Amplification of 9p24.1, causing PD-L1 overexpression, plays a significant role in EBV-positive DLBCL and EBV-positive cHL, whereas EBVMCU, DLBCL-CI, FA-DLBCL, and LyG primarily depend on an (local) immunosuppressive condition. In conclusion, the molecular pathogenesis of EBV LPD is less reliant on driver mutations and instead rely on EBV latent genes and immune evasion; both factors provide promising targets for future therapy.
P2, N=41, Recruiting, Milton S. Hershey Medical Center | Not yet recruiting --> Recruiting
5 days ago
Enrollment open
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HLA-DRB1 (Major Histocompatibility Complex, Class II, DR Beta 1) • HLA-B (Major Histocompatibility Complex, Class I, B) • HLA-C (Major Histocompatibility Complex, Class I, C)
P=N/A, N=100, Recruiting, St. Jude Children's Research Hospital | Trial completion date: Mar 2027 --> Dec 2027 | Trial primary completion date: Mar 2026 --> Dec 2026
5 days ago
Trial completion date • Trial primary completion date
We identify EBV-encoded LMP1 as a factor in T cell dysfunction through enhanced HRS:CD8 interactions, and its expression level correlates with T cell terminal exhaustion in a distance-dependent manner. This spatial framework dissects viral-mediated immune evasion in the cHL TME, highlighting potential therapeutic opportunities to target virus-associated T cell dysfunction for precision immunotherapy in virus-associated malignancies.
Discontinuation of the culprit drug resulted in the remission of cutaneous symptoms. Because lymph node lesions in DIHS/DRESS also demonstrate HL-like histology, this case suggests that HH, while a novel and distinct histiocytic/dendritic cell disorder, may be associated with lymph nodal lesions occurring in the context of DIHS/DRESS.
In the absence of systemic involvement, the patient was diagnosed with primary classical Hodgkin lymphoma of the bladder. This rare presentation highlights the importance of considering classical Hodgkin lymphoma in the differential diagnosis of bladder tumors with atypical morphology.
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.