TNFRSF8 positive

Understanding the subtypes and molecular characteristics of ALCL is essential for optimizing therapeutic strategies. Therefore, this review summarizes recent research advances on ALK +/- ALCL to provide insights for optimizing treatment approaches.

This case demonstrates that IVLBCL can present with diffuse interstitial lung disease and generalized lymphadenopathy, expanding its recognized phenotypic spectrum. It may represent a variant with CD30-mediated nodal homing and immune activation.

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.

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.

Furthermore, treatment with AVD (adriamycin/vinblastine/dacarbazine) in combination with brentuximab vedotin (BV) was initiated to achieve a complete metabolic response. Histopathologically, SV has a high proportion of HRS cells, with high CD30-positive and low EBER-positive rates. Therefore, CD30-targeted therapies such as BV may be preferable for SV, even in localized NS-HL patients, thereby improving patient prognosis.

P1, N=26, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed | Trial completion date: May 2026 --> Dec 2025

CHOP or CHOP-like regimens have long been the standard frontline therapy; however, the addition of brentuximab vedotin has improved overall survival and established a new standard of care for CD30-positive PTCL...Epigenetic modulators, including histone deacetylase inhibitors and an EZH1/2 inhibitor, have demonstrated particularly high activity in TFH-derived subtypes, supporting the integration of biomarker-driven patient selection as a path toward precision medicine in PTCL. This review summarizes current insights into the genetic landscape, recent clinical advances in novel agents, and future perspectives on therapeutic stratification, highlighting the need to translate molecular insights into durable clinical benefits for patients with PTCL.

In further studies, RNA sequencing confirmed the presence of NPM1::ALK gene fusion in this case; whole-exome sequencing (WES) detected somatic mutations in multiple genes of the JAK-STAT pathway (including JAK1, PTPN6, MTOR, and TYK2). It is noteworthy that such genetic alterations are more commonly observed in ALK-negative anaplastic large cell lymphoma (ALK-ALCL) but are less commonly reported in ALK+ALCL.