TNFRSF8 (TNF Receptor Superfamily Member 8)

A component of teratoma was also present. We believe this to be the first report of such a unique association.

Ultimately, the patient was diagnosed with fluid overload-associated large B-cell lymphoma and treated with rituximab, cyclophosphamide, vincristine sulfate, and prednisone, but passed away three months after diagnosis. It may be mistaken for other conditions such as primary effusion lymphoma or other diffuse large B-cell lymphomas. The presence of a Human Herpesvirus-8-negative effusion-based lymphoma in an elderly immunocompetent patient without nodal or tissue involvement should prompt consideration of fluid overload-associated large B-cell lymphoma.

P2, N=82, Completed, Seagen, a wholly owned subsidiary of Pfizer | Active, not recruiting --> Completed

Nonetheless, some patients experienced high-grade AEs or symptom recurrence and stopped BV/PV therapy. Future studies may provide clarification and guide clinical practice.

Pediatric PCLs show heterogeneous behavior and therapeutic responses. Early biopsy of atypical or treatment-refractory eruptions, comprehensive histopathology and immunophenotyping, targeted EBV testing when suggested, and appropriate use of skin-directed radiotherapy (EBRT/TSEBT) and transplantation in selected refractory disease are essential. Multidisciplinary management and equitable access to specialized therapies are critical to optimize outcomes.

Although ex vivo expanded TILs are predominantly terminally differentiated, exhausted and transcriptionally highly distinct from the initial TILs, there is also a large progenitor exhausted CD8 T cell (Tpex) population and DN numbers increase. Future work to amplify subpopulations of TILs with memory cell phenotypes, such as the DN cells, will likely further improve this therapy.

An 85-year-old male presented with multiple rapidly progressive, painful, ulcerative lesions, initially misdiagnosed as PG and treated with oral cyclosporine with no clinical response... The case documents an exceptionally rare cutaneous presentation of A-DLBCL, expanding the extremely limited literature on this enigmatic entity. Furthermore, it underscores the fundamental role of early skin biopsy in the differential diagnosis of non-specific ulcerative lesions, which is critical for ensuring appropriate treatment administration within the therapeutic window in cases of malignancy.

Diffuse large B-cell lymphoma (DLBCL) can undergo stepwise immunophenotypic and molecular evolution over decades, progressing from a germinal Center B-cell-like (GCB)-like phenotype to an activated B-cell -like/non-GCB pattern (MUM1+, CD30+) and ultimately to an aggressive anaplastic variant.The cell-of-origin profile and its associated molecular features are not necessarily static; thus, therapeutic strategies for relapsed DLBCL should be tailored to the current disease state rather than relying on the signature at initial diagnosis.Longitudinal re-evaluation through repeat biopsies is imperative to capture the evolving landscape of the malignancy, ensuring that treatment selection is guided by the most recent pathological and molecular findings.

After R-CHOP-like therapy, EBV+DLBCL patients achieved complete and overall response rates of 55.5% (30/54) and 83.3% (45/54), respectively...EBV+ DLBCL in this Chinese cohort was primarily non-GCB. Elevatedβ2-microglobulin and bone marrow invasion independently predicted inferior PFS, while elevatedβ2-microglobulin and anemia predicted inferior OS.

The CD30 antibody-drug conjugate, brentuximab vedotin, and PD-1 inhibitors, nivolumab and pembrolizumab have transformed the care of patients with Hodgkin lymphoma and have been incorporated into earlier lines of therapy. Novel immunotherapies for patients with relapsed/refractory Hodgkin lymphoma include CAR-T products, EBV-specific T cells, bispecific antibodies, and checkpoint inhibitor combinations. We review the rationale for each and summarize safety, efficacy, and progress in clinical development.

The 36-month PFS (from first scan) was 73.0% (54.5, 85.0) for BV/Ipi/Nivo compared to 45.8% (26.3, 63.4) for BV/Nivo (HR=0.45, CI 0.19-1.08, one-sided p=0.03). The study did not meet its primary endpoint of superior CR rate for the triplet, but it supports the use of checkpoint-ADC induction prior to auto SCT, and there is an intriguing signal of disease control for patients wishing to defer or avoid SCT for the triplet of BV/Ipi/Nivo.