TNFRSF13B (TNF Receptor Superfamily Member 13B)

In conclusion, both pleural effusions and peripheral blood from TB and LUAD exhibit significant distinct immune landscapes. These results delineate disease-specific molecular mechanisms underlying immune regulation in pleural malignancies and infections.

P1/2, N=6, Active, not recruiting, Pharming Technologies B.V. | Recruiting --> Active, not recruiting

Notably, CSNK1E inhibition impaired the growth and tumor-initiating capacity of drug-persistent cells and potentiated the efficacy of R-CHOP-based treatment both in vitro and in vivo. Together, our study reveals the stem-like transcriptional and functional properties of drug-persistent cells, and identifies CSNK1E as a critical mediator and therapeutic vulnerability to improve the efficacy of standard immunochemotherapy in DLBCL.

P2, N=20, Active, not recruiting, Pharming Technologies B.V. | Recruiting --> Active, not recruiting

Following enzalutamide (ENZ) treatment, GSTA1 expression is inhibited...TNFRSF13B induces c-Fos expression, forming a transcriptional complex with c-Jun, thereby regulating chromogranin A (CHGA) and promoting the neuroendocrine phenotype. Our study suggested that GSTA1 deficiency leads to elevated ROS levels and activation of TNFRSF13B and c-FOS, which subsequently transcriptionally regulate CHGA and ultimately drive neuroendocrine differentiation in PCa.

CD320, SLC44A1, and TNFRSF13B are promising, clinically relevant targets for CAR T-cell therapy in MM. Their stage-specific expression and prognostic significance support their potential to enhance existing immunotherapeutic strategies.

Gene silencing experiments indicated that XBP-1 might be involved in the TACI-mediated regulation of EBV lytic activities in EBV-immortalized B cells. This study underscores the impact of TNFRSF13B variants on EBV infection and host immune responses, offering insights into CAEBV pathogenesis and potential therapeutic strategies.

Flow cytometry analysis in a 4NQO-induced mouse model showed that ERBB3 inhibition reduced CCDC50⁺ B cells while restoring MHC-II expression, indicating a shift toward immune activation. These findings highlight a dual role of ERBB3 in HNSCC, acting both as an oncogenic contributor and an immune-modulatory regulator, and position ERBB3 as a promising context-dependent therapeutic target.

Findings confirm that NHL, particularly DLBCL, is the most prevalent malignancy in this cohort. Given the link between malignancies and underlying IEI, immunologic evaluation is recommended, particularly for NHL patients. The observed predominance of hematologic malignancies among CVID patients and the association with lymphoproliferation further emphasize the need for heightened malignancy surveillance and early immunologic workup in this subgroup. Further research on biomarkers for malignancy prediction in IEI is warranted.

We identified (i) biallelic mutations in TNFRSF13B, (ii) the HLA-class II marker (DPA1*03), and (iii) multiple single nucleotide polymorphisms in known B-cell related genes, as additional genetic risk factors. Moreover, pathogenic mutations in other known IEI genes were presented in 16% of patients with heterozygous TNFRSF13B variants.

These lesions exhibit distinct histopathologic features, such as amyloid deposition, and have a favorable prognosis with minimal risk of progression to systemic amyloidosis. This study supports the hypothesis that AL-amyloidomas are part of the broader spectrum of indolent B-cell lymphomas.

This study assessed for the first time in an unbiased and comprehensive manner the role of IEI/IBMFS in childhood hematological malignancy predisposition. Although the overall yield of this exploratory study was limited, our findings support the importance of research on childhood cancer predisposition at the intersection of hematological malignancies and IEI/IBMFS. We identified several variants in both dominant and recessive genes of which it would be interesting to investigate their causality. However, for now, sequencing of IEI/IBMFS-associated genes should be restricted to research context or in case of clinical suspicion.