FGF4 (Fibroblast growth factor 4)

P2, N=60, Not yet recruiting, Tongji Hospital

Drug-gene interaction mining mapped 78 target proteins to clinically relevant compounds, including tolrestat, alcuronium, metyrosine, and 4-phenylbutyric acid...Physicochemical and pharmacokinetic profiling further prioritised tolrestat as a computationally favourable candidate (MW = 357.35, LogP = 3.64, TPSA = 81.86 Ų), exhibiting acceptable drug-likeness, high predicted gastrointestinal absorption, and low synthetic complexity (SA = 2.34), in contrast to alcuronium (MW = 666.89, SA = 7.86), which showed multiple rule violations. Collectively, this in silico study proposes a robust diagnostic gene signature for HCC and identifies tolrestat as a promising repurposing candidate that warrants experimental validation, demonstrating the utility of integrating machine learning, network biology, and molecular simulation in translational cancer research.

As KLF5 specifically regulates SETα, this implicates SET isoform switching at the KLF5/FGF signalling axis during primitive endoderm specification. Together, we propose a model of how distinct roles of SETα and SETβ may regulate cell identity in the early blastocyst.

Although MAPK alterations are pervasive in CRC, their distribution varies meaningfully by ancestry, age, and treatment exposure. These findings highlight NF1, MAPK3, RPS6KA4, and PDGFRB as potential biomarkers in EOCRC and H/L patients, supporting the need for ancestry-aware precision oncology approaches.

This suggests that besides SMARCA4 deficiency, alterations in other genes may cooperatively contribute to the tumorigenesis of bladder undifferentiated tumors. These findings provide a reference for subsequent exploration of precise diagnostic and prognostic assessment and treatment strategies for this disease.

Furthermore, incorporation of myeloid cells generated DMG-specific microglia that reduced treatment efficacy and revealed CAR T cell functional states most vulnerable to microglia-mediated immunosuppression. Thus, we present a representative DMG model offering a months-long experimental window in vitro, which we leveraged to delineate CAR T cell functionality and microglial impact, aiding therapy development for this devastating disease.

FGF4 promotes TNBC progression by activating IL6/STAT3 to reprogram macrophages into immune-suppressive M2 effectors, fostering a tumor-permissive microenvironment. Targeting FGF4 may disrupt this crosstalk, offering a novel immunotherapeutic strategy for TNBC.

Despite identifying these molecular features, poor prognosis was predicted, and no clinically actionable targets were detected, underscoring the need for future therapeutic development. This paradigm highlights molecular profiling as a critical adjunct to conventional diagnostics in maRPF, bridging the gap between histopathological ambiguity and biologically grounded clinical decision-making.

Our study results indicate that only specific types of FGFs and FGFRs may have a causal relationship with BC. Th research provides a new perspective on the mechanisms of action of different types of FGFs and FGFRs in BC, and offers potential genetic support for personalized medicine and precision therapy.

Moreover, SCC could carry canonical NSCLC) activating mutations. Our data suggest that deep molecular analyses resolve tumor heterogeneity and may help with new algorithm-based treatment strategies for SCC.

This study used ZHBTc4 ES cells, which have tetracycline-regulated Oct-4 expression, to explore the capabilities of EWS-Oct-4...Finally, comparative transcriptomic analysis revealed that ES cells expressing EWS-Oct-4 and those expressing Oct-4 had highly similar global gene expression profiles, with distinct variations in differentially expressed genes. These findings indicate that EWS-Oct-4 can effectively replace Oct-4, which has significant implications for advancements in stem cell research and regenerative medicine.