FGF1 (Fibroblast Growth Factor 1)

Genetic silencing and pharmacological inhibition of RORγ (GSK805/XY101) suppressed proliferation, induced apoptosis in vitro, and significantly reduced xenograft tumor growth in vivo. Notably, RORγ antagonists synergized with pemigatinib to overcome resistance in pemigatinib-refractory models. Collectively, these findings identify the RORγ-FGF1-FGFR2 axis as a critical oncogenic driver in iCCA and highlight RORγ inhibition as a promising therapeutic strategy to suppress tumor progression and enhance sensitivity to FGFR inhibitors.

These glial inputs involve astrocytic neurexins and the perineuronal net (PNN) component phosphacan, suggesting both intrinsic and extrinsic mechanisms underlie FGF1-induced AgRP silencing. Combined with evidence that FGF1 increases assembly in the arcuate nucleus, our findings reveal a cell-type-specific model for how FGF1 elicits long-term reprogramming of hypothalamic circuits to achieve diabetes remission.

Overall, our findings indicate that three biomolecules (5A-Androstan-3B,17B-diol, 17A-methyl; Kaurenoic acid; and Humulene) from PF have the potential to exert therapeutic effects on multiple targets in the 'Pathways in Cancer' pathway.

The identified 9 hub genes demonstrate significant potential as reliable diagnostic biomarkers for mCRC. Moreover, these molecular markers may contribute to disease pathogenesis through their dynamic interactions with tumor-infiltrating immune cells, suggesting a crucial role in the tumor microenvironment.

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.

Recent findings suggest that its tumorigenesis and FGF23 overproduction depend on the FGFR1 pathways, which may be activated via FN1::FGFR1 or FN1::FGF1 fusion, as well as by α-Klotho overexpression in the majority of fusion-negative PMTs. This review discusses the clinical, histologic, immunohistochemical, and molecular genetic features, along with potential therapies and differentiation from potential mimics.

Overall, our study reveals two circRNAs that might have a potential role in primary to metastasis transition in the BRAF-mutated melanoma within TIME via the circRNA-miRNA-mRNA axis.

Among tested mutants, FGF1HSBCD exhibits the highest affinity for heparin and HS/HSPGs, showing over 20-fold increase in affinity for glypican-4 and requiring 0.23 M higher salt concentration for elution from heparin column compared to the initial FGF1HS molecule. Finally, we demonstrated FGF1HSBCD potential to act as a molecular sensor of HSPGs level in cancer cell lines overproducing HSPGs, implicating that FGF1HSBCD can be used as HSPGs biosensor or as a drug delivery carrier in protein-drug conjugates (PDC) targeting HSPGs.

Besides radionuclides, eFGF1 can also deliver doxorubicin (DOX) into cancer cells. Considering these characteristics, eFGF1-DOTA-Tb[161Tb] and eFGF1-DOX emerge as promising candidates for FGFR-targeted cancer therapy, and further evaluation in vivo is warranted.

P=N/A, N=288, Recruiting, University of Milano Bicocca | Not yet recruiting --> Recruiting

In addition, we showed that cells obtained by long-term exposure to taltobulin are resistant to both taltobulin and other microtubule-targeting drugs, and exhibit elevated levels of FGFR1 and cyclin D. We also found that the presence of FGF-ligand trap prevents the development of long-term resistance to taltobulin. Our results shed light on how blocking the FGF1/FGFR1 axis by honokiol and FGF ligand trap could help develop more effective cancer therapies, potentially preventing the emergence of drug-resistant relapses.

P=N/A, N=288, Not yet recruiting, University of Milano Bicocca