B Acute Lymphoblastic Leukemia

Given the critical importance of CD22 targeting, this experience serves as a foundation for new approaches targeting CD22 while providing ongoing support for dual-targeting approaches and insights into toxicity mitigation. NCT02315612.

P1/2, N=104, Recruiting, Amgen | Not yet recruiting --> Recruiting

P1/2, N=83, Recruiting, AstraZeneca | Not yet recruiting --> Recruiting

Blinatumomab combined with low-dose chemotherapy and TKIs demonstrated a trend toward improved MRD negativity, lower relapse rates, and reduced hematologic toxicity compared to conventional chemotherapy. These findings support further investigation in larger trials to confirm clinical benefit.

Based on our results, the CD49f molecule can be used as a measurable residual disease marker in both pediatric and adult B-cell acute lymphoblastic leukemia patient groups, and its expression correlates with genetic abnormalities and focal adhesion kinase-Src pathway activation. Orv Hetil. 2025; 166(50): 1983-1992.

P1, N=54, Active, not recruiting, Fate Therapeutics | Trial primary completion date: Sep 2024 --> Jun 2025

P1, N=50, Not yet recruiting, The General Hospital of Western Theater Command

Higher initial CASP8AP2 gene expression was associated with favorable impact on event-free survival in pediatric ALL patients. Post-induction levels did not show similar correlation. Future larger studies are needed to confirm the favorable association and to search for other possibly related prognostic factors to further refine risk stratification.

P=N/A, N=179, Recruiting, Novartis Pharmaceuticals | N=500 --> 179

P=N/A, N=270, Active, not recruiting, Ruijin Hospital

P1, N=71, Active, not recruiting, City of Hope Medical Center | Trial completion date: Sep 2025 --> Jul 2026 | Trial primary completion date: Sep 2025 --> Jul 2026

Ferroptosis was induced in B-ALL cells using erastin...PRDX1 knockdown further reduced the viability of B-ALL cells treated with the ferroptosis activator ML210, and treatment with the ferroptosis inhibitor liproxstatin-1 significantly reversed the suppressive effect of PRDX1 knockdown on xenograft tumor growth. Mechanically, PRDX1 deletion triggered ferroptosis in B-ALL cells by inhibiting the cAMP pathway. PRDX1 deficiency modulates ferroptosis in B-ALL cells by blocking the cAMP pathway, which offer a novel perspective on the pathogenesis of B-ALL.