage plate, leading to chromosomal separation defects and non-modal nucleiIn the mechanism, biochemical, functional and mass spectrometry analysis showed that the coagulation complex in HyperD-ALL cells was damaged, resulting in reduced chromosomal coagulation, loss of filament hardness, and abnormal positioning of the chromosome passenger complex protein Aurora B kinase (AURKB) and Survivin in early filament divisionin addition, HyperD-ALL cells also exhibit staining monomer coagulation defects and damage to spindle assembly checkpoints (SAcs), which, therefore, in the downstream of coagulant complex defects, due to AURKB defects and damage to SAC activity, resulting in fission-splittingUnder AURKB and/or SAC inhibition, healthy CD34-dry/progenitor cells appear chromosomal structure/coagulation defects and super-dicosmoverall, hyperdipidal B-ALL is associated with defective coagulin complexes, AURKB, and SAcs