Publications by authors named "J Codony-Servat"
Background: KRAS-mutant non-small cell lung cancer (NSCLC) shows a relatively low response rate to chemotherapy, immunotherapy and KRAS-G12C selective inhibitors, leading to short median progression-free survival, and overall survival. The MET receptor tyrosine kinase (c-MET), the cognate receptor of hepatocyte growth factor (HGF), was reported to be overexpressed in KRAS-mutant lung cancer cells leading to tumor-growth in anchorage-independent conditions.
Methods: Cell viability assay and synergy analysis were carried out in native, sotorasib and trametinib-resistant KRAS-mutant NSCLC cell lines.
Purpose: High-mobility group box 1 protein (HMGB1) is subject to exportin 1 (XPO1)-dependent nuclear export, and it is involved in functions implicated in resistance to immunotherapy. We investigated whether HMGB1 mRNA expression was associated with response to immune checkpoint inhibitors (ICI) in non-small cell lung cancer (NSCLC).
Patients And Methods: RNA was isolated from pretreatment biopsies of patients with advanced NSCLC treated with ICI.
Vaccine antibodies against a synthetic epidermal growth factor variant enhance the antitumor effects of inhibitors targeting the MAPK/ERK and PI3K/Akt pathways.
Transl Oncol
February 2024
Article Synopsis
- The EGFR pathway helps some cancers resist treatments, but scientists are trying a new method using vaccines that create anti-EGF antibodies to improve drug effectiveness.
- In experiments with different cancer cell types, vaccines given to rabbits were used to create anti-EGF antibodies, which were tested alongside various cancer drugs.
- The results showed that these anti-EGF antibodies worked well with cancer drugs and helped stop cancer cells from growing, suggesting they could be used in future clinical trials for patients.
KRAS G12C mutations in non-small cell lung cancer (NSCLC) partially respond to KRAS G12C covalent inhibitors. However, early adaptive resistance occurs due to rewiring of signaling pathways, activating receptor tyrosine kinases, primarily EGFR, but also MET and ligands. Evidence indicates that treatment with KRAS G12C inhibitors (sotorasib) triggers the MRAS:SHOC2:PP1C trimeric complex.
View Article and Find Full Text PDFArticle Synopsis
- Lung cancer cells, particularly NSCLC, increase their ability to survive oxidative stress by upregulating the xCT transporter for cystine, which helps maintain high intracellular cysteine levels necessary for making glutathione.* -
- The NRF2 transcription factor regulates the xCT transporter and is kept in check by KEAP1; mutations in KEAP1 or NRF2 can enhance cystine uptake and support cancer cell survival, while limited cystine can lead to ferroptosis, a form of cell death.* -
- Targeted therapies in certain NSCLC types can trigger pyroptosis and apoptosis, leading to the breakdown of the cell membrane after caspase-3 activation, contributing to death of the cancer cells.*