BICC1 (BicC Family RNA Binding Protein 1)

The complementary activity of lirafugratinib and futibatinib against FGFR2 kinase domain mutations supports their sequential use, when precise resistance mutations are detected in patients.

NGS represents the most suitable approach in molecular profiling of FGFR aberrant transcripts. Rings trial based on artificial reference samples play a pivotal role in optimizing routine diagnostic procedures filling the gap in clinical stratification of iCCA patients.

This study found that accelerated biological aging was associated with a higher risk of CRC and implied potential intervention opportunities by adherence to healthy lifestyles. Aging-related DNAm and altered gene expression might contribute to this biological association, which yielded insights into the etiology and potential therapeutic targets of CRC.

This study establishes a visceral pain model centered on pancreatic parenchymal nociception rather than secondary neural effects, and for the first time proposes an interconnected regulatory network linking epigenetic modifications, immune reprogramming, and neural plasticity, revealing dual pain pathogenesis mechanisms: (1) immune microenvironment reshaping that potentiates neuroinflammation, and (2) direct ion channel regulation enhancing neuronal excitability. These findings provide a mechanistic foundation for developing methylation-based prognostic biomarkers and multimodal analgesic therapeutic strategies targeting the immuno-neural nexus.

With a growing incidence of BTC and growing use of targeted therapies for FGFR2 alterations, the emergence of secondary resistance-causing point mutations following treatment with approved inhibitors is becoming increasingly challenging. Beyond selective inhibitors, lenvatinib may represent a viable therapeutic option.

This study identified a genetic causal relationship between HGB levels and the risk of PAAD. Through transcriptomic analysis, we constructed a prognostic model based on HGB-associated key genes. The model displayed reliable predictive capacity and offers new perspectives for clinical strategies aimed at preventing PAAD.

We report the case of a 55-year-old female with advanced iCCA harboring an FGFR2-BICC1 fusion, who experienced a rapid clinical response to tasurgratinib following disease progression on gemcitabine, cisplatin, and durvalumab (GCD). This is the first report to describe the real-world clinical efficacy of tasurgratinib in an iCCA patient with FGFR2-BICC1 fusion. Our findings suggest that tasurgratinib can provide a rapid and durable response with manageable toxicity in molecularly selected patients who have progressed on standard therapies.

The good comparability between cryopreserved and fresh insulinoma cells allows for inclusion of cryopreserved insulinoma patient samples in future studies, which allows for reduced assay-based variability. The online version contains supplementary material available at 10.1186/s44356-025-00025-4.

Oncogenic FGFR2 fusion/rearrangement was associated with small duct type iCCA, especially in cases with positive serum HBsAg and absent cholangiolocarcinoma components and peripheral liver steatosis. This study provides a comprehensive comparison of three assays for detecting FGFR2 fusion/rearrangement, along with clinicopathologic characterization of oncogenic FGFR2 fusion in iCCA.

Our study demonstrated that NEDD4L acts as a tumor suppressor in GC, while BICC1 functions as a pro-tumorigenic factor. The NEDD4L/BICC1 axis plays a significant role in the metastasis and progression of GC.