Identifies a prognostic tool and evaluates immune responses in drug-resistant childhood ALL, suggesting new treatment strategies.
ALL is the commonest childhood hematological malignancy; modern multi-agent chemotherapy cures about 80% of patients, yet roughly 20% experience primary or secondary chemotherapy resistance that sharply reduces long-term survival. The molecular circuits driving this resistance remain poorly defined, and validated biomarkers for early risk stratification are lacking. Growing data implicate reprogramming of the immune microenvironment as a critical determinant of treatment response and relapse risk. We therefore interrogated transcriptomic profiles from GEO and TARGET datasets to identify genes differentially expressed between chemosensitive and chemoresistant ALL, distilled a 13-gene resistance-associated prognostic index (RAPI-13) by LASSO regression, and validated the signature in independent cohorts. Functional enrichment, immune-infiltration deconvolution and single-cell RNA-seq revealed that high-risk patients harbor activated oncogenic signaling (IL-2/STAT5, NOTCH, PI3K/AKT/mTOR) together with immune-evasion signatures. Mechanistic studies showed that CD40 agonist treatment polarizes tumor-associated macrophages toward the pro-inflammatory M1 state, restores anti-leukemic immunity and re-sensitizes resistant blasts to chemotherapy. In cell-line-derived xenografts and humanized mice, triple therapy combining CD40 agonist, daunorubicin and PD-L1 blockade achieved superior leukemia control, prolonged survival and fostered immune memory formation. These findings provide a clinically applicable prognostic tool and pre-clinical rationale for integrating CD40-centered immunotherapy into frontline protocols to overcome chemotherapy resistance in childhood ALL.
No takes yet. Share an insight, caveat, or question.
Li et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: