MET expression

These results indicate c-Met protein overexpression can be assessed before or after treatment since most patients maintain consistent c-Met status. As targeted therapies may elevate c-Met overexpression over time, retesting may be necessary in those with an oncogenic driver alteration initially diagnosed as c-Met negative.

Moreover, comprehensive in vitro and in vivo experiments demonstrate that nitidine significantly inhibits tumor progression through an LRPPRC-MET-G4-dependent mechanism. Collectively, our study suggests an epigenetic regulatory mechanism involving LRPPRC-MET-G4-mediated MET upregulation and provides a promising therapeutic strategy for MET-driven tumors using molecular glues that target the LRPPRC-MET-G4 interface.

In this study, we demonstrated that HOXA9 drove the expression of the fusion gene EPHB4-MET and exerted a tumorigenesis signature. HOXA9 may be a useful target for both diagnosis and treatment in patients with EPHB4-MET fusion genes in lung cancer.

Following discontinuation of Savolitinib due to drug-induced liver injury, Tislelizumab, previously associated with resistance, was reintroduced as a "rechallenge" successfully re-establishing disease control. Coupled with a systematic review of pertinent literature, this article explores the clinical features, therapeutic challenges, potential resistance mechanisms, and management approaches for such patients. It also outlines future research avenues for combination or sequential therapies, aiming to furnish a more holistic reference for clinical decision-making.

P2, N=252, Not yet recruiting, Shanghai Allink Biotherapeutics Co., Ltd.

HP BMSC transplantation correlates with early molecular events in acute liver failure mice, including upregulation of VEGF, HGF, and c-Met expression and changes in CD24⁺CD38⁺ B lymphocyte subsets, providing correlative evidence for involvement of the VEGF/c-Met pathway.

In HER3/c-Met dual-positive cell lines, SDP0505 demonstrated enhanced cell binding and internalization over the in-house synthesized U3-1402 analog...SDP0505 represents a novel HER3 × c-Met ADC with superior internalization and anti-tumor activity in preclinical models, especially in EGFR TKI-resistant PDX models. These results supported the initiation of a Phase I clinical trial in China.

Given the importance of plasma membrane-associated MET in initiating its canonical signaling cascades, as well as the demonstrated non-canonical signaling from nuclear localized MET in different tumor cell types and in response to various environmental stimuli, we developed assay capability to measure levels of pY1235MET and total MET within the plasma membrane or nucleus; these assays enable future explorations of the biological and clinical relevance of MET subcellular localization patterns. Finally, using tissue microarrays of over 50 resected tumor specimens from patients with colorectal carcinoma or non-small cell lung cancer, we demonstrated that tumor levels of pY1235MET do not always track total MET expression, suggesting that measurement of activated MET in tumor could hold potential as an independent biomarker to identify additional patients who might benefit from MET-directed targeted therapy-beyond those with tumor MET amplification, MET overexpression, or established MET-activating mutations.

P1, N=31, Active, not recruiting, AbbVie | Recruiting --> Active, not recruiting | Phase classification: P1/2 --> P1 | Trial completion date: Sep 2028 --> Dec 2027 | Trial primary completion date: Sep 2028 --> Dec 2027

Notably, the magnitude of OC effects correlated with MET expression, an established target of OC and a prognostic factor associated with reduced relapse-free survival within the triple-negative subtype. Collectively, these findings identify OC as a modulator of cancer cell metabolism and mitochondrial dynamics, with particular relevance in MET-high triple-negative breast cancers.

Vebreltinib plus an EGFR-TKI demonstrates favorable efficacy and manageable safety in real-world NSCLC patients with MET-driven resistance, with notable intracranial activity. Immunohistochemistry 3 + may serve as a practical predictive biomarker.

FAXDC2 acts as a tumor suppressor in HCC, and its knockdown promotes cell proliferation, migration, invasion, and EMT via upregulating c-Met expression and enhancing its phosphorylation in HepG2 cells. Therefore, the FAXDC2/c-Met axis may serve as a noval potential therapeutic target for HCC intervention.