TNFRSF8 expression

P2, N=30, Recruiting, M.D. Anderson Cancer Center | Trial completion date: Jan 2026 --> Jan 2027 | Trial primary completion date: Jan 2026 --> Jan 2027

P1, N=22, Completed, Seagen, a wholly owned subsidiary of Pfizer | Active, not recruiting --> Completed

While response rates were similar, PFS was shorter. These findings suggest that BV remains a potential therapeutic option in this patient population and merits further prospective investigation.

Subsequently, dual-luciferase reporter assays and chromatin immunoprecipitation (ChIP)-qPCR demonstrated that Meq directly bound to the CD30 promoter to activate its transcription, and the primary binding regions located at -1383 to -1162 bp and -97 to +75 bp relative to the transcription start site. Collectively, this study demonstrated Meq could bind to CD30 promoter at two binding regions and up-regulate its expression, and provided a critical foundation to investigate the role of the CD30 signaling pathway in MD-induced tumorigenesis.

This understanding provides a strong rationale for COO- and TME-guided therapeutic strategies, such as combining the anti-CD30 antibody-drug conjugate brentuximab vedotin with immunomodulatory agents. This report elucidates the enigma of CD30 and outlines a path towards personalized medicine for DLBCL.

RDD of the lung and mediastinum is rare, with a wide range of ages. Histologically, there are often lymphoid follicles with germinal centers and interstitial fibrosis or sclerosis. This together with the expression of BCL2 and CD30 in the histiocytes can lead to misdiagnosis of lymphomas or other lymphoproliferative diseases or missed diagnosis, particularly in the mediastinum. Careful histological examination for the diagnostic feature of emperipolesis together with characteristic Cyclin D1, OCT2, S100 protein, and CD68 positivity are important clues for accurate diagnosis.

AITL with HRS-like cells is prone to misdiagnosis as CHL due to overlapping morphological and immunophenotypic features. Integration of EBER, TCR/IG clonality assessment, and molecular profiling, particularly the identification of TET2 and RHOA mutations is essential for accurate classification. Recognizing this entity is critical for avoiding diagnostic pitfalls and guiding appropriate therapeutic strategies.

He commenced first-line systemic therapy with methotrexate, but had no response. He was switched to brentuximab vedotin and has received eight cycles with partial response...Approach to mycosis fungoides in children: consensus-based recommendations. J Am Acad Dermatol 2024; 91: 1078-85).

P1, N=43, Active, not recruiting, UNC Lineberger Comprehensive Cancer Center | Recruiting --> Active, not recruiting | Trial completion date: Sep 2041 --> Nov 2039 | Trial primary completion date: Sep 2026 --> Dec 2025

P1/2, N=38, Active, not recruiting, UNC Lineberger Comprehensive Cancer Center | Recruiting --> Active, not recruiting | Trial completion date: Aug 2038 --> Nov 2039 | Trial primary completion date: Sep 2027 --> Dec 2025

The antibody-drug conjugate brentuximab vedotin (BV) has significantly improved outcomes for CD30-expressing lymphomas. The ECHELON-2 trial established BV combined with cyclophosphamide, doxorubicin, and prednisone (CHP) as a frontline standard for systemic anaplastic large cell lymphoma, demonstrating superior survival over the traditional CHOP regimen...We assess alternative strategies, such as BV-based combinations with immunotherapies or alternative chemotherapies, the integration of other targeted agents, and the transformative potential of advanced cellular treatments like anti-CD30 chimeric antigen receptor (CAR)-T cell therapy for relapsed/refractory disease. The collective evidence signals a paradigm shift from a one-size-fits-all approach toward personalized, precision-driven strategies aimed at maximizing efficacy, minimizing toxicity, and improving long-term quality of life for patients with CD30-positive lymphomas.

GI mastocytosis is highly predictive of SM in BM; however, most SM-BM+ patients are SM-GI-. The SM-BM- patients are very unlikely to be SM-GI+. Because GI neoplastic mast cells are often tryptase negative, diagnostic evaluation should include CD117 and CD25 immunohistochemistry, as well as KIT D816V mutation analysis by ddPCR as needed.