NFIB (Nuclear Factor I B)

Taken together, this study highlighted that NFIB serves as a tumor suppressor gene in bladder cancer, and suppresses cell migration, invasion and EMT through the modulation of the PI3K-AKT signaling pathway, revealing NFIB as a potential biomarker for monitoring early metastasis of bladder cancer and a target for therapy. The online version contains supplementary material available at 10.1007/s10616-026-00900-4.

This case highlights ACC's propensity for "benign-mimicking" sonographic features (well-defined margins, posterior enhancement, hypovascularity), contributing to misdiagnosis. It underscores that integrating elastography (for assessing stiffness), contrast-enhanced ultrasound (for evaluating washout patterns), CT/MRI (for detecting suspicious perineural spread), and molecular biomarkers (e.g., low Ki-67) is crucial to improving diagnostic accuracy and optimizing follow-up management for ACC.

We report here an exceedingly rare case of a benign neoplasm diagnosed as benign tubular SG adenoma that was unexpectedly found to harbor a MYBL1::NFIB fusion gene. This case expands the spectrum of SG tumors driven by fusions of MYBL1, and challenges the specificity of MYBL1 fusions for cutaneous AdCC.

Mutational disruption of key DNA-contacting residues abolishes DNA binding and transcriptional activation, linking atomic-level recognition to oncogenic transcriptional regulation. Together, these findings elucidate the structural mechanism underlying NFIB function in cancer and establish a framework for therapeutic strategies targeting NFIB-driven malignancies.

A balanced translocation in MYB-NFIB fusion gene appears to be fundamental in the pathogenesis. Surgery forms the mainstay treatment option followed by adjuvant radiation in high risk cases, as extrapolated from studies in salivary gland tumour.

In situ hybridization and RT-PCR confirmed the presence of HPV42 in digital papillary adenocarcinoma. Our study confirms the presence of mutations in TP53 and Jak1 and suggests that HPV42 does not contribute to malignant adnexal tumors of the head and neck.

These findings provide critical insights into early tumorigenesis, highlighting the potential of precursor cells as biomarkers for early detection and therapeutic targets of esophageal squamous cell cancer. By elucidating the cellular dynamics underlying esophageal preneoplasia, this research lays the foundation for strategies to prevent malignant progression, offering broader implications for improving cancer diagnostics and treatment approaches.

WGS in SGC is achievable in clinically relevant timeframes, providing genomic information for deeper understanding of disease pathophysiology, to clarify histologic subtype and can identify actionable genomic targets which may not be found through routine sequencing technologies. Further use of WGS has the potential to improve care for patients with SGC.

Notwithstanding advancements, issues with clinical integration, model interpretability, and data quality still exist. Future directions highlight federated learning models, explainable AI, and large-scale clinical validation as key to integrating AI into precision oncology for patients with AdCC.

Recent reports have indicated that the minor allele of the nuclear transcription factor I/B (NFIB), rs28379954 T>C, affects the metabolism of risperidone and clozapine, which are mediated by CYP2D6 and CYP1A2, respectively. First, we reanalyzed the association between rs28379954 T>C and CYP2D6 activity in three independent cohorts exposed to CYP2D6 substrates (propafenone, tamoxifen, and sparteine) which revealed no association...We identified significant downregulation of several metabolic pathways related to hepatic functionality, PPAR signaling, and drug metabolism for NFIB, NFIC, and NFIX, whereas pathways associated with cancer biology were significantly induced. In summary our findings provide further insight into hepatic CYP regulation via the NFI network with implications for the understanding of interindividual variability of drug metabolism.

Emerging breakthroughs in targeted therapies warrant attention, including antisense oligonucleotides targeting MYB-NFIB fusion genes, clinical trial data of NOTCH inhibitors (e.g., AL101), and PARP inhibitor-based combinatorial regimens leveraging DNA damage repair mechanisms. By integrating fundamental research and clinical translational evidence, this review provides a theoretical framework for optimizing LGACC diagnosis and treatment paradigms.