HGF (Hepatocyte growth factor)

While TNF-α and HGF/IL-12p40 showed promise, most inflammatory biomarkers demonstrated limited accuracy, specifically for outcome prediction in CD; however, this does not preclude their potential usefulness for other clinical or experimental applications. Current evidence does not support the clinical use of this approach and further studies are needed.

These results suggest that cardiac surgery with CPB increases the plasma levels of several growth factors, thus potentially promoting pancreatic cancer cell proliferation, as seen in the in vitro study using serum from non-cancer patients.

Pharmacological inhibition of FAK with single agent VS-4718 did not significantly reduce macroscopic tumor volume; however, its use in combination with the mitogen-activated protein kinase kinase (MEK) inhibitor selumetinib resulted in both a significant reduction in tumor volume and the preservation of dorsal root ganglion architecture. Our findings establish a critical role for FAK in schwannoma development and provide rationale for evaluation of combination FAK plus MEK inhibition in future clinical trials for NF2-associated SWN.

CXCL1/CXCR2 and HGF/c-MET may represent compensatory pathways that sustain proliferation and survival in resistance to KRASG12C inhibitors. The simultaneous blockade of these signals may offer a novel strategy for bypassing resistance.

The results of this study may help develop an effective treatment for EGFR-TKI-mediated rashes. The findings will be published in academic journals upon the completion of the trial.

Notably, MI102 effect exhibited superior tumor cell selectivity compared with the MET inhibitor tivantinib. At the transcriptional level, RNA-seq revealed that MI102 globally downregulated MYCN-associated oncogenic programs. Collectively, these findings establish pharmacological downregulation of MYCN as a promising therapeutic strategy for HCC and reveal a functional link between MET signaling and MYCN-driven oncogenic pathways.

Furthermore, CYH33 possessed potent activity against the growth of LUSC with hyperactivated PI3K signaling. Collectively, the dual-targeting of CYH33 that directly blocked PI3Kα in tumor cells and disrupted CAF-mediated pro-metastatic signaling supported PI3Kα inhibitors as a potential therapeutic approach for advanced LUSC.

MET-altered NSCLC is a challenging and heterogeneous molecular subset, and our knowledge is rapidly evolving. Work is ongoing to define the spectrum of actionable mutations, to develop standardized and clinically meaningful biomarker-driven identification of these alterations, and to determine the most effective treatment approaches, with the goal of expanding the treatment landscape and improving outcomes for a subset of patients with limited treatment options.

GSCC is a highly malignant tumor with a poor prognosis. Whether immune-related drugs are optimal for metastatic GSCC requires further exploration.

In conclusion, the strategy of using the interface residues has been successfully explored for the discovery of new c-Met binders. [68Ga]Ga-SMIC-1014 shows a high tumor imaging performance and potential as a c-Met-targeted diagnostic probe.

CD177+ neutrophils drive liver regeneration by promoting endothelial transmigration, ECM degradation and HGF-α release. These findings reveal a neutrophil-mediated mechanism driving surgical liver regeneration and support the potential of CD177+ neutrophil infusion to establish a proregenerative hepatic environment for therapeutic strategies in liver failure.

Notably, this function is absent from the closely related MST1R/RON RTK, suggesting it is a unique feature of the MET receptor. Together, these findings uncover a previously unrecognized layer of MET regulation with potential implications for the development of selective therapies targeting MET-driven cancers.