Leukemia

P1, N=10, Active, not recruiting, Baylor College of Medicine | Trial completion date: Jul 2026 --> Jul 2027

P2, N=25, Not yet recruiting, Jennifer Woyach | Initiation date: May 2026 --> Sep 2026

P1, N=46, Recruiting, City of Hope Medical Center | Trial completion date: Feb 2030 --> May 2028 | Trial primary completion date: Feb 2030 --> May 2028

P=N/A, N=50, Recruiting, French Innovative Leukemia Organisation | Trial completion date: Jun 2026 --> Jul 2028 | Trial primary completion date: Dec 2025 --> Jul 2026

The children presented with severe pain and vesicular lesions; one had noncontiguous dermatomal involvement. The findings underscore the role of immunosuppression, particularly HIV and leukemia therapy, in atypical HZ presentations.

The integration of alternative genotype parameterizations and regularized machine learning highlights pathways for future predictive research. However, given the retrospective nature of the study and inherent risks of internal optimism, these scores serve as biologically informed proof-of-concept models that strictly require robust prospective external validation.

Blinatumomab was administered after one cycle of high-dose methotrexate/cytarabine, resulting in MRD negativity after one cycle...Inotuzumab ozogamicin induced a second hematological remission with MRD negativity, although disease control was not durable. This case highlights the importance of repeat immunophenotypic and cytogenetic assessment at relapse after blinatumomab treatment.

This may be due to late presentation and poor adherence to imatinib which needs further investigations. To improve the survival of patients with CML in Rwanda, access to all available lines of TKI and better follow-up should be considered.

Pharmacologic inhibition of IGF2BP1-RNA interactions with the small-molecule BTYNB induced potent and selective cytotoxicity in patient-derived AMKL models. Together, these findings uncover a developmental co-dependency between SNHG29 and IGF2BP1 that defines a lineage-restricted oncogenic circuit and an actionable therapeutic vulnerability in AMKL.

Using B-ALL cell lines and patient-derived xenografts, we show that FATP2-expressing TP53-mutant B-ALL resistance to CAR-T is dependent on exogenous lipid uptake to fuel fatty acid oxidation (FAO) and cell survival, which can be pharmacologically targeted through inhibition of neutral lipolysis and CPT1. These findings identify FATP2-mediated fatty acid uptake and downstream FAO as a potential target to improve existing CAR-T efficacy in human B-ALL.