Functional outcomes and survival after surgical stabilization for inoperable non-small-cell lung cancer with spinal metastasis of the thoracic and lumbar spines: a retrospective comparison between epidermal growth factor receptor-tyrosine kinase inhibitor and platinum-based chemotherapy groups.
The proportions of adenocarcinoma, never-smokers, and metastasis to the liver were higher in the exon 20 in-frame insertion mutation group, whereas coexistence of EGFR mutation was more frequently found in the HER2 amplification group.
Distant metastasis was found in 9 of 41 patients (22.0%) and 6 of 15 patients (40.0%) with high expression of MET and high co-expressions of EGFR and MET, respectively; statistically significant differences were detected in both high expression of MET (P = .003) and high co-expressions of EGFR and MET (P = 3.41 × 10<sup>-5</sup> ).
These results indicate that extracts of <i>A nantoensis</i> could inhibit signal transduction at least involved in EGFR as well as the PI3K/AKT and Ras-ERK pathways, which are crucial players of tumor cell migration and invasion.
The concordance rate demonstrated the feasibility of EGFR mutations in corresponding metastases using Amplification Refractory Mutation System when the primary tumor tissue is unavailable in the lung adenocarcinoma patients, and the inconsistency indicates that corresponding metastasis being screened simultaneously with the primary tumor samples may present some supplementary information for the patients.
VPS33B overexpression suppressed CRC proliferation, intrahepatic metastasis and chemoresistance of cisplatin (DDP) in vivo and in vitro through modulating the epidermal growth factor receptor (EGFR)/RAS/ERK/c-Myc/p53/miR-133a-3p feedback loop and the downstream cell cycle or EMT-related factors.
The results indicate that CUL1 knockdown prohibited the metastasis behaviors of breast cancer cells through downregulation (dephosphorylation) of the EMT signaling pathways of EGFR and Akt/GSK3β/β-catenin in breast cancer.
Six independent prognostic factors including sex (P = 0.008), the presence of visceral metastasis (P = 0.008), the number of metastases in the vertebral body (P = 0.011), Frankel score (P < 0.001), D-dimer (P = 0.002), and sensitive epidermal growth factor receptor mutation (p < 0.001) were identified and entered into the nomogram.
Conclusions Incorporation of EGFR mutation status in advanced NSCLC further differentiates survival curves of M categories in 8th TNM classification and more precisely predicts survival compared to number of metastasis or number of metastatic sites alone.
Several of these pathways including AKT, EGFR, and mTOR are known to contribute to tumor development and metastasis, and cannabinoids may reverse their effects, thereby by inducing apoptosis, autophagy and modulating the immune system.
Furthermore, miR-103a-3p inhibited growth and metastasis via effects on the KRAS pathway and epithelial-to-mesenchymal transition in EGFR wild-type NSCLC cell lines, respectively, which substantially reduced EGFR expression and activity.
Altogether, our findings unravel the interplay between integrin-α2β1/-α5β1 and EGFR in anoikis resistance and suggest that the resistant cells are cancer initiating or cancer stem cells, which may serve as a promising target to combat metastasis of cancer.