Burkitt Lymphoma

P1/2, N=161, Completed, Acerta Pharma BV | Active, not recruiting --> Completed | Trial completion date: Apr 2026 --> Oct 2025

SULT1C2P1 and KCNK5 emerged as M1-associated prognostic biomarkers. Our findings establish EBV as a key modulator of BL genomic instability and immune remodeling, leading us to hypothesize that EBV status defines distinct BL subtypes with unique therapeutic vulnerabilities, thereby enabling the future development of EBV-stratified precision therapies.

Curcumin and vitamin D₃ demonstrated cytotoxic, pro-apoptotic effects in Daudi cells, both independently and in combination. Preclinical and clinical studies are warranted to validate these effects and establish translational applications.

This study highlights the potential of lectins in immunotherapy for the treatment and eradication of malignant cells. The SadP-based lectibody demonstrates improved efficacy and yield when compared to the previously engineered StxB-scFv UCHT1 lectibody, therefore opening the possibility for its use in an in vivo model.

P1/2, N=145, Recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2026

The patient achieved complete remission with R-CHOP therapy, aligning with LBCL-IRF4-R's favorable prognosis. This case underscores the need for integrated morphology, immunophenotyping, and NGS to resolve complex diagnostic challenges. It presents a key diagnostic pitfall where secondary 11q aberrations in LBCL-IRF4-R can mimic HGBL-11q, revealing limitations of current genetic algorithms and advocating for expanded molecular diagnostic criteria.

Fimepinostat was tolerable at a dose of 35 mg/m2 in children with relapsed and refractory solid and CNS tumors, but lacked significant clinical activity. Discovery of drugs to target Myc continues to be a high priority for childhood cancers.

P1, N=35, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed | Trial completion date: Jun 2026 --> Nov 2025 | Trial primary completion date: Jun 2026 --> Nov 2025

We further discuss the theory that aberrant activation-induced cytidine deaminase (AID) expression, in the setting of EBV infection and chronic malaria exposure, is the most likely aetiology of endemic BL. This review provides a comprehensive summary of key molecular differences between EBV-positive and EBV-negative BL, that may guide the development of future targeted therapeutic strategies.

Our findings suggest that clinical malaria did not result in the impairment of T-cell activation, but rather induced shifts in cytokine secretion in favor of IL-10. We further demonstrate that malaria-induced T-cell immune alterations are not EBV-specific but rather affect overall immune suppression.

In addition, anti-9G4 cTCR-T cells showed ∼17-fold lower IFN-γ secretion compared to anti-9G4 CAR-T cells, despite achieving similar cytotoxicity. Together, our findings suggest that anti-9G4 precision cellular therapies provide a strategy to selectively target pathogenic B cells in SLE, while minimizing risks of infection and cytokine-related toxicities.