ArticleLeukemia2026
Unraveling cellular and molecular mechanisms of relapse in CD19/CD22 dual-targeting chimeric antigen receptor T-cell therapy for B-cell acute lymphoblastic leukemia.
Article in Leukemia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
CD19/CD22 dual-target chimeric antigen receptor (CAR19/22) T cell therapies mark a key advance over single-target options for refractory B-cell malignancies. However, over 20% of patients relapse and underlying mechanisms remain less understood. This study evaluated relapse in 91 B-cell acute lymphoblastic leukemia (B-ALL) patients treated with CAR19/22 T cells a clinical trial (ChiCTR-OPN-16008526). The complete remission rate was 91.9%, and 32.9% (26/79) of responders relapsed at a median of approximately 7 months. Among late relapses (>7 months), 92.3% was CAR T functional insufficiency showing lack of persistence or recovery of CD19⁺ B lymphocytes. Early relapses showed greater heterogeneity with 30.8% attributable to CAR T functional insufficiency and 30.8% to antigen insufficiency. Notably, two early relapses (15.4%) exhibited concurrent CD19/CD22 downregulation and harbored a preexisting PAX5 deletion or frameshift insertion. These PAX5-mutated subclones persisted and expanded at relapse, with one patient acquiring additional CD19 mutations. PAX5 knockout in leukemic cells reduced CD19/CD22 expression and proximal enhancer activities, causing in vitro resistance to CAR19/22 T cells. Collectively, CAR T functional insufficiency and antigen insufficiency are the most (61.5%) and second (15.4%) frequent drivers of relapse, respectively. Disruptive PAX5 mutations define a distinct molecular mechanism of early relapse, guiding rational targeted strategies.
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