NFKBIE (NFKB Inhibitor Epsilon)

P2, N=22, Recruiting, Zulfa Omer | Not yet recruiting --> Recruiting

P2, N=62, Recruiting, Zulfa Omer | Not yet recruiting --> Recruiting | Initiation date: Jun 2025 --> Dec 2025

FTO regulates NFKBIE expression via m6A-dependent demethylation, establishing a pivotal FTO-NFKBIE regulatory axis that drives TNBC progression. FTO overexpression promotes TNBC cell proliferation, migration, and invasion, effects that are partially reversible through NFKBIE restoration.

Notably, NFKBIE silencing also led to the downregulation of components of the Hedgehog signaling pathway, suggesting that NFKBIE may regulate tumor progression through modulation of this critical pathway. In conclusion, high NFKBIE expression is strongly associated with GBM progression and poor prognosis, and targeting its expression may offer a promising therapeutic strategy for GBM treatment.

No significant difference was found in the overall survival between CD10-MUM1+ FL and conventional FL patients. In summary, this study demonstrated that CD10-MUM1+ FL has unique clinical, pathological ​and genetic features.

While univariable analysis revealed shorter TTFT for Binet A patients with any ATM aberration compared to ATM-wildtype, multivariable analysis identified only del(11q), trisomy 12, SF3B1, and EGR2 mutations as independent prognosticators of shorter TTFT among Binet A patients and within M-CLL and U-CLL subgroups. These findings highlight del(11q), and not ATM mutations, as a key biomarker of increased risk of early progression and need for therapy, particularly in otherwise indolent M-CLL, providing insights into risk-stratification and therapeutic decision-making.

We then applied our analysis pipeline to scRNA-seq measurements of HSPCs isolated from aged mice, as well as human myeloid neoplasm patients. These analyses identified the same myeloid-primed progenitor expansion as in the IκB- models, suggesting that it is a common feature across different settings of myeloid bias.

These findings necessitate revisiting the prognostic impact of high-risk factors, current management strategies, new bi- and tri-specific T-cell engagers, combination therapies, novel therapeutic targets, and next-generation clinical trials for high-risk MCL patients. This article provides a comprehensive update on recognizing and managing high-risk MCL, encompassing current practices and future directions.

Our study also suggested genetic heterogeneity between Asian and European populations by identifying ancestry-specific genetic associations. Overall, this study has implicated novel disease genes and molecular mechanism for DLBCL.

Genetic complexity (≥3 CNVs) observed in 51% of analysed patients was significantly associated with impaired FFS and OS. We demonstrate that targeted sequencing from peripheral blood and bone marrow reliably detects diagnostically and prognostically important genetic factors in MCL patients, facilitating genetic characterization in clinical routine.

The findings of this study demonstrate that Bailixiang tea possesses the ability to alleviate lung tissue damage and inhibit the development of LPS-induced cytokine storm in mice. These effects are attributed to the tea's ability to suppress the TLR2/MAPK8 and TLR2/NF-κB pathways. Consequently, this research highlights the potential application of Bailixiang tea as a treatment option for cytokine storm.