B Acute Lymphoblastic Leukemia

The morphology of multiple clefts nuclei in blasts was strongly correlated with TCF3::PBX1 fusion in patients with B-ALL/LBL. Therefore, testing for TCF3::PBX1 fusions is recommended for patients with the morphology of multiple clefts nuclei in blasts.

P1, N=30, Recruiting, St. Jude Children's Research Hospital | Not yet recruiting --> Recruiting

P1, N=28, Not yet recruiting, Children's Hospital Medical Center, Cincinnati

The ALL/MRD2014 trial underscores the importance of MRD status and allo-HSCT in Ph+ ALL. Continuous dasatinib-based regimens offer favorable outcomes in MRD-negative patients.

P=N/A, N=50, Recruiting, Rennes University Hospital | Not yet recruiting --> Recruiting

P1, N=20, Recruiting, OHSU Knight Cancer Institute | Trial primary completion date: Dec 2025 --> Dec 2026

P=N/A, N=77, Recruiting, Institute of Hematology & Blood Diseases Hospital, China | Not yet recruiting --> Recruiting

Furthermore, it allows detailed, long-term studies of cell-cell interactions and treatment responses using live-cell imaging and AI-assisted cell tracking. Future integration with a perfusion-based drug screening system promises to enhance personalized cancer therapy by optimizing broad drug screening approaches and enabling real-time evaluation of therapeutic efficacy.

The treatment landscape for relapsed or refractory acute lymphoblastic leukemia (RR ALL) has evolved significantly with the introduction of monoclonal antibodies such as blinatumomab and inotuzumab ozogamicin. As monoclonal antibodies increasingly move into frontline therapy, their role in relapse settings must be redefined. Future research should focus on unraveling the molecular underpinnings of resistance and refining treatment paradigms to improve survival and quality of life for patients with RR ALL.

P2, N=23, Not yet recruiting, First Affiliated Hospital of Zhejiang University

P2, N=53, Recruiting, Institute of Hematology & Blood Diseases Hospital, China | Not yet recruiting --> Recruiting

As one of the key factors in the TME, abnormally elevated CD10- neuts correlate with CAR T therapy resistance. Targeting these neutrophils could enhance the effectiveness of CAR T treatment.

This case highlights the need to supplement banding cytogenetics with appropriate molecular (cyto)genetic techniques whenever the karyotype does not reveal characteristic aberrations. Although KMT2A rearrangements in both lymphoblastic and myeloid acute leukemias usually arise through karyotypically visible chromosomal recombinations, this is not always the case.

There was no significant difference between ABCB1 C3435 T polymorphism and mucositis, myelosuppression, nephrotoxicity, gastrointestinal toxicity in pediatric ALL treated with MTX. Our meta-analysis suggests that the ABCB1 C3435 T mutation may enhance the MTX-induced hepatotoxicity in childhood acute lymphoblastic leukemia.

P2, N=16, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed | Trial completion date: Feb 2025 --> Mar 2024

These results suggest that CDKN2A/B deletion may be one of the factors affecting poor prognosis. It provides a new perspective for clinical treatment, risk stratification, and prognostic assessment in pediatric ALL patients.

At 14 months of age he had medullary and CNS relapse, and at 16 months of age underwent CD19 CAR-T therapy. At 6 years of age he remains in remission with tolerable developmental delays and a good quality of life.

Not available.

P2, N=78, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed | Trial completion date: Nov 2025 --> Dec 2024

Identification of FIP1L1::PDGFRA rearrangements is important as they enable treatment with a tyrosine kinase inhibitor, which has significantly improved the overall prognosis for PDGFRA-rearranged neoplasms. Prospective studies assessing imatinib dosage, duration, and long-term safety are warranted in this cohort.

Both in vitro and in vivo experiments demonstrated that indirubin inhibited ALL cell proliferation and induced cell cycle arrest and apoptosis; the underlying mechanism may involve the PI3K-AKT signaling pathway. The action and mechanism of indirubin in ALL through network pharmacology, as well as in vivo and in vitro experimental validation were elucidated, offering new insights and potential therapeutic avenues for the treatment of ALL.

Biopsies showed new onset myeloid sarcoma (MS), with continued remission of B-ALL. 18F-FDG PET/CT showed numerous markedly hypermetabolic soft tissue lesions located in the skin and subcutaneous tissues, muscles, osseous structures, mucosa, pleura, mediastinum, peritoneum, retroperitoneum, and testes.

P2, N=36, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Sep 2025 --> Sep 2026 | Trial primary completion date: Sep 2025 --> Sep 2026

These findings link active signaling to uridine dependency in B-ALL cells and an associated risk of relapse. Targeting uridine synthesis through DHODH inhibition offers a promising therapeutic strategy for chemo-resistant B-ALL as a novel therapeutic approach for resistant disease.

We observed multiple phenotypes identifying subtypes of acute leukaemia cases, extending our previous studies in Ethiopia. This study extends previous studies by describing phenotypically defined subsets of ALL and AML which, in addition to diagnosis, may have useful prognostic value for clinicians.

Central nervous system (CNS) involvement, serum ferritin levels higher than four times normal and rituximab no more than two doses were associated with lower PFS...Mature B-ALL/B-NHL with BM involvement was a heterogeneous group of malignancies in both clinical features and genetic alternations. Genetics analysis was helpful for making accurate diagnoses and guiding appropriate therapeutic strategies.

CAR T-cell therapy is a groundbreaking advancement in treating r/r B-ALL, offering high rates of durable remissions.

The CDI model, validated across multiple cohorts, demonstrated substantial predictive power for relapse-free survival (RFS) and was identified as an independent risk factor. This study offers a comprehensive analysis of PCD patterns in pediatric B-ALL, yielding valuable insights into potential novel therapeutic strategies and opportunities for personalized treatment approaches.

In conclusion, the dysregulation EBF1 led to CSRP2 upregulation and resulting in progression of B-ALL. The EBF1/CSRP2 axis could be of great potential as therapeutic targets for B-ALL treatment.

The correlation coefficients (r) of MRD levels were 0.831 between CM-IGH and LT-IGH, 0.702 between CM-IGH and MFC, and 0.776 between LT-IGH and MFC. The CM-IGH assay demonstrates substantial concordance with LT-IGH and MFC in detecting MRD in pediatric patients with B-ALL, highlighting the complementary value of IGH clonality assays and MFC.

Our single-cell data demonstrate that chromosomal changes are acquired prior to additional mutations and that RAS signaling mutations are present in all HeH cases, often as subclonal mutations. This single-cell multi-omics study enabled us to extensively characterize the genetic and surface protein heterogeneity in patients with HeH B-ALL.

P=N/A, N=330, Recruiting, Children's Oncology Group | Trial completion date: Dec 2028 --> Jun 2029 | Trial primary completion date: Dec 2028 --> Jun 2029

Combination testing with the conventional chemotherapeutic agents currently used to treat infants with ALL demonstrated additivity with cytarabine. Dactinomycin is extensively used for the treatment of solid tumors in children and has an acceptable safety profile when used to treat infants in this context. However, despite being readily translational and exhibiting promising in vitro cytotoxicity, dactinomycin showed limited efficacy in vivo and therefore does not represent a priority candidate for integrating into therapy for infants with ALL.

P2, N=64, Recruiting, National Cancer Institute (NCI) | Trial completion date: Feb 2025 --> Feb 2026 | Trial primary completion date: Feb 2025 --> Feb 2026

P1/2, N=47, Recruiting, Juventas Cell Therapy Ltd. | Trial primary completion date: Dec 2024 --> Jul 2025

CD9 can be used as a surrogate biomarker in predicting disease prognosis by recognising the patients with high-risk factors i.e., lymphadenopathy, elevated white blood cells, possible occurrence of BCR::ABL1, and the scarcity of ETV6::RUNX1 within the CD9+ group.

P2, N=97, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jan 2025 --> Jan 2026

P1/2, N=26, Recruiting, Vironexis Biotherapeutics Inc. | Initiation date: Dec 2024 --> Mar 2025

P1/2, N=50, Not yet recruiting, Juventas Cell Therapy Ltd. | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Dec 2024 --> Dec 2026

P2/3, N=1800, Recruiting, Institute of Hematology & Blood Diseases Hospital, China | Not yet recruiting --> Recruiting

P2, N=40, Recruiting, M.D. Anderson Cancer Center | Trial completion date: Feb 2025 --> Feb 2027 | Trial primary completion date: Feb 2025 --> Feb 2027

P1, N=22, Completed, Cedars-Sinai Medical Center | Active, not recruiting --> Completed | N=10 --> 22 | Trial completion date: Mar 2025 --> Nov 2024