IRF4 (Interferon regulatory factor 4)

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.

She received six cycles of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy, which she tolerated well. Post-treatment PET-CT revealed a complete metabolic response, and subsequent follow-up has shown no evidence of disease recurrence. This report illustrates that isolated splenomegaly can be the first and only manifestation of DLBCL and emphasizes the role of splenectomy as both a diagnostic and therapeutic option in carefully selected patients.

Grade 3A FL is characterized by marked clinical and biological heterogeneity. Our findings indicate that Ki-67 expression serves as a valuable prognostic marker that can inform therapeutic decision-making in patients with grade 3A FL. The proposed model integrating Ki-67 and clinical variables enhances PFS prediction and supports individualized treatment strategies for these patients.

Mechanistically, Tazemetostat appears to reduce IKZF1 binding to the IRF4 promoter and super-enhancer, explaining how the combination with IMiDs/CELMoDs which also have this effect may reach the threshold required to suppress IRF4 expression and ultimately inhibit MM cell growth in resistant cell lines. Our findings highlight a potential strategy for treating MM patients with IMiD resistance.

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.

This suggests that IKZF3 is a good biological indicator for tumors and may become a new therapeutic target for tumors. A systematic elaboration of the latest research progress on the IKZF3 gene structure, physiological functions, tumor regulation, and treatment resistance can provide reference and scientific basis for future tumor therapy.

Finally, targeting PRKCN with an orally bioavailable inhibitor suppresses MM cell growth and overcomes drug resistance in vitro, and elicits robust efficacy in cell line-derived xenografts and a patient-derived xenograft, which is connected with the mitigated PRKCN expression and activation loop phosphorylation as well as blunted mTOR-IRF4 axis. Collectively, our study delineates PRKCN function that links aberrant NF-κB signaling and mTOR-IRF4 axis, supporting clinically targeting PRKCN in MM.

This finding highlights the functional relevance of IMiD's inherent polypharmacology in circumventing primary resistance mechanisms at the cellular level. Together, our results identify the ARID2-containing PBAF complex as a critical vulnerability in resistant myeloma cells and provide a mechanistic rationale for designing combination strategies that co-target this complex, with the potential to enhance therapeutic efficacy by overcoming drug resistance.

Treatment with topical corticosteroids has provided considerable improvements, showing resolution of lesions. To the best of our knowledge, this is the first case of LyP type E affecting a pediatric patient with lesions confined to the oral mucosa.

These results suggest that clonal complexity captures tumor-intrinsic features and biological diversity in DLBCL, especially in the ABC subtype, offering novel insights into the disease pathogenesis.

The histomorphologic and immunohistochemical features of the histiocytic sarcoma in this Lemur catta were characteristic of this condition in other species. This report documents the first case of histiocytic sarcoma in Lemur catta, providing novel histopathological and immunohistochemical insights of this condition in prosimians.

Their diagnosis requires careful consideration to accurately distinguish rare indolent entities, recently defined large B‑cell lymphomas, and reactive mimics. Recent classifications, including the newly introduced WHO Classification of Pediatric Tumors, increasingly reflect these unique aspects.