MET mutation

A plasma sample serves as a supplement for identifying GPS when a tissue sample is unavailable. Moreover, the integration of FISH, NGS, and ddPCR provided a comprehensive assessment of MET amplification.

Primary and acquired MET mutations in NSCLC exhibit distinct genomic characteristics. Patients harboring concurrent EGFR mutations in NSCLC may derive less benefit from MET-TKI and ICI, whereas those harboring TP53 co-mutations tend to experience more favorable outcomes compared with TP53 wild-type NSCLC patients when treated with MET-TKI.

Our results further reveal that the MUC1-C-driven STAT1 inflammatory response promotes resistance of patient-derived (i) EGFR mutant NSCLC cells with MET amplification to the combination of osimertinib+MET TKIs, and (ii) EGFR(T790M/C797S) NSCLC cells to the 4th generation EGFR TKI TQB3804. Of clinical significance, we report that NSCLC cells dependent on MUC1-C for TKI resistance are druggable with an antibody-drug conjugate (M1C ADC) in vitro and in a PDX tumor model. These findings demonstrate that MUC1-C (i) is essential for TKI resistance of NSCLC cells by driving an inflammatory memory response and (ii) is a target for M1C ADC treatment of TKI-refractory NSCLCs.

Savolitinib plus osimertinib demonstrated numerically higher clinical activity versus savolitinib plus placebo in all patients and patients with higher MET biomarker cutoffs.

P2, N=100, Active, not recruiting, Gustave Roussy, Cancer Campus, Grand Paris | Trial primary completion date: Sep 2025 --> Apr 2028

The present study marks the initial discovery of MET exon 14 skipping and EGFR Del19 in a single patient, who achieved partial response through a treatment plan involving Osimertinib and Gumarontinib. These findings provide valuable perspectives on treatment approaches for individuals sharing similar genetic profiles.

These cells exhibited markedly enhanced cytotoxicity against tumour cells overexpressing c-Met, accompanied by increased release of key effector cytokines such as interferon-γ. This research framework offers a precise, synergistic therapeutic strategy to overcome limitations in CAR-T therapy response within serous ovarian carcinoma.

P1/2, N=862, Recruiting, DualityBio Inc. | Trial completion date: Jan 2028 --> May 2028 | Trial primary completion date: Sep 2027 --> Dec 2027

In summary, in advanced NSCLC, hybrid capture-based NGS, such as F1CDx, may capture more actionable genomic alterations as compared with ODxTT, an amplicon-based NGS.

In conclusion, we characterize the breadth of angiocentric glioma patterns in terms of demographics, anatomic location, and MYB fusion patterns. The updated molecular diagnosis of angiocentric glioma as of 2021 warrants continued exploration of the scope of MYB oncogene fusions as drivers of prognosis and targets for future therapies.

P1/2, N=231, Recruiting, Regeneron Pharmaceuticals | Active, not recruiting --> Recruiting

These data suggest SETD2-mutated lung adenocarcinoma presents at significantly earlier stages, has a unique molecular profile compared to non-mutated tumors, and trends towards improved RFS in early-stage tumors. Future study is warranted on both patient outcomes and immunopathologic characteristics of SETD2-mutated lung adenocarcinoma.