T Acute Lymphoblastic Leukemia

P3, N=40, Active, not recruiting, Fujian Medical University Union Hospital

To our knowledge, this is the first report of the translocation involving NUP98 and SETBP1 genes in T-LBL. It is necessary to collect additional cases and conduct carefully designed experiments to establish the recurrence of this fusion in other T-LBL cohorts and confirm its role as a novel oncogenic rearrangement in T-LBL, providing a basis for managing such patients.

These findings support a role for seasonal triggers in ALL and warrant further investigation in larger, genetically stratified cohorts.

These findings highlight genomic context in shaping BH3 mimetic responses and point to rational combination of this class of drugs with anti-leukemic agents such as asparaginase.

In conclusion, among heavily treated r/r B-ALL, PET/CT scans identified a higher incidence of non-CNS EMD and hidden EMDs in MRD-positive patients. The treatment strategy of CAR-T followed by consolidation improved the long-term survival of patients with non-CNS EMD.

P=N/A, N=60, Not yet recruiting, Washington University School of Medicine | Trial completion date: Mar 2028 --> Jun 2028 | Initiation date: Feb 2026 --> May 2026 | Trial primary completion date: Mar 2028 --> Jun 2028

P1/2, N=96, Recruiting, Beijing Biotech

It was demonstrated that the IONPs primarily bound to the membrane of Jurkat cells and formed ordered assembly structures under MF, which disrupted cellular homeostasis by activating the calcium-NFAT-FasL signaling pathway, hyperpolarizing mitochondria, reprogramming metabolism, and disrupting cytoskeletal assembly. In conclusion, the MAMS strategy sensitized Jurkat cells to VCR by multilevel interference with the homeostasis of cells, providing a promising approach for developing more effective and less cytotoxic T-ALL treatment regimens.

By integrating clinical and transcriptomic data from diagnostic T-ALL samples, we found that high MRD patients show a specific transcriptional profile. Moreover, we identified a transcriptional signature characterized by the differential expression of HSH2D, LAT2, BCL2, MAST4, METRN, and PITPNM2 genes that is tightly associated with an increased MRD, which could improve the prediction of poor treatment response in T-ALL patients, especially during early treatment phases.

Mechanistically, miR-15b/16-2 represses the expression of the genes encoding BCL-2 and CYCLIN D3, thereby promoting apoptosis and cell cycle dysregulation in T-ALL cells, characterized by an accumulation of G0-phase cells and a defective transition to the G2/M phase. Overall, these findings support a novel tumor-suppressive function for miR-15b/16-2 in T-ALL and highlight its potential as a promising therapeutic target.

P1, N=18, Not yet recruiting, M.D. Anderson Cancer Center