• TSPAN32 is consistently downregulated across all B-ALL subtypes. • Low TSPAN32 predicts poor survival, independent of age and genotype. • TSPAN32 levels inversely correlate with blast percentage in B-ALL. • TSPAN32 is unaffected by glucocorticoids, suggesting alternative regulation. B-cell acute lymphoblastic leukemia (B-ALL) is an aggressive hematologic malignancy characterized by the uncontrolled proliferation of immature B-cell precursors. Despite therapeutic advances, outcomes remain poor in adults and relapsed patients, underscoring the need for novel targets. TSPAN32, a tetraspanin family member, is primarily expressed in hematopoietic tissues and implicated in immune regulation. In this study, we have evaluated the TSPAN32 expression across various B-ALL subtypes and correlated it with clinical data. TSPAN32 expression was significantly reduced in all subtypes compared to healthy bone marrow. Expression was relatively uniform within the B-ALL population, unaffected by differentiation stage. A significant negative correlation between TSPAN32 expression and blast percentage was also observed. Survival analysis revealed that lower TSPAN32 expression correlated with poorer overall survival. Gene expression analysis in sample diverging for the expression of TSPAN32 identified key pathways, including immune modulation and ECM processes, associated to TSPAN32 expression. In conclusion, TSPAN32 emerges as a molecule involved in the biology of B-ALL. Its prognostic value, consistent expression across age groups, and involvement in key signaling pathways highlight its potential as a biomarker for B-ALL.
Scuderi et al. (Sun,) studied this question.