Burkitt Lymphoma

Hierarchical analysis of MYC, BCL2, BCL6 rearrangements and 11q aberration is therefore essential. It directly impacts diagnosis, prognostic stratification, and therapeutic management.

The patient was treated with rituximab-based multi-agent chemotherapy and showed a favorable response. This case highlights the importance of early radiologic-pathologic correlation and prompt biopsy in atypical pediatric mandibular swellings to enable timely diagnosis and management.

Together, our results indicate that CD8+ T cells both in the TME and in circulation of children with BL are not terminally exhausted but remain poised for functional re-invigoration. These findings support the potential integration of immune checkpoint inhibitors into combination chemotherapeutic regimens to improve outcomes for these children.

This case highlights the diverse presentations of Burkitt's lymphoma and a favorable prognosis with treatment. Clinicians should maintain a high index of suspicion for a malignant etiology of acute pancreatitis in patients without classic risk factors.

Multiparameter optimization yielded compound 18, which demonstrated improved efficacy in a MYC-dependent Burkitt lymphoma xenograft model at a significantly lower dose than the RUVBL1/2 inhibitor CB-6644. This work establishes SMT as a powerful tool to facilitate the drug discovery SAR campaigns and evaluates the therapeutic potential of RUVBL1/2 inhibition in MYC-dependent cancers.

Together, our data indicate that ZDHHC11 promotes BL cell growth at least in part by stimulating expression of MEF2B, which promoted BL cell survival through both BCL6-dependent and independent pathways. Our work highlighted the importance of the MEF2B-BCL6 axis, which strongly supports BL growth and identified ZDHHC11 as a novel regulator of this axis.

P1/2, N=20, Recruiting, New York Medical College | Trial completion date: Aug 2025 --> Aug 2027 | Trial primary completion date: Aug 2024 --> Aug 2026

Therefore, we upgraded the treatment plan to R-CHOP chemotherapy (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone), and achieved a complete remission (CR)...We observe that the combination of HD-MTX and intrathecal chemotherapy exhibits remarkable efficacy in managing post-transplant CNS-PTLD that is resistant to conventional R-CHOP chemotherapy. CAR-T therapy emerges as a potential option for patients suffering from relapsed or refractory CNS-PTLD.

Here, we identify EBV latent membrane protein 1 (LMP1), a key viral oncogene necessary for B cell immortalization and which mimics aspects of CD40 signaling, drives resistance to ferroptosis induction by erastin, a small molecule that blocks cystine uptake...PFKFB4 was also necessary for LMP1-mediated Burkitt B cell ferroptosis resistance. Collectively, these results identify PFKFB4 as a key host cell EBV metabolism remodeling target critical for infected B cell redox defense.

EBV-activated JunB played an obligatory role in repression of the G1/S phase inhibitor CDKN2C /p18 INK4c in LCLs but not Burkitt B cells. These findings establish an LMP1-JunB-p18 INK4c axis as essential for EBV-driven lymphoblastoid B cell proliferation, suggest JunB-mediated cross-talk between Epstein-Barr nuclear antigens and LMP1, and highlight JunB as a potential therapeutic target for EBV-associated lymphoproliferative disorders.

P1, N=16, Completed, Calibr, a division of Scripps Research | N=36 --> 16 | Trial completion date: Aug 2036 --> Oct 2025 | Trial primary completion date: Aug 2036 --> Oct 2025 | Enrolling by invitation --> Completed

We therefore characterized the impact of pan-HDAC inhibitor, panobinostat, and class I HDAC inhibitor, nanatinostat, on the growth, survival, and lytic reactivation of four EBV-positive cell lines: P3HR1-ZHT BL, Jijoye BL, IBL-1 immunoblastic lymphoma, and de novo infection derived lymphoblastoid cell lines (LCL). Functional validation through a Cas9-RNP approach revealed that the CD137 receptor is indeed involved in preventing successful lytic reactivation. These data have important implications for how we approach oncolytic therapies for EBV-associated malignancies.