The patient underwent induction chemotherapy with cytarabine and mitoxantrone, followed by salvage therapy with venetoclax and azacitidine, resulting in morphologic remission. Subsequent haploidentical hematopoietic stem cell transplantation achieved remission, with ongoing hematologic recovery. This case underscores the limitations of conventional molecular assays in detecting cryptic fusions and highlights the critical role of comprehensive genomic profiling in refining subclassification and optimizing therapeutic strategies in pediatric AML.
Collectively, our findings establish TSPAN6 as a migrasome-related regulator driving adverse immunotherapy outcomes and responses. Targeting TSPAN6, potentially with mitoxantrone, presents a potential strategy to enhance immunotherapy efficacy.
Compound 30, but not 16 or 40, sensitized ABCG2-expressing HEK-293-R5 cells to mitoxantrone. Distinct docking modes of compounds 30 and 40 to ABCG2 predict the structural determinants for the inhibition of ATPase. These results reveal novel rigid, extended nucleoside inhibitors of ABC transporters with varied activities that attenuate MDR in cells.
Adverse events during induction and reinduction were consistent with those reported in previous infant acute lymphoblastic leukaemia studies. Infections remain a substantial cause of morbidity and mortality in this immunocompromised patient population and extended beyond the induction and reinduction chemotherapy phases.