MET-H

We established HER3-and/or MET-KO SW1116 cell lines, and HER3/MET-double KO resulted in the inhibition of in vitro cell proliferation and in vivo tumor growth in nude mice by SW1116 cells. Furthermore, the combination of patritumab, an anti-HER3 fully human mAb, and PHA665752, a MET inhibitor, markedly inhibited in vitro cell proliferation, 3D-colony formation, and in vivo tumor growth in nude mice by SW1116 cells The dual targeting of HER3/MET has potential as CRC therapy.

Furthermore, CCN4 cells also exerted the prominent tumor-inhibitory effect on xenograft tumor growth. Collectively, this study suggests that DAP10 is a potent stimulator in CAR structure for NK cell activation, and CCN4-based immunotherapy may represent a promising strategy for the treatment of c-Met-positive LUAD.

Our findings reveal that HGF and TNFα are critical for the crosstalk between breast cancer cells and CAFs in the TME and that the HGF/c-Met signaling pathway is a promising therapeutic target for radiosensitizing breast cancer.

In our series, high c-MET expression correlated with poor survival outcomes. Further studies are warranted to validate the clinical relevance and applicability of c-MET as a prognostic factor in ER+/HER2- early BC.

Magnetic activated cell sorting was used to separate the CD44v6+ from CD44v6- cells, and Met levels were regulated using lentiviral particles and the selective Met inhibitor, PHA665752...Further, a cJun binding site was identified 1700 bp upstream of the Nanog transcription start site and mutation of the cJun binding site reduced Nanog expression. In conclusion, the HGF/Met signaling pathway is important for maintenance of stemness in CD44v6+ HCC cells by enhancing expression of cJun, which binds 1700 bp upstream of the Nanog transcription start site.

In this FIH phase I trial, CT053PTSA was well tolerated and had a satisfactory safety profile. Further trials evaluating the clinical activity of CT053PTSA are ongoing.

Teliso-V plus erlotinib showed encouraging antitumor activity and acceptable toxicity in EGFR TKI-pretreated patients with EGFR-M+, c-Met+ NSCLC.

In this study, simple NGS output data analysis from RNA-based NGS assay allowed reliable prediction of MET highamplification status in NSCLC. Although copy number variation analysis is usually restricted to DNA panels, this study shows that focused analysis can be useful to triage and select samples with candidate MET gene amplifications from an RNA-based NGS assay.

Targeting SIGLEC15 may offer a potential novel therapeutic opportunity for THCA patients. However, the detailed exact cellular mechanisms of SIGLEC15 in THCA still needed to be elucidated by further studies.

P2, N=3, Active, not recruiting, National Cancer Institute (NCI) | N=169 --> 3 | Trial completion date: Dec 2022 --> Sep 2023 | Trial primary completion date: Dec 2022 --> May 2022

P2, N=43, Completed, Armando Santoro, MD | Unknown status --> Completed